Objective:To evaluate the efficacy of ultrasound-guided superior laryngeal nerve block(SLNB) combined with intravenous anesthesia for improving pediatric fiberoptic bronchoscopy.Methods:Forty pediatric patients of either sex, aged 3-6 yr, of American Society of Anesthesiologists Physical Status classificationⅠor Ⅱ, with body mass index of 18-24 kg/m 2, undergoing fiberoptic bronchoscopy in Cangzhou Central Hospital in 2022, were divided into 2 groups ( n=20 each) by a random number table method: ultrasound-guided SLNB plus intravenous anesthesia group (group A) and topical anesthesia plus intravenous anesthesia group (group B). After sedation with dexmedetomidine and esketamine, ultrasound-guided bilateral SLNB was performed with 1% lidocaine 0.5 ml (for each side)in group A, and topical anesthesia was performed with 1% lidocaine in nasal and pharyngeal cavities in group B. After completion of the surgery procedure, propofol was continuously infused at 5 mg·kg -1·h -1 until completion of diagnosis and treatment. An increment of propofol 1 mg/kg was intravenously given if severe bucking or body movement occurred during operation. Mean arterial pressure (MAP), heart rate (HR) and SpO 2 were recorded on admission to the operating room (T 0), immediately after sedation (T 1), immediately after bronchoscopy entering the glottis (T 2), 5 min after start of treatment (T 3) and at the end of examination (T 4). The occurrence of intraoperative hypoxemia, HR <60 bpm, and MAP <50 mmHg were recorded, and the additional dose of propofol was recorded. The venous blood samples were collected at T 0 and T 4 to determine plasma cortisol concentrations by chemiluminescence.The surgeon′s satisfaction score was recorded. The complications of SLNB were also recorded within 2 h after operation in group A. Results:Compared with group B, HR was significantly decreased at T 2 and T 3, SpO 2 was increased, the intraoperative additional dosage of propofol and incidence of hypoxemia were decreased, and the surgeon′s satisfaction score was increased, and the concentrations of cortisol were decreased at T 4 in group A ( P<0.05). No HR<60 bpm and MAP<50 mmHg were found in two groups. No SLNB-related complications were observed after operation in group A. Conclusions:Ultrasound-guided SLNB combined with intravenous anesthesia is safer for pediatric fiberoptic bronchoscopy and can improve the analgesic effect and is more helpful in inhibiting intraoperative stress responses when compared with conventional anesthesia.
Objective:To evaluate the role of transient receptor potential vanillic acid 4 (TRPV4) in dexmedetomidine-induced improvement in cognitive function in mice with mechanical ventilator-caused brain injury.Methods:Ninety clean-grade healthy male C57BL6 mice, weighing 20-25 g, aged 8-12 weeks, were divided into 5 groups ( n=18 each) using a random number table method: control group (group C), mechanical ventilation group (group V), HC-067047 group (group H), dexmedetomidine group (group D), and dexmedetomidine+ GSK1016790A group (group DG). In group C, the animals breathed air spontaneously for 6 h without mechanical ventilation. In group V, the animals were mechanically ventilated for 6 h. In group H, TRPV4 blocker HC-067047 10 mmol was injected into the cerebral ventricle at 3 and 6 h of mechanical ventilation. In D and DG groups, dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before mechanical ventilation. In group DG, TRPV4 agonist GSK1016790A 5 μmol was injected into the cerebral ventricle at 60 min before mechanical ventilation. Morris water maze test was performed on 6 mice in each group at 1 day before mechanical ventilation and 3 and 7 days after mechanical ventilation. Six mice in each group were randomly selected and sacrificed at 1 day after mechanical ventilation, and the brain tissue was taken for determination of the neuronal apoptosis in hippocampal CA1 area by TUNEL method, and the apoptosis index was calculated. Six mice in each group were randomly selected and sacrificed at 1 day after mechanical ventilation, and the hippocampal tissues were taken for determination of the expression of TRPV4, serine-threonine protein kinase (Akt), phosphorylated Akt (p-Akt), Bcl-2, Bax and caspase-3 by Western blot. Results:Compared with group C, the escape latency was significantly prolonged and the number of crossing the original platform was reduced at 3 and 7 days after mechanical ventilation, the expression of TRPV4 and caspase-3 was up-regulated, the ratio of Bcl-2/Bax was decreased, and the apoptosis index of neurons was increased in group V and group DG ( P<0.05). Compared with group V, the escape latency was significantly shortened and the number of crossing the original platform was increased at 3 and 7 days after mechanical ventilation, the expression of TRPV4 and caspase-3 was down-regulated, the expression of p-Akt was up-regulated, the ratio of Bcl-2/Bax was increased, and the apoptosis index of neurons was decreased in group D and group H ( P<0.05). Compared with group D, the escape latency was significantly prolonged at 3 and 7 days after mechanical ventilation, the number of crossing the original platform was reduced, the expression of TRPV4 and caspase-3 was up-regulated, the expression of p-Akt was down-regulated, the ratio of Bcl-2/Bax was decreased, and the apoptosis index of neurons was increased in group DG ( P<0.05). Conclusions:TRPV 4 is involved in dexmedetomidine-induced improvement in cognitive function, which is related to up-regulation of p-Akt expression and inhibition of apoptosis in hippocampal neurons in mice with mechanical ventilation-caused brain injury.
