Stroke is a life-threatening condition that impairs the arteries and causes neurological impairment. The incidence of stroke is increasing year by year with the arrival of the aging population. Thus, there is an urgent need for early stroke diagnosis. Short-chain fatty acids (SCFAs) can modulate the central nervous system and directly and indirectly impact behavioral and cognitive functions. This study aimed to investigate the connection between SCFA metabolism and stroke development via bioinformatic analysis. Initially, the Gene Set Enrichment Analysis (GSEA) and immune cell infiltration analysis were performed based on RNA data from stroke patients to comprehend the mechanisms governing stroke pathogenesis. The functional analysis, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Protein-Protein Interaction (PPI), was performed based on the Differentially Expressed Gene (DEG) selected by the limma package. 1220 SCFA metabolism-related genes screened from Genecards databases were intersected with 242 genes in main modules determined by Weighted Gene Co-Expression Network Analysis (WGCNA), and the final 10 SCFA key genes were obtained. GO analysis revealed that these genes were involved in immune response processes. Through lasso regression analyses, we established a stroke early diagnosis model and selected 6 genes with diagnostic value. The genes were validated by the area under curve (AUC) values and had a relatively good diagnostic performance. Finally, 4 potential therapeutic drugs targeting these genes were predicted using the Drug Signatures Database (DSigDB) via Enrichr. In conclusion, this paper analyzes the involvement of SCFAs in the complex gut-brain axis mechanism, which contributes to developing new targets for treating central nervous system diseases and provides new ideas for early ischemic stroke diagnosis.
Stroke is a life-threatening condition that impairs the arteries and causes neurological impairment. The incidence of stroke is increasing year by year with the arrival of the aging population. Thus, there is an urgent need for early stroke diagnosis. Short-chain fatty acids (SCFAs) can modulate the central nervous system and directly and indirectly impact behavioral and cognitive functions. This study aimed to investigate the connection between SCFA metabolism and stroke development via bioinformatic analysis. Initially, the GSEA and immune cell infiltration analysis were performed based on RNA data from stroke patients to comprehend the mechanisms governing stroke pathogenesis. The functional analysis, including GO, KEGG, and PPI, was performed based on the DEG selected by the limma package. 1220 SCFA metabolism-related genes screened from Genecards databases were intersected with 242 genes in main modules determined by WGCNA, and the final 10 SCFAs key genes were obtained. GO analysis revealed that these genes were involved in immune response processes. Through lasso regression analyses, we established a stroke early diagnosis model and selected 6 genes with diagnostic value. The genes were validated by the AUC values and had a relatively good diagnostic performance. Finally, 4 potential therapeutic drugs targeting these genes were predicted using the DSigDB via Enrichr. In conclusion, this paper analyzes the involvement of SCFAs in the complex gut-brain axis mechanism, which contributes to developing new targets for treating central nervous system diseases and provides new ideas for early stroke diagnosis.
西医认为,应激性溃疡发病的直接原因是胃酸分泌过多,损伤黏膜的屏障保护功能,治疗方法主要有抑制胃酸分泌药、抗酸药、胃黏膜保护药、肠内营养及止血药物等.中医认为,其病机主要包括脾胃亏虚、胃肠腑实、热毒炽盛、寒热错杂、气机郁滞、血行瘀滞等,多采用单味药、辨证论治、针灸治疗等.目前,中医药治疗应激性溃疡存在以下问题:相关文献报道以实验研究居多,且模型多为水浸束缚应激,应激类型尚不全面;临床研究较少,且缺乏大样本研究,说服力需加强;中医药治疗应激性溃疡的具体作用机制研究尚不全面等.今后,应加强对临床大样本研究,进一步完善应激性溃疡的中医证型,以期为应激性溃疡的中医规范治疗提供系统的思路和方法.
