目的 探讨气腹状态下不同潮气量(VT)所对应每搏量变异度(SVV)之间的线性关系.方法 择期行腹腔镜结直肠根治术患者57例,在常规麻醉后通过FloTrac传感器进行每搏量变异度监测,在建立人工气腹并调整至Trendelenburg体位后对VT进行设置.按随机顺序设置为6、8、10 mL/kg(以标准体质量计算),记录每搏量变异度等相关数据.结果 随着VT增加,SVV呈进行性增加,且其数值之间有显著的相关性(SVV6与SVV8:r=0.927,P<0.01;SVV8与SVV10:r=0.926,P<0.01;SVV6与SVV10:r=0.867,P<0.01).结论 气腹状态下不同VT所对应SVV之间存在一定的线性关系.根据线性回归方程,可以基于给定VT的已知SVV来计算任何不同VT的SVV.

Objective:To evaluate the role of spinal peroxisome proliferation-activated receptor-γ (PPAR-γ) in protectin D1 (PD1)-induced reduction of neuropathic pain (NP) in rats.Methods:Forty-eight clean-grade healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 4 groups ( n=12 each) by a random number table method: sham operation group (Sham group), NP group, NP plus PD1 group (NP+ PD group), and NP plus PD1 plus GW9662 group (NP+ PD+ GW group). Neuropathic pain was induced by spared nerve injury in anesthetized rats.In NP+ PD and NP+ PD+ GW groups, PD1 900 ng (diluted to 20 μl in dimethyl sulfoxide [DMSO]) was intrathecally injected once a day for 8 consecutive days starting from 30 min before establishing the model.In NP+ PD+ GW group, the PPAR-γ antagonist GW9662 200 ng (diluted to 20 μl in DMSO) was intrathecally injected once a day for 8 consecutive days starting from 45 min before establishing the model.The equal volume of DMSO was intrathecally injected in Sham group.The mechanical paw withdrawal threshold (PWT) was measured before establishing the model and at 1, 3, 5, 7, 10 and 14 days after establishing the model.Six rats in each group were sacrificed on day 14 after establishing the model, and their lumbar enlargements were removed for determination of the expression of PPAR-γ, TNF-α and IL-6 by Weston blot.Six rats in each group were sacrificed on day 14 after establishing the model, L 4, 5 segments of the spinal cord were removed, and the co-expression of PPAR-γ with neuron-specific nucleoprotein (NeuN), glial fibrillary acidic protein (GFAP) or serum calcium binding adapter molecule 1 (Iba-1) was determined by immunofluorescence staining. Results:Compared with group Sham, PWT was significantly decreased at each time point after establishing the model, the expression of PPAR-γ was down-regulated, and the expression of TNF-α and IL-6 was up-regulated in the other three groups ( P<0.05). Compared with group NP, PWT was significantly increased at 7-14 days after establishing the model, the expression of PPAR-γ was up-regulated, and the expression of TNF-α and IL-6 was down-regulated in group NP+ PD, and no significant change was found in the parameters mentioned above in group NP+ PD+ GW ( P>0.05). Compared with group NP+ PD, PWT was significantly decreased at 7-14 days after establishing the model, the expression of PPAR-γ was down-regulated, and the expression of TNF-α and IL-6 was up-regulated in group NP+ PD+ GW ( P<0.05). The results of immunofluorescence staining of the spinal cord showed that PPAR-γ was co-expressed with NeuN and GFAP. Conclusion:The mechanism by which PD1 mitigates NP is related to promoting the activation of PPAR-γ in spinal cord neurons and astrocytes and inhibiting inflammatory responses in rats.

Objective To observe the pain threshold of spared nerve injury ( SNI) rats and the transient receptor potential cation channel subfamily A member 1 (TRPA1) mRNA expression of dorsal root ganglion (DRG) in the 4th cervical vertebra and the 5th cervical vertebra in rats at different time points after modeling; and to discuss the significance of peripheral TRPA1 mRNA in different stages of neuropathic pain model. Methods Thirty healthy adult male Sprague-Dawley rats, weighing 200-230 g, were selected and randomly divided into three groups:control group (6 cases), sham operation group (6 cases) and spared nerve injury model group ( SNI group, 18 cases ) . In SNI group, the left common peroneal nerve and the sacral nerve were ligated, but the sural nerve was preserved. In the sham operation group, the skin muscles were dissected and the nerves were not ligated, and the incision was directly sutured. Rats in control group were not given any treatments. All rats were tested for bilateral hind limb mechanical withdrawal threshold (MWT) 3 days and 1 day before surgery, and 1, 3, 5, 7, 9, 12, 14 days after surgery. Three rats were sacrificed in sham operation group and control group, respectively. At 1, 3, 5, 7 and 14 days after treatment, 3 rats of SNI group were sacrificed everyday. The DRGs in the 4th cervical vertebra and the 5th cervical vertebra of the rats were taken and the expression of TRPA1 mRNA was detected by quatitative-polymerase chain reaction ( q-PCR) . Results The MWT values of the left hind limbs in SNI group were decreased progressively after SNI, which were significantly different from sham operation group (P<0. 01), showing obvious postoperative pain. MWT values at each time point of SNI group were significant different from sham operation group ( P<0. 01 ) . There was a significant difference in the decrease between each adjacent time point in SNI group (P<0. 05). The results of q-PCR showed that TRPA1 mRNA was expressed in DRG of normal rats. There was no significant difference in the expression of TRPA1 mRNA between sham operation group and control group (P>0. 05). Compared with the sham operation group, the level of TRPA1 mRNA was significantly increased 1 day and 3 days after SNI, and the TRPA1 mRNA was significantly decreased 7 days after surgery ( P<0. 01 ) . Conclusions SNI model rats have neuropathic pain. Peripheral TRPA1 mRNA participates in the generation and maintenance of pain in SNI model, and its roles in different stages are different.

Neuropathic pain (NP) is a direct pain caused by a lesion or disease of the somatosensory nervous system,which is the consequence of a complex interplay of mechanisms in the peripheral and central nervous systems and the most intractable pain syndrome.Transient receptor potential cation channel,subfamily A,member 1 (TRPA1) is involved in the formation of neuropathic pain and plays a crucial role in the integration of nociceptive signals.During NP,a large amount of oxidative stress products are released to cause hyperalgesia.TRPA1-specific antagonists are expected to be used in the treatment of neuropathic pain.This review summarizes the mechanism of TRPA1 activation and regulation and research progress in TRPA1 in NP,so as to provide new insights for pain management.

通过简单的临床观察并不能完全掌握麻醉深度水平,进一步的监测麻醉深度可以提高麻醉质量,降低麻醉并发症,有效保障患者围术期的安全与康复.本文综述麻醉深度监测技术,为临床应用提供参考.