Objective:To evaluate the role of transient receptor potential vanilloid receptor 1 (TRPV1)/nuclear factor-κB (NF-κB) signaling pathway in dexmedetomidine-induced alleviation of ventilator-induced lung injury (VILI) in rats.Methods:One hundred clean-grade healthy male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 5 groups ( n=20 each) using a random number table method: control group (group C), VILI group (group V), AMG9810 group (group A), dexmedetomidine group (group D), and dexmedetomidine + RTX group (group DR). VILI model was prepared by mechanical ventilation with a tidal volume of 40 ml/kg for 4 h. In group A, TRPV1 inhibitor AMG9810 30 mg/kg was intraperitoneally injected at 1 h before mechanical ventilation.Dexmedetomidine 5.0 μg/kg was intravenously infused at 20 min before mechanical ventilation, and dexmedetomidine was intravenously infused at the rate of 5.0 μ g·kg -1·h -1 during ventilation in group D and group DR.In group DR, RTX 70 μ g/kg was intraperitoneally injected for 3 consecutive days before mechanical ventilation.At 4 h of mechanical ventilation, the concentrations of interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and IL-6 in bronchoalveolar lavage fluid (BALF) were detected, oxygenation index (OI) and wet/dry lung weight (W/D) ratio were measured, the histopathological changes of lung tissues were observed, and lung injury was assessed and scored.The expression of TRPV1 and NF-κB in lung tissues was detected by Western blot, and real-time polymerase chain reaction was used to detect the expression of TRPV1 and NF-κB mRNA. Results:Compared with group C, the concentrations of IL-1β, TNF-α and IL-6 in BALF were significantly increased, OI was decreased, the W/D ratio and lung injury scores were increased, and the expression of TRPV1 and NF-κB protein and mRNA was up-regulated in group V ( P<0.05). Compared with group V, the concentrations of IL-1β, TNF-α and IL-6 in BALF were significantly decreased, OI was increased, the W/D ratio and lung injury scores were decreased, and the expression of TRPV1 and NF-κB protein and mRNA was down-regulated in A, D and DR groups ( P<0.05). Compared with group D, the concentrations of IL-1β, TNF-α and IL-6 in BALF were significantly increased, OI was decreased, the W/D ratio and lung injury scores were increased, and the expression of TRPV1 and NF-κB protein and mRNA was up-regulated in group DR ( P<0.05). Conclusions:The mechanism by which dexmedetomidine alleviates VILI is partially related to inhibition of the activation of TRPV1/NF-κB signaling pathway and inhibition of the inflammatory responses in lung tissues of rats.
Objective:To investigate the effect of baicalin on cognitive function of mice with brain injury induced by mechanical ventilation and its mechanism.Methods:Seventy two C57BL6 mice, weighing 20-25 g, aged 8-12 weeks, were randomly divided into control group (group C), mechanical ventilation group (group V), baicalin group (group B), baicalin+ Akt inhibitor MK-2206 group (group BM) according to random number table method, with 18 in each group.Mice in group C did not have mechanical ventilation and breathed air independently for 6 hours.Mice in group V received mechanical ventilation for 6 hours.Mice in group B and group BM were intraperitoneally injected with baicalin 100 mg/kg 30 minutes before mechanical ventilation, and mice in group BM were injected intraventricular with Akt inhibitor MK-2206 300 μg/kg 60 minutes before mechanical ventilation.Six mice in each group were randomly selected to test their learning and memory abilities by Morris water maze test 1st day before mechanical ventilation and 3rd day and 7th day after mechanical ventilation.One day after mechanical ventilation, six mice in each group were killed, and the brain tissue was taken.TUNEL method was used to detect the neuronal apoptosis in hippocampal CA1 area, and the apoptosis index was calculated.One day after mechanical ventilation, six mice in each group were killed, and the hippocampus was taken, Western blot was used to detect the protein expressions of caspase-3, caspase-9, Akt, p-Akt, GSK-3β and p-GSK-3β.SPSS 22.0 software was used for statistical analysis of data, repeated measure ANOVA and one-way ANOVA were used for comparison between multiple groups.LSD- t test was used for further pairwise comparison. Results:The results of water maze test showed that the time and group interaction of the four groups were not significant ( F=1.14, P>0.05), the main effect of time and group were both significant ( F=47.36, 59.65, both P<0.05). At 3rd day and 7th day after mechanical ventilation, the escape latencies of mice in group V were higher than those in group C (both P<0.05), and the numbers of platform crossing were lower than those in group C (both P<0.05). And 3 days and 7 days after mechanical ventilation, the escape latencies of mice in group B were lower than those in group V (both P<0.05) and the numbers of platform crossing were higher than those in group V (both P<0.05). The escape latenies of mice in BM group on the 3rd and 7th day were higher than those in group B (both P<0.05), and the numbers of platform crossing were lower than those in group B on the 3rd day and 7th day after mechanical ventilation(both P<0.05). TUNEL and Western blot results showed that apoptosis index of hippocampal neurons and expression levels of apoptosis-related proteins caspase-3 and caspase-9 were significant different in the four groups ( F=51.42, 41.21, 40.19, all P<0.05). The apoptosis index of hippocampal neurons ((40.6±3.9)%), the expression levels of caspase-3 (4.93±0.92) and caspase-9 (4.81±0.88) in the hippocampus of mice in group V were higher than those in group C ((13.7±1.4)%, (1.87±0.27), (1.71±0.25), all P<0.05), the apoptosis index of hippocampal neurons ((15.6±1.6)%), the expression levels of caspase-3 (1.95±0.30) and caspase-9 (1.76±0.28) in group B were lower than those in group V ((40.6±3.9)%, (4.93±0.92), (4.81±0.88), all P<0.05), the apoptosis index of hippocampal neurons ((27.8±2.7)%), the expression levels of caspase-3 (3.58±0.61) and caspase-9 (3.49±0.57) in BM group were higher than those in group B ((15.6±1.6)%, (1.95±0.30), (1.76±0.28), all P<0.05). Expression level of p-Akt, p-GSK-3β in hippocampal tissues of the four group of mice were significantly different ( F=37.54, 43.23, both P<0.05). The expression level of p-Akt (0.51±0.06) and p-GSK-3β (0.47±0.05) of hippocampal tissues of mice in group V were lower than those of group C ((1.07±0.10), (1.11±0.12), both P<0.05), the expression level of p-Akt (0.99±0.10) and p-GSK-3β (1.08±0.09) of hippocampal tissues of mice in group B were higher than those of group V (both P<0.05), the expression level of p-Akt (0.83±0.08) and p-GSK-3β (0.81±0.07) of hippocampal tissues of mice in group BM were lower than those in group B (both P<0.05). Conclusion:Baicalin can improve the cognitive function of mice with brain injury induced by mechanical ventilation, which is related with activation of Akt/GSK-3β signaling pathway and inhibition of hippocampal neuron apoptosis.