目的:探讨黄连解毒汤对脑梗死合并胃损伤大鼠干细胞因子/酪氨酸激酶受体(SCF/C-kit)信号通路的影响.方法:将80只健康10周龄雄性Wistar大鼠随机分为模型组、黄连解毒汤组、奥美拉唑组、假手术组、正常组,以上各组再分设4 d组、7 d组,共10组.采用线栓法建立大脑中动脉梗死模型.黄连解毒汤组给予黄连解毒汤(27 mg/ml)混悬液,奥美拉唑组给予奥美拉唑(15 mg/ml)悬浊液,其余组给予1 ml 0.9%氯化钠溶液灌胃,4 d组连续灌胃4 d,7 d组连续灌胃7 d.采用HE染色法观察大鼠胃组织病理形态学变化,并进行病理损伤评分;采用实时荧光定量检测大鼠胃组织SCF、C-kit mRNA表达水平;采用Western blot检测大鼠胃组织中SCF、C-kit蛋白表达水平.结果:与正常组、假手术组比较,模型组、黄连解毒汤组、奥美拉唑组大鼠胃黏膜病理评分均明显升高(4、7 d组均P<0.01),胃组织SCF、C-kit mRNA和蛋白表达水平均明显降低(P<0.01);正常组、假手术组间比较差异无统计学意义(P>0.05).与模型组比较,黄连解毒汤组、奥美拉唑组大鼠胃黏膜病理评分均显著降低(4、7 d组均P<0.01),胃组织SCF、C-kit mRNA和蛋白表达水平均明显升高(P<0.01).与奥美拉唑组比较,黄连解毒汤组大鼠胃黏膜病理评分均明显降低(P<0.05),胃组织SCF、C-kit mRNA和蛋白表达水平均明显升高(P<0.05).结论:黄连解毒汤对脑梗死合并胃损伤大鼠的胃黏膜具有一定的保护作用,其机制可能与黄连解毒汤升高大鼠胃组织SCF、C-kit mRNA及蛋白的表达水平有关.
目的 观察黄连解毒汤对急性期脑梗死大鼠胃动力的影响.方法 将60只大鼠随机分为正常对照组、假手术组、脑梗死组、枸橼酸莫沙必利组、黄连解毒汤常规剂量组及黄连解毒汤高剂量组,每组各10只,脑梗死组、枸橼酸莫沙必利组、黄连解毒汤常规剂量组及黄连解毒汤高剂量组采用线栓法制备大脑中动脉梗死模型(MCAo),假手术组大鼠仅暴露大脑中动脉而不凝闭,正常对照组不进行手术干预.造模结束后,黄连解毒汤常规剂量组和高剂量分别按生药5.39、10.78 g/kg灌胃,枸橼酸莫沙必利组按0.05 mg/kg予枸橼酸莫沙必利片灌胃,假手术组及脑梗死组予0.9%氯化钠注射液2 mL灌胃,正常对照组不做任何处理.共灌胃7 d,比较各组大鼠灌胃第4、7 d胃动素(MTL)水平情况,比较各组大鼠灌胃第1、4、7 d胃电图慢波振幅与频率情况,并分析脑梗死组大鼠胃动力障碍变化趋势.结果 与正常对照组和假手术组同期比较,脑梗死组第4、7 d MTL水平均升高(P<0.05);与脑梗死组同期比较,枸橼酸莫沙必利组、黄连解毒汤常规剂量组及黄连解毒汤高剂量组第4、7 d MTL水平均降低(P<0.05);与枸橼酸莫沙必利组同期比较,仅黄连解毒汤高剂量组第4 d MTL水平降低(P<0.05);与黄连解毒汤常规剂量组同期比较,黄连解毒汤高剂量组第4 d MTL水平降低(P<0.05).与正常对照组和假手术组同期比较,脑梗死组大鼠第1、4、7 d胃电图慢波振幅均降低(P<0.05),其中脑梗死组第4 d胃电图慢波振幅最低(P<0.05);与脑梗死组同期比较,枸橼酸莫沙必利组、黄连解毒汤常规剂量组及黄连解毒汤高剂量组第1、4、7 d胃电图慢波振幅均升高(P<0.05);与枸橼酸莫沙必利组同期比较,仅黄连解毒汤高剂量组第1、4、7 d胃电图慢波振幅均升高(P<0.05);与黄连解毒汤常规剂量组同期比较,黄连解毒汤高剂量组第1、4、7 d胃电图慢波振幅均升高(P<0.05).与正常对照组和假手术组同期比较,脑梗死组第1、4、7 d胃电图慢波频率均升高(P<0.05),其中脑梗死组第4 d胃电图慢波频率最高(P<0.05);与脑梗死组同期比较,仅枸橼酸莫沙必利组、黄连解毒汤常规剂量组及黄连解毒汤高剂量组第4 d胃电图慢波频率均降低(P<0.05),而3个治疗组第1、4、7 d胃电图慢波频率组间比较差异均无统计学意义(P>0.05).结论 黄连解毒汤对急性期脑梗死大鼠胃动力障碍具有明确的治疗作用,可有效提升胃电图慢波振幅,增强胃的收缩力量,同时可降低胃电图慢波频率,降低胃的蠕动速度,并可降低胃动素的水平,综合调控脑梗死急性期大鼠胃动力的紊乱,让胃动力趋向于正常运动水平,且其调节作用有一定的量效关系,高剂量疗效优于常规剂量.