Objective:To evaluate the effects of dexmedetomidine on alveolar epithelial barrier function in rats with ventilator-induced lung injury (VILI), and the role of protein kinase C (PKC).Methods:One hundred clean-grade male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 5 groups ( n=20 each) using a random number table method: control group (group C), VILI group (group V), PKC inhibitor group (group B), dexmedetomidine group (group D), and dexmedetomidine plus PKC agonist group (DP group). The VILI model was developed by mechanical ventilation with a tidal volume of 40 ml/kg for 4 h in anesthetized animals.Group C breathed air autonomously for 4 h without mechanical ventilation.Group V was mechanically ventilated for 4 h. In group B, bisindolvlmaleimide I 0.12 mg/kg was injected intramuscularly 1 h before mechanical ventilation.In D and DP groups, dxmedetomidine 5.0 μg/kg was injected intravenously at 20 min before mechanical ventilation, and dexmedetomidine was intravenously infused at the rate of 5.0 μg·kg -1·h -1 during mechanical ventilation.In group DP, PKC agonist phorbol-12-myristic acid-13-acetate 15 μg/kg was intraperitoneally injected at 30 min before mechanical ventilation.At 4 h of mechanical ventilation, oxygenation index (OI), lung permeability index (LPI) and wet/dry lung weight (W/D) ratio were measured, the pathological changes of lung tissues were observed, and lung injury was assessed and scored.The expression of PKC, occludin and ZO-1 protein was detected by Western blot, and the expression of PKC mRNA, occludin mRNA and ZO-1 mRNA was determined by real-time polymerase chain reaction. Results:Compared with group C, OI was significantly decreased, LPI, W/D ratio and lung injury score were increased, the expression of PKC protein and mRNA was up-regulated, and the expression of occludin and ZO-1 protein and mRNA was down-regulated in V and DP groups ( P<0.05), and no significant change was found in the parameters mentioned above in B and D groups ( P>0.05). Compared with group V, OI was significantly increased, LPI, W/D ratio and lung injury score were decreased, the expression of PKC protein and mRNA was down-regulated, and the expression of occludin and ZO-1 protein and mRNA was up-regulated in B, D and DP groups ( P<0.05). Compared with group D, OI was significantly decreased, LPI, W/D ratio and lung injury score were increased, the expression of PKC protein and mRNA was up-regulated, and the expression of occludin and ZO-1 protein and mRNA was down-regulated in group DP ( P<0.05). Conclusions:Dexmedetomidine can reduce the damage to alveolar epithelial barrier function in rats with VILI, and the mechanism is related to inhibition of PKC activation and up-regulation of the expression of occludin and ZO-1.
Objective:To evaluate the relationship between the mechanism underlying methylprednisolone-induced alleviation of ventilator-induced lung injury (VILI) and p38 mitogen-activated protein kinase (p38 MAPK)/nucleotide binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) pathway in lung tissues of rats.Methods:Sixty clean-grade male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 3 groups ( n=20 each) using a random number table method: control group (group C), mechanical ventilation group (group V), and methylprednisolone group (group M). Group C breathed air spontaneously for 4 h without mechanical ventilation.Group V was mechanically ventilated (RR 40 times/min, V T 40 ml/kg, I∶E 1∶1, PEEP 0, FiO 2 21%) for 4 h. Group M received intravenous methylprednisolone 10 mg/kg at 20 min before mechanical ventilation.At 4 h of mechanical ventilation, broncho-alveolar lavage fluid (BALF) was collected to measure the concentrations of interleukin-1beta (IL-1β), IL-18, and tumor necrosis factor-alpha (TNF-α) and wet/dry lung weight ratio (W/D ratio), and lung tissues were obtained for microscopic examination of the histopathological changes and for detection of the expression of p38MAPK, phosphorylated p38MAPK (p-p38MAPK), NLRP3, apoptosis-related speck-like protein containing a CARD (ASC), and cysteinyl aspartate-specific protease-1 (caspase-1) (using Western blot). Results:Compared with group C, the W/D ratio of lung tissues and concentrations IL-1β, IL-18 and TNF-α in BALF were significantly increased, and the expression of p-p38MAPK, NLRP3, ASC and caspase-1 was up-regulated in group V ( P<0.05), and no significant change was found in group M ( P>0.05). Compared with group V, the W/D ratio of lung tissues and concentrations of IL-1β, IL-18 and TNF-α in BALF were significantly decreased, and the expression of p-p38MAPK, NLRP3, ASC and caspase-1 was down-regulated in group M ( P<0.05). Conclusion:The mechanism by which methylprednisolone alleviates VILI may be related to inhibition of p38MAPK/NLRP3 pathway activity and reduction of inflammatory responses in lung tissues of rats.
Objective:To explore the predictive effect of brachial artery peak velocity variation (ΔVp) during end expiratory occlusion (EEO) on volume response in elderly patients.Methods:Elderly patients planning to undergo elective gastrointestinal surgery under general anesthesia, American Society of Anesthesiologists (ASA) ⅠorⅡ, cardiac function ⅠorⅡ, after anesthesia induction, EEO and volume expansion (VE) tests were successively performed in all patients. The hemodynamic indexes such as mean arterial pressure (MAP), heart rate (HR) and central venous pressure (CVP) were recorded before EEO, during EEO, before VE, after VE. Meanwhile, stroke volume variation (SVV) before EEO, the difference (Δ) before and after the experiment was recorded and calculated. At the timepoints before EEO and before VE, the peak velocity of brachial artery was measured by ultrasound while the variation peak velocity of brachial artery (ΔVp) was calculated. Patients with increment rate of stroke volume (ΔSV) ≥15% were included in the responders group and ΔSV<15% in the non-responders group. A total of 84 patients were included, 43 patients in the responders group while 41 patients in the non-responders group. The receiver operating characteristic curve (ROC) curve was used to evaluate the predictive effect of each index on volume responsiveness.Results:Before and after EEO and VE, ΔMAP and ΔSV in the responders group were significantly higher than those values in the non-responders group ( P<0.05). there was no significant difference of ΔHR and ΔCVP between the two groups ( P>0.05). During EEO and before VE, ΔVp in the responders group were significantly higher than those values in the non-responders group ( P<0.05). The SVV in the responders group before EEO is significantly higher than that value in the non-responders group ( P<0.05). Area under the curve (AUC) of ΔVp, ΔMAP, ΔHR, ΔCVP in the EEO experiment and SVV before EEO by predicted fluid responsiveness were 0.862, 0.615, 0.514, 0.524, 0.797, respectively. The AUC of ΔMAP, ΔHR, ΔCVP in VE experiment and ΔVp before VE by predicted fluid responsiveness were 0.667, 0.521, 0.542, 0.779, respectively. During EEO, ΔVp≥30.2% is the cut off value;the sensitivity is 91.1%, the specificity is 81.8%. SVV≥8.7% before EEO is the cut off value. The sensitivity is 84.5% while the specificity is 73.4%. ΔVp≥27.6% before VE is the cut off value; the sensitivity is 81.5% while the specificity is 72.8%. Conclusions:During EEO, ΔVp≥30.2% could effectively predict fluid responsiveness of elderly patients during operation.
目的 评价甲泼尼龙对呼吸机相关性肺损伤(VILI)大鼠肺组织瞬时受体电位香草酸4(TRPV4)/基质金属蛋白酶2/9(MMP-2/MMP-9)信号通路的影响.方法 清洁级雄性SD大鼠100只,采用随机数字表法分为5组(n=20):对照组(C组)、机械通气组(V组)、甲泼尼龙组(Mp组)、甲泼尼龙+GSK1016790A组(MpG组)、HC-067047组(H组).C组不行机械通气,自主呼吸空气4 h;V组机械通气(RR 40次/min,VT 40 mL/kg,I:E 1:1,PEEP 0,FiO221%)4 h;Mp组在机械通气前20 min静脉输注甲泼尼龙10.0 mg/kg;MpG组在给予甲泼尼龙前20 min静脉输注GSK1016790A 0.025 mg/kg;H组机械通气前30 min静脉输注HC-06704710.0 mg/kg.机械通气4 h时,检测支气管肺泡灌洗液(BALF)中白细胞介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)、总蛋白浓度,测定肺通透指数(LPI)、肺湿/干质量比(W/D),观察肺组织病理学结果.Western blot法检测肺组织TRPV4、MMP-2、MMP-9的表达水平.结果 与C组比较,V组和MpG组BALF中IL-1(ng/mL:84.56±5.35 vs.144.85±9.39、121.56±7.69)、TNF-α(ng/mL:179.65±45.73 vs.486.18±94.79、316.93±69.71)、总蛋白(mg/mL:321.29±28.76 vs.687.78±65.78、476.39±46.67)升高,肺组织LPI[(2.47±0.17)×10-3 vs.(6.19±0.29)×10-3、(4.24±0.25)×10-3]、W/D比值(4.42±0.19 vs.8.83±0.61、6.32±0.41)升高,TRPV4(1.85±0.25 vs.5.81±0.92、3.87±0.65)、MMP-2(0.44±0.06 vs.1.16±0.23、0.85±0.11)、MMP-9(0.19±0.03 vs.0.46±0.09、0.34±0.07)表达上调(P<0.05);与V组比较,Mp组、MpG组和H组BALF中IL-1(ng/mL:144.85±9.39 vs.89.78±5.91、121.56±7.69、94.23±6.78)、TNF-α(ng/mL:486.18±94.79 vs.186.42±49.37、316.93±69.71、193.71±51.41)、总蛋白(mg/mL:687.78±65.78 vs.348.78±31.52、476.39±46.67、359.68±36.12)降低,肺组织LPI[(6.19±0.29)×10-3 vs.(2.85±0.14)×10-3、(4.24±0.25)×10-3、(2.97±0.21)×10-3]、W/D比值(8.83±0.61 vs.4.75±0.22、6.32±0.41、4.82±0.25)降低,TRPV4(5.81±0.92 vs.2.13±0.29、3.87±0.65、2.35±0.37)、MMP-2(1.16±0.23 vs.0.48±0.08、0.85±0.11、0.52±0.08)、MMP-9(0.46±0.09 vs.0.22±0.04、0.34±0.07、0.25±0.05)表达下调(P<0.05),肺组织病理损伤减轻;与Mp组比较,MpG组BALF中IL-1(ng/mL:89.78±5.91 vs.121.56±7.69)、TNF-α(ng/mL:186.42±49.37 vs.316.93±69.71)、总蛋白(mg/mL:348.78±31.52 vs.476.39±46.67)升高,肺组织LPI[(2.85±0.14)×10-3 vs.(4.24±0.25)×10-3]、W/D比值(4.75±0.22 vs.6.32±0.41)升高,TRPV4(2.13±0.29 vs.3.87±0.65)、MMP-2(0.48±0.08 vs.0.85±0.11)、MMP-9(0.22±0.04 vs.0.34±0.07)表达上调(P<0.05).结论 甲泼尼龙可减轻大鼠VILI,与其抑制TRPV4/MMP-2/MMP-9信号通路有关.