目的 观察调胃承气汤对脑出血急性期大鼠胃肠组织SCF/c-kit信号通路的影响,探讨其调节胃肠动力障碍的作用机制.方法 选取40只健康Wistar大鼠,按照随机数字法将其分为假手术组、模型组、西药组和中药组,每组10只.除假手术组只进针不注射外,其他组均采用自体血注入法建立脑出血大鼠模型.成功造模后,中药组和西药组分别给予113.4 mg/mL的调胃承气汤悬浊液和0.135 mg/mL的莫沙必利悬浊液10 mL/(kg·d)灌胃,假手术组和模型组予以等容量生理盐水灌胃,均连续灌胃7 d.分别采用Western blot法和RT-PCR法检测大鼠胃、小肠、大肠、盲肠组织中c-kit、SCF蛋白及mRNA表达情况.结果 模型组大鼠胃肠各组织中的c-kit、SCF蛋白及mRNA相对表达量均明显低于假手术组(P均<0.05);中药组和西药组大鼠胃肠各组织中的c-kit、SCF蛋白及mRNA相对表达量均明显高于模型组(P均<0.05),中药组和西药组各指标比较差异均无统计学意义(P均>0.05),但中药组各指标有高于西药组的趋势.结论 调胃承气汤改善脑出血急性期胃肠动力障碍的作用机制与提高SCF/c-kit信号通路相关蛋白及mRNA的表达有关.
目的:探讨清胰利胆颗粒联合床旁连续性肾脏替代治疗(CRRT)对重症急性胰腺炎(SAP)患者炎性因子、免疫功能及外周血叉状头/翅膀状螺旋转录因子(Foxp3)、维甲酸相关孤独受体γt(RORγt)mRNA表达的影响.方法:选取2017年3月~2019年12月期间我院收治的SAP患者80例,根据随机数字表法分为对照组(n=40)和研究组(n=40),对照组患者予以床旁CRRT疗法治疗,研究组在对照组的基础上联合清胰利胆颗粒治疗,比较两组疗效、炎性因子、免疫功能、外周血Foxp3、RORγtmRNA相对表达量及不良反应.结果:研究组治疗后临床总有效率为87.50%(35/40),高于对照组患者的70.00%(28/40)(P<0.05).研究组治疗后免疫球蛋白G(IgG)、免疫球蛋白A(IgA)、免疫球蛋白M(IgM)、Foxp3 mRNA相对表达量较治疗前升高,且高于对照组(P<0.05).两组治疗后白介素-6(IL-6)、白介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)、RORγtmRNA相对表达量较治疗前降低,且研究组低于对照组(P<0.05).两组在治疗过程中均未出现严重不良反应.结论:清胰利胆颗粒联合床旁CRRT疗法治疗SAP,疗效显著,可有效改善患者炎性因子、免疫功能,其主要作用机制可能与外周血Foxp3、RORyt mRNA相对表达量有关.