Objective: We evaluated the efficacy of electroacupuncture combined with tropisetron in treating carboprost tromethamine-induced nausea and vomiting during cesarean section under lumbar anesthesia. Methods: A total of 264 patients aged 22-40 years were enrolled, who received carboprost tromethamine and suffered nausea and vomiting during cesarean section under lumbar anesthesia. The patients were divided randomly into the control group, electroacupuncture group, tropisetron group, and electroacupuncture + tropisetron group. Results: Compared to the control group, the nausea and vomiting scores decreased at T-3 in both the electroacupuncture and electroacupuncture + tropisetron groups, and decreased at T-4 in the electroacupuncture group, tropisetron group, and electroacupuncture + tropisetron group; the motilin, gastrin, and 5-hydroxytryptamine (5-HT) levels decreased at T-5 in the other 3 groups. Compared to the electroacupuncture + tropisetron group, the nausea and vomiting scores increased at T-3 in the control and tropisetron groups, and increased at T-4 in the other 3 groups; the motilin, gastrin, and 5-HT levels increased at T-5. Conclusions: Our study suggested that electroacupuncture combined with tropisetron could effectively relieve carboprost tromethamine-induced nausea and vomiting during cesarean section under lumbar anesthesia. The effect was better than its single application, and the reduced 5-HT, motilin, and gastrin levels might be involved in the underlying mechanism.
Objective:To evaluate the accuracy of lung recruitment maneuver (LRM) combined with brachial artery peak velocity variation (ΔVp) in predicting fluid responsiveness.Methods:Sixty-four patients of both sexes, aged 18-64 yr, with body mass index 19-26 kg/m 2, of American Society of Anesthesiologists physical status Ⅰor Ⅱ, with New York Heart Association class Ⅰor Ⅱ, scheduled for elective open gastrointestinal surgery under general anesthesia, were enrolled in this study.LRM (positive airway pressure was maintained at 30 cmH 2O for 10 s) and volume loading test were performed in sequence after anesthesia induction.ΔVp was measured by ultrasonography at the beginning of LRM.Mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP) and stroke volume (SV) were recorded before LRM (T 1), during LRM (T 2), before volume expansion (T 3) and after volume expansion (T 4). The changing rate of each index before and after LRM (ΔMAP LRM, ΔHR LRM, ΔCVP LRM, ΔSV LRM) and before and after volume expansion (ΔMAP VE, ΔHR VE, ΔCVP VE, ΔSV VE) were calculated.ΔSV VE≥15% was considered to be a positive response after volume expansion, and patients were divided into response group (≥ 15%, R group) and non-response group (< 15%, NR group). Results:There were 34 cases in R group and 30 cases in NR group.Compared with NR group, MAP at T 2 and SV at T 1, 2 were significantly decreased, ΔMAP LRM, ΔMAP VE, ΔSV LRM and ΔSV VE were increased, and ΔVp was increased in group R ( P<0.05). There was a positive correlation between ΔVp and ΔSV VE ( r=0.829, P<0.05), a negative correlation between ΔSV LRM and ΔSV VE ( r=-0.876, P<0.05), and a negative correlation between ΔVp and ΔSV LRM ( r=-0.819, P<0.05). The area under the receiver operating characteristic curve of LRM combined with ΔVp was 0.808, and the cut-off value was 32.3%, the sensitivity 75.3%, and the specificity 88.2%. Conclusion:LRM combined with ΔVp (≥32.3%) can accurately predict the intraoperative fluid responsiveness in patients.
Objective:To evaluate the effect of dexmedetomidine on the extracellular signal-regulated kinase(ERK)/sodium-potassium ATPase(Na + -K + -ATPase)signaing pathway in lung tissues of rats with mechanical ventilation-induced lung injury (VILI). Methods:Forty-eighty clean-grade male Sprague-Dawley rats, weighing 270-320 g, aged 4-5 months, were divided into 4 groups ( n=12 each) using a random number table method: control group (group C), VILI (alpha2-adrenergic receptor antagonist) group (group V), dexmedetomidine group (group D), and dexmedetomidine plus yohimbine group (group DY). Group C underwent no mechanical ventilation and breathed air spontaneously for 4 h. Mechanical ventilation (respiratory rate 40 breaths/min, tidal volume 40 ml/kg, inspiratory/expiratory ratio 1∶1, PEEP 0, fraction of inspired oxygen 21%) lasted 4 h in group V. Dexmedetomidine was infused intravenously in a dose of 5.0 μg/kg at 20 min before ventilation followed by an infusion of 5.0 μg·kg -1· h -1 throughout ventilation in group D. In group DY, yohimbine 0.1 mg/kg was injected intravenously at 10 min before dexmedetomidine, and the other treatments were similar to these previously described in group D. Blood samples and lung tissues were taken at 4 h of mechanical ventilation to determine the wet/dry weight ratio (W/D ratio), lung permeability index (LPI), alveolar fluid clearance rate (AFC), and expression of extracellular signal-regulated kinase (ERK), phosphorylated extracellular signal-regulated kinase (p-ERK), and Na + -K + -ATPase in lung tissues (by Western blot) and to observe pathological changes of lung tissues. Results:Compared with group C, LPI and W/D ratio were significantly increased, AFC was decreased, p-ERK expression was up-regulated, and Na + -K + -ATPase expression was down-regulated in group V and group DY ( P<0.05), and no significant change was found in the incidence of the parameters mentioned above in group D ( P>0.05). Compared with group V, LPI and W/D ratio were significantly decreased, AFC was increased, p-ERK expression was down-regulated, Na + -K + -ATPase expression was up-regulated ( P<0.05), and the pathological changes of lung tissues were significantly attenuated in group D, and no significant change was found in the incidence of the parameters mentioned above in group DY ( P>0.05). Compared with group D, LPI and W/D ratio were significantly increased, AFC was decreased, p-ERK expression was up-regulated, Na + -K + -ATPase expression was down-regulated ( P<0.05), and the pathological changes of lung tissues were accentuated in group DY. Conclusion:The mechanism by which dexmedetomidine alleviates VILI may be related to activating alpha2-adrenergic receptors and inhibiting ERK/Na + -K + -ATPase signaling pathway in rats.
目的 评价甲泼尼龙对机械通气相关性肺损伤(VILI)大鼠肺泡内液体清除的影响.方法 清洁级雄性SD大鼠60只,采用随机数字表法分为三组(n=20):对照组(C组)、机械通气组(V组)和甲泼尼龙组(Mp组).C组不行机械通气,自主呼吸空气4h;V组机械通气(RR40次/min,VT 40 mL/kg,I∶E1∶1,PEEP0,FiO2 21%)4h;Mp组机械通气前20 min静注甲泼尼龙10 mg/kg.机械通气4h时,取血标本和肺组织,测定肺湿/干质量(W/D)比值与肺通透指数(LPI),观察肺组织病理学结果,测定肺泡内液体清除率(AFC).Western blot法检测肺组织细胞外信号调节激酶(ERK)、磷酸化细胞外信号调节激酶(p-ERK)、肺泡上皮细胞钠离子通道(ENaC)、钠钾三磷酸腺苷酶(Na+-K+-ATPase)的表达水平.结果 与C组比较,V组大鼠肺组织LPI和W/D比值升高[(2.17±0.07) ×10-3 vs.(6.46±0.31)×10-3,4.32±0.18 vs.8.74±0.53],AFC降低(%:30.56±5.35 vs.13.85 ±2.39),p-ERK表达上调(0.51 ±0.03 vs.1.19±0.13),ENaC和Na+-K+-ATPase表达下调(1.86±0.23 vs.0.71 ±0.08,1.82±0.21 vs.0.65±0.05),P均<0.05,Mp组上述指标差异无统计学意义(P>0.05);与V组比较,Mp组大鼠肺组织LPI和W/D比值降低[(6.46±0.31) ×10-3 vs.(2.67±0.11) ×10-3,8.74±0.53 vs.4.77±0.21],AFC升高(%:13.85 ±2.39 vs.28.23 ±4.78),p-ERK表达下调(1.19±0.13 vs.0.86±0.08),ENaC和Na+-K+-ATPase表达上调(0.71 ±0.08 vs.1.71 ±0.18,0.65 ±0.05 vs.1.65±0.14),P均<0.05.结论 甲泼尼龙可通过促进肺泡内液体清除来减轻大鼠VILI,其机制与抑制ERK磷酸化,上调ENaC和Na+-K+-ATPase表达有关.
目的 评估呼气末正压(PEEP)抬高期间肱动脉峰流速差值对患者术中容量反应性的预测作用.方法 择期全麻下行胃肠手术患者67例,男45例,女22例,年龄40~72岁,BMI 18~25 kg/m2,ASAⅠ或Ⅱ级,心功能Ⅰ或Ⅱ级.麻醉诱导后所有患者均先后进行PEEP抬高试验和容量负荷试验.将扩容后每搏量增加≥15%的患者纳入有反应组(R组,n=35),扩容后每搏量增加<15%的患者纳入无反应组(NR组,n=32).分别在PEEP抬高前、PEEP抬高时记录HR、MAP、中心静脉压(CVP)、每搏量(SV),同时超声测量肱动脉峰流速记录肱动脉峰流速最大值(Vpmax)、肱动脉峰流速最小值(Vpmin)、肱动脉峰流速变异度(ΔVp),计算上述指标的差值(Δ).采用受试者工作特征曲线(ROC曲线)评估ΔVpmin、ΔΔVp预测容量反应性的效能.结果 PEEP抬高期间R组ΔVpmin、ΔΔVp明显高于NR组(P<0.05).ΔVpmin、ΔΔVp预测容量反应性的ROC曲线下面积(AUC)分别为0.887(95%CI 0.808~0.965)和0.817(95%CI 0.710~0.924).讨论PEEP抬高期间肱动脉峰流速差值可有效预测术中容量反应性,其中ΔVpmin有较好的预测作用.