目的 观察参附注射液联合亚低温治疗心脏骤停(CA)患者的临床效果.方法 选取2015年1月~2018年12月山东省青岛市海慈医疗集团收治的138例CA患者作为研究对象,按照随机数字表法将其分为对照组和观察组,每组69例.对照组给予亚低温(32~34℃)治疗,观察组在对照组基础之上,再静脉输注100 mL的参附注射液.心肺复苏后30 min、2h、12h和24 h采用酶联免疫法检测超氧岐化酶(SOD)、一氧化氮(NO)、丙二醛(MDA)、神经元特异性烯醇化酶(NSE)、人S100B蛋白(S-100B);CA 12、24、48、72 h检测患者脑氧代谢指标,包括动静脉血氧含量差(Ca-jvO2)、颈静脉球部血氧饱和度(SjvO2)和脑氧摄取率(CERO2);采用格拉斯哥昏迷量表(GCS)评估患者的昏迷状态;统计复苏有效率和病死率.结果 与复苏后30 min比较,对照组复苏2、12、24 h,SOD和NO水平明显下降,MDA水平明显升高,差异均有统计学意义(均P<0.05).与复苏后30 min比较,观察组复苏2、12、24 h,SOD水平明显下降,NO和MDA水平明显升高,差异均有统计学意义(均P<0.05).与复苏后30 min比较,两组患者复苏后2、12、24 h,NSE和S-100B水平均明显升高,差异均有统计学意义(均P<0.05).复苏后2、12、24 h观察组SOD和NO水平明显高于对照组,MDA、NSE和S-100B水平明显低于对照组,差异均有统计学意义(均P< 0.05).与CA 12 h比较,两组患者CA 24、48、72 h,SjvO2水平和GCS评分明显升高,而Ca-jvO2水平明显降低,差异均有统计学意义(均P< 0.05).两组患者CA 24 h CERO2水平明显高于12h,CA 48、72 hCERO2水平明显低于12h,差异均有统计学意义(均P<0.05).CA 48、78 h观察组Ca-jvO2、CERO2水平和GCS评分明显高于对照组,而SjvO2水平明显低于对照组,差异均有统计学意义(均P<0.05).观察组治疗有效率明显高于对照组,而病死率明显低于对照组,差异均有统计学意义(均P< 0.05).结论 参附注射液联合亚低温治疗对CA患者心肺复苏心肌组织和脑组织的保护作用明显,能够改善预后.
AIM:Ischemia/reperfusion (I/R) injury is the major cause of neurological deficit following stroke. Our previous study showed neuroprotective effects of hispidulin against cerebral ischemia reperfusion injury (IRI). In this study, we further examined the involvement of pyroptosis in this neuroprotective function.MATERIALS AND METHODS:IRI was simulated in a rat model by middle cerebral artery occlusion (MCAO) surgery, and the animals were treated with different doses of hispidulin. The neurological function of the rats was evaluated by the neural function defect score (NFDS), balance beam test and limb placement test. The infarct volume and brain water content were measured 72 h following IRI. Neuronal cell survival and pyroptosis in the ischemic cortex were respectively detected by Nissl staining and TUNEL assay. The relative expression of pyroptosis markers was determined by qRT-PCR, Western blotting and ELISA as appropriate. IRI was simulated in vitro in primary cerebral astrocytes using the OGD/R procedure. AMPKα was blocked genetically or pharmacologically using siRNA and compound C respectively. CCK-8 and LDH release assays were performed using suitable kits.RESULTS:Hispidulin improved the neurological symptoms of the rats after IRI, in addition to decreasing the infarct size and brain edema. Mechanistically, hispidulin exerted its neuroprotective effects in vivo and in vitro by suppressing NLRP3-mediated pyroptosis by modulating the AMPK/GSK3β signaling pathway.CONCLUSION:Hispidulin is a neuroprotective agent with clinical potential against IR-induced neurological injury.
Objective To investigate the dynamic characteristic changes of gastrointestinal mucosa and its relationship with disease progression in rats with acute cerebral infarction. Methods Fifty-six male Wistar rats were selected as the study subjects, and they were divided into three groups: normal control, sham operation and cerebral infarction model groups by random number table method. The middle cerebral artery occlusion (MCAO) model was prepared by the modified Longa thread embolic method. The levels of gastrin (GAS) were monitored in each group after modeling for 24 hours, 4 days and 7 days; after the rats were killed, the sections of gastric antrum and small intestine were taken and stained with hematoxylin-eosin (HE) staining method, the histopathological changes of gastric and small intestinal mucosa were observed under light microscope, in the mean time the gastric and small intestinal mucosal pathological scores were also performed, and the differences of pathological scores among the three groups were compared. Results There were no statistical significant differences in GAS, gastrointestinal mucosa and small intestinal mucosal pathological scores between the normal control group and sham operation group at each time point (all P > 0.05); the GAS level in cerebral infarction model group was decreased gradually with time prolongation, reaching the lowest level 7 days after modeling, but the GAS level in cerebral infarction model group was significantly higher than that in normal group and shamoperation group (ng/L: 205.02±7.68 vs. 130.51±8.03, 145.29±7.68, both P < 0.05). The pathological scores of gastrointestinal mucosa and small intestinal mucosa in the cerebral infarction model group were increased first and then decreased with time prolongation, peaked on 4th day and decreased significantly on 7th day, the pathological scores of gastrointestinal mucosa and small intestinal mucosa in the cerebral infarction model group at each time point were significantly higher than those in the normal control group and sham-operated group (gastric mucosal pathological score: 82.50±2.95 vs. 21.38±1.57, 36.10±3.41; small intestinal mucosal pathological score: 62.00±2.78 vs. 18.25±1.39, 25.55±1.75, all P < 0.05). Under light microscopy, the normal control group showed complete normal morphological appearance, normal structure, orderly arrangement of villi and no infiltration of inflammatory cells; in shamoperation group, inflammatory cells infiltrated the lamina propria at each time point, and there were villi slightly uneven, enlarged stroma, congestion, edema occasionally seen and no obvious ulcer; in cerebral infarction model group, the various layers of gastrointestinal mucosal were not very clear, the glands were arranged irregularly and the capillaries dilated, and in part of tissues, congestion, hemorrhage, edema and inflammatory cell infiltration were seen obviously. Conclusion The injury of gastrointestinal mucosa in acute stage of cerebral infarction should be related to the stress stimulation and disease progress of cerebral infarction itself, not due to the abnormal secretion of GAS.