目的 比较针刺复合基础麻醉与单纯基础麻醉应用于腹膜透析置管手术的有效性及安全性.方法 选取首次行腹膜透析置管术的患者69例,采用随机数字表法分为针刺复合基础麻醉组(AA组)和单纯基础麻醉组(BA组).手术开始前20 min,2组均静脉泵注0.3 μg/kg右美托咪定镇静,AA组于手术开始前连续电刺激双侧内关穴及三阴交穴至术毕.术中视觉模拟评分法(Visual Analogue Scale,VAS)评分大于5分,可给予静脉注射芬太尼1 μg/kg,如芬太尼总量达5 μg/kg后VAS评分大于5分者,则改为全身麻醉完成手术.记录2组手术切皮时、牵拉及切开腹膜时、建立皮下隧道时、缝皮时、术后2h、术后12h及术后24 h的VAS评分.记录术中镇痛药芬太尼的追加量,手术医生对麻醉效果的满意度,术中转全身麻醉率及麻醉手术相关不良反应.结果 2组术中VAS评分在手术切皮开始逐渐增高至缝皮时降低,2组术后VAS评分逐渐降低,2组术中、术后VAS评分在组间、时点间、组间·时点间交互作用差异均有统计学意义(P<0.05),AA组追加镇痛药芬太尼的总剂量明显少于BA组(P<0.05).与BA组比较,AA组手术医师满意度高,转全身麻醉率较低,差异均有统计学意义(P<0.05).结论 腹膜透析置管手术中采用针刺复合基础麻醉较单纯基础麻醉安全、有效.
Objective To evaluate the efficacy of transversus abdominis plane block (TAPB) with different doses of dexmedetomidine mixed with ropivacaine in the pediatric patients undergoing laparoscopic surgery with general anesthesia.Methods Eighty patients of both sexes,aged 3-6 yr,weighing 10-30kg,scheduled for elective single-channel laparoscopic appendectomy,were divided into 4 groups (n =20each) using a random number table method:0.5 μg/kg dexmedetomidine plus ropivacaine group (group DR1),1.0 μg/kg dexmedetomidine plus ropivacaine group (group DR2),1.5 μg/kg dexmedetomidine plus ropivacaine group (group DR3),and ropivacaine group (R group).Bilateral TAPB was performed under ultrasound guidance after the end of anesthesia induction.In group TR,0.25% ropivacaine 0.5 ml/kg was injected,the 0.5 ml/kg mixture of 0.5,1.0 and 1.5 μg/kg dexmedetomidine and ropivacaine at a final concentration of 0.25% was injected in DR1,DR2 and DR3 groups.Anesthesia was maintained by intravenously infusing remifentanil and inhaling sevoflurane.Cisatracurium was intermittently injected to maintain muscle relaxation.Ibuprofen was taken orally to maintain postoperative FLACC score <4.The intraoperative consumption of remifentanil,tracheal extubation time,duration of anesthetic recovery room stay,requirement for ibuprofen,and occurrence of opioids-and TAPB-related complications were recorded.Results There was no significant difference in the intraoperative consumption of remifentanil or tracheal extubation time between four groups (P>0.05).Compared with group R,the requirement for ibuprofen was significantly decreased in DR2 and DR3 groups,the duration of anesthetic recovery room stay was significantly prolonged in group DR3 (P<0.05),and no significant change was found in the requirement for ibuprofen in group DR1 or in the duration of anesthetic recovery room stay in DR1 and DR2 groups (P>0.05).Compared with group DR1,the duration of anesthetic recovery room stay was significantly prolonged,and the requirement for ibuprofen was decreased in group DR3,and the requirement for ibuprofen was significantly decreased (P<0.05),and no significant change was found in the duration of anesthetic recovery room stay in group DR2 (P>0.05).Compared with group DR2,the duration of anesthetic recovery room stay was significantly prolonged (P<0.05),and no significant change was found in the other parameters in group DR3 (P> 0.05).No patients developed opioids-or TAPB-related complications.Conclusion TAPB with 1.0 μg/kg dexmedetomidine mixed with ropivacaine provides good efficacy for the pediatric patients undergoing laparoscopic surgery with general anesthesia.
Objective To compare internal jugular vein diameter and brachial artery peak velocity variation (VVp) in predicting fluid responsiveness.Methods Sixty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients,of New York Heart Association I,aged 18-64 yr,scheduled for elective gastrointestinal surgery under general anesthesia,were included in this study.Six percent hydroxyethyl starch 130/0.47 ml/kg was infused at a rate of 0.4 ml · kg-1 · min-1 after induction of anesthesia.The patients with the changing rate of stroke volume variation (ASVV) more than or equal to 15% were included in responsiveness group and patients with ASVV less than 15% were included in non-responsiveness group after volume expansion.Immediately after volume expansion and at 3 min after volume expansion,mean arterial pressure,central venous pressure and heart rate were recorded,the maximum diameter of the internal jugular vein at the end of inspiration (IJVmax) and the minimum diameter of the internal jugular vein at end of expiration (IJVmin) and brachial artery peak velocity were measured using an ultrasonic instrument,and the variation of internal jugular vein respiration (VIJV) and VVp were calculated.The receiver operating characteristic curve was used to evaluate the accuracy of IJV IJVmin,VIJV and VVp in predicting fluid responsiveness.Results There were 31 patients in responsiveness group and 29 patients in non-responsiveness group.Compared with non-responsiveness group,mean arterial pressure,central venous pressure,IJVmax and IJVmin were significantly decreased and heart rate,VIJV and VVp were increased immediately after volume expansion in responsiveness group (P<0.05).The areas under receiver operating characteristic curve (AUC) of IJV IJVmin,VIJV and VVp were 0.753,0.948,0.837 and 0.832,respectively.AUC IJVmax,AUCVIJV and AUCVVp were significantly decreased when compared with AUC IJVmin (P<0.05).Conclusion The accuracy of IJVmax is higher than that of VVp in predicting intraoperative fluid responsiveness in the patients.