目的 观察胃肠承气洗消溶液联合杂合式血液净化技术对重度有机磷中毒患者的治疗效果,并观察其对患者血浆细胞因子的影响.方法 患者90例随机分为3组,对照组采用西医常规治疗;治疗1组采用一般治疗联合杂合式血液净化治疗;治疗2组采用一般治疗以及胃肠承气洗消溶液鼻饲联合杂合式血液净化治疗;比较各组患者的临床疗效以及细胞因子水平.结果 治疗1组、治疗2组患者胆碱酯酶上升较对照组快,且急性呼吸衰竭的发生率以及中间综合征的发生率较低,入住ICU治疗时间较短,病死率低,且治疗2组疗效优于治疗1组(均P<0.05),但两治疗组患者的病死率的差异无统计学意义(P>0.05).对照组患者在治疗第10日TNF-α、IL-6、TGF-β1均较治疗前下降(P<0.05);治疗1组与治疗2组患者在治疗12 h后、第5日、第10日后各细胞因子均较治疗前下降(P<0.05),且同一治疗时间治疗1组、治疗2组患者各细胞因子均低于对照组(P<0.05),在治疗第10天,治疗2组各细胞因子水平均低于治疗1组(P<0.05).结论 胃肠承气洗消溶液联合杂合式血液净化技术治疗急性重度有机磷中毒疗效较好,其机制除早期清除毒物以外,还可能与血液净化治疗清除炎症介质,中药胃肠承气洗消溶液抑制减轻炎症反应有关.
Objective To explore the dynamic changes of gastric mucosal injury in acute stage of cerebral infarction. Methods Fifty male Wistar rats were selected and randomly divided into the control group(n=8),sham operation group (n=24), and cerebral infarction group(n=8).The middle cerebral artery occlusion model in the cerebral infarction group was established by the line embolus.The blood vessels of the rats in the sham operation group were only ligated with-out the nylon fish line insertion.The control group was not treated.In the sham operation group and the cerebral infarction group,8 rats were taken on day 1,4 and 7,respectively.The serum level of gastrin(GAS)was detected at any time in the control group.After the blood was collected,the gastric tissues were stained by HE staining.The pathological grading of gastric mucosa was observed and photographed under microscope.Results The serum GAS level of rats in the cerebral infarction group at each time was significantly higher than that in the control group and sham operation group(all P<0.05),but there was no difference in serum GAS content between the control group and sham operation group(P>0.05). The level of serum GAS in the cerebral infarction group decreased with time(P<0.05).In the control group and the sham operation group,the gross morphology of the gastric mucosa did not significantly change,and the pathological score of the gastric mucosa was 0.The degree of gastric mucosal injury in cerebral infarction group was worse than that of the control group and the sham operation group, but the pathological scores of gastric mucosa were higher than those in the control group and sham operation group(all P<0.05),and the highest pathological score of gastric mucosa was on the 4 th day of modeling.Conclusion In the acute phase of acute cerebral infarction,gastric mucosal injury can be seen in rats,and its mucosal injury is related to cerebral infarction itself.Hypergastrinemia may not be the main factor of gastric mucosal injury.