Objective To observe the influence and safety of dexmedetomidine 1 μg/kg given before the induction of anesthesia on the analgesic and sedate effects of remifentanil in pediatric postoperative analgesia.Methods Sixty children scheduled for bowel resection surgery were randomly divided into 2 groups:dexmedetomidine combined with remifentanil group (group DR,n=30) and remifentanil group (group R,n=30).Dexmedetomidine 1 μg/kg was given before the induction of anesthesia in group DR,normal saline in group R.Analgesic mixture including remifentanil 24 μg/kg,granisetron 0.1 mg/kg,diluted to 100 ml,was given to both groups.The postoperative analgesia and sedation was assessed with FACES Face Ratings and Ramsay score at the end of operation,and at 2,6,12 and 48 h after surgery.Times of pressed the analgesic pump,the incidence of side effects and parent' s satisfaction scores were recorded.Results FACES and Ramsay scores in group DR were significantly better than those in group R (P < 0.05).There was no occurrence of respiratory depression in both groups.Parent' s postoperative satisfaction score in group DR was higher than that in group R (P<0.05).There were 5 patients vomiting in group R,but only 1 in group DR (P < 0.05).Conclusion With application of dexmedetomidine 1 μg/kg given before the induction of anesthesia,the analgesic and sedation effects of remifentanil can be improved,with high comfort level and patient' s satisfaction,which is better than application of remifentanil only.
Objective To evaluate the effect of dexmedetomidine on the expression of aquaporin 5 (AQP5) in lung tissues in a rat model of ventilator-induced lung injury.Methods One hundred pathogen-free male Sprague-Dawley rats,weighing 270-320 g,were divided into 5 groups (n=20 each) using a random number table:control group (group C),mechanical ventilation group (group V) and different doses of dexmedetomidine groups (DEX1-3 groups).The animals were mechanically ventilated,with tidal volume 40 ml/kg,respiratory rate 50 breaths/min,inspiratory/expiratory ratio 1 ∶ 1,and inspired oxygen fraction ratio 21%.In DEX1 3 groups,dexmedetomidine 0.5,1.0 and 2.0 μg/kg were infused intravenously,respectively,over 20 min before ventilation,and then dexmedetomidine was infused intravenously for 4 h at a rate of 0.5,1.0 and 2.0 μg · kg 1 · h-1,respectively,during ventilation.Immediately before tracheal intubation and at 1,2 and 4 h of ventilation,blood samples were collected from the femoral artery for blood gas analysis,and arterial oxygen partial pressure (PaO2) was recorded.At 4 h of ventilation,the animals were sacrificed,and the lungs were removed for examination of the pathological changes of lung tissues (with light microscope) and for determination of lung permeability index (LPI),wet/dry weight ratio (W/D ratio) and expression of p38 mitogen-activated protein kinase (p38MAPK),phosphorylated p38MAPK (p-p38MAPK) and AQP5 in lung tissues (by Western blot).The p-p38MAPK/p38MAPK ratio was calculated.The expression of AQP5 mRNA in lung tissues was detected by real-time polymerase chain reaction.Results Compared with group C,PaO2 was significantly decreased,W/D ratio and LPI were increased,the expression of p-p38MAPK was up-regulated,and p-p38MAPK/p38MAPK ratio was increased,and the expression of AQP5 protein and mRNA was dow.n-regulated in V and DEX1 groups (P<0.05),and no significant change was found in the parameters mentioned above in DEX2.3 groups (P>0.05).Compared with group V,PaO2 was significantly increased,W/D ratio and LPI were decreased,the expression of p-p38MAPK was down-regulated,and p-p38MAPK/p38MAPK ratio was decreased,and the expression of AQP5 protein and mRNA was up-regulated in DEX2.3 groups (P<0.05),and no significant change was found in the parameters mnentioned above in group DEX1 (P>0.05).The pathological changes of lung tissues were significantly attenuated in DEX2,3 groups as compared with group V.Conclusion The mechanism by which dexmedetomidine mitigates ventilator-induced lung injury may be related to inhibition of p38MAPK phosphorylation and up-regulation of AQP5 expression in rats.
Objective To investigate the effect of hyperbaric oxygen ( HBO) preconditioning on activation of plasma protein C in a rat model of asphyxial cardiac arrest?resuscitation. Methods A total of 105 adult male Sprague?Dawley rats, aged 70-90 days, weighing 260-320 g, were randomly divided into 3 groups: cardiac arrest group ( group CA, n=5) , cardiac arrest?resuscitation group ( group CA∕R, n=50) , and hyperbaric oxygen preconditioning group ( group H, n=50 ) . Cardiac arrest was induced by campling the endotracheal tube at the end of expiration. The animals underwent HBO preconditioning once a day for 3 consecutive days before cardiac arrest was induced in group H. The rats were placed in the HBO chamber, 10 min later the pressure was increased at a constant rate until the hyperbaric oxygen reached 2 atmosphere absolute, and maintained at this level for 45 min, after the oxygen concentration>95%, and then the pressure was decreased at a constant rate ( within 20 min) until the normal pressure was reached. The rats underwent no resuscitation in group CA. Five rats were selected from CA∕R and H groups at 3, 6, 12 and 24 h after restoration of spontaneous circulation, and at 30 min of cardiac arrest in group CA, and blood samples were taken from the abdominal aorta for determination of the plasma activated protein C ( APC) concentrations. The time from asphyxia to cardiac arrest, time for spontaneous regular cardiac rhythm, and successful resuscitation were recorded. Results Compared with group CA, the plasma APC concentrations were significantly decreased at each time point after restoration of spontaneous circulation in CA∕R and H groups ( P<0.05) . Compared with group CA∕R, the time from asphyxia to cardiac arrest was significantly prolonged, the time for spontaneous regular cardiac rhythm was shortened, the success rate of resuscitation was increased, and the plasma APC concentrations were increased at each time point after restoration of spontaneous circulation in group H ( P<0. 05 ) . Conclusion HBO preconditioning can promote activation of plasma protein C after resuscitation in a rat model of asphyxial cardiac arrest, and is helpful in improving hypercoagulation.