分析卒中相关性肺炎对病人生命转归及预后的影响,尽管目前西医诊治卒中相关性肺炎已有规范的指南,但该病的控制在临床上仍有极大的困难.介绍中医药疗法辨证论治的特点,在个体化精准治疗下更显优势.主要对中药注射液、中药汤剂、针灸及其他中医药疗法治疗卒中相关性肺炎的现状进行综述.
Focal cerebral ischemia is associated with ischemia/reperfusion (I/R) injury. Hispidulin is a flavonoid compound with a variety of pharmacological properties. The neuroprotective effects of hispidulin have not been fully elucidated. Herein, we demonstrated that pretreatment of animals with hispidulin improved the neurological outcomes and decreased the infarct size and brain edema in the cerebral focal I/R model. Mechanistically, we showed in vivo and in vitro that hispidulin exerted a protective effect against I/R injury by inducing the Nrf2 antioxidant pathway through modulation of AMPK/GSK3β signaling. Taken together, our results suggest that hispidulin may be a useful neuroprotective agent against ischemia/reperfusion (I/R) injury.
将某医院急诊科2013年1月至2016年6月收治的急性重度有机磷中毒患者,仅采取常规治疗的28例作为对照组(A组),剩余患者随机分为常规治疗加杂合式血液净化治疗组(B组)和常规治疗加杂合式血液净化治疗、胃肠洗消溶液鼻饲治疗组(C组),并比较三组临床疗效.结果显示,与A组比较,B组、C组患者血清胆碱酯酶上升快、呼吸衰竭、中间综合征发生率低,ICU治疗时间短,死亡率低,且C组疗效优于B组(均P<0.05),但C组与B组死亡率的差异无统计学意义.三组患者治疗3d、5d、10d后APACHE Ⅱ评分均较治疗前下降(P<0.05),且同一治疗时间B组、C组APACHE Ⅱ评分均低于A组(P<0.05),C组APACHE Ⅱ评分低于B组(P<0.05).提示杂合式血液净化技术联合胃肠洗消溶液治疗急性重度有机磷中毒疗效较好.
报道1例口服美托洛尔及苯海拉明所致重度休克患者的临床表现及救治过程.治疗前及时留取血、尿标本,及时进行毒物检测,有助于指导治疗;尽早行血液净化清除毒物在救治中起到关键性作用.
蓖麻毒素毒性极高,中毒病例临床较少见.报道2例蓖麻子中毒患者的临床表现及救治经过.
目的:探讨枳实对脑梗塞大鼠急性期胃动素(MTL)、胃泌素(GAS)的调节作用.方法:24只大鼠制备大脑中动脉梗塞模型,随机分为脑梗塞组、枳实组、西咪替丁组,并设正常对照组,每组8只.分别给予生理盐水、枳实、西咪替丁、生理盐水灌胃,4天后放免法测定血浆胃动素(MTL)、血清胃泌素(GAS)含量.结果:枳实组与西咪替丁组大鼠血清GAS含量明显低于脑梗塞组(P<0.01),但仍高于正常组大鼠(P<0.01),二者比较差异无统计学意义(P>0.05);枳实组大鼠血浆MTL含量明显低于脑梗塞组(P<0.01),西咪替丁组含量较脑梗塞组有所降低(P>0.05),两组含量仍高于正常组大鼠(P<0.01),枳实组较西咪替丁组血浆MTL明显降低(P<0.01).结论:枳实对脑梗塞急性期胃酸分泌及胃肠动力有一定的调节作用.
目的:研究高龄老年脓毒症患者的发病情况及临床特征。方法回顾分析2010年8月至2011年5月我院急诊科入住高龄老年脓毒症病例62例,根据预后分为死亡组(15例)和存活组(47例),比较两组病例的临床特征。结果高龄老年脓毒症发生率28%(62/223):病死率24%(15/62)。呼吸道感染所致脓毒症比例高,死亡组与存活组在体温、心率、呼吸、白细胞计数、超敏C反应蛋白的方面比较差异无统计学意义(P>0.05),但两组数据均高于正常;在血小板计数、血清白蛋白及APACHEⅡ评分方面比较差异有统计学意义(P<001)。死亡组血小板计数、血清白蛋白低于存活组,APACHEⅡ评分高于存活组。结论高龄老年脓毒症在急诊科是一种常见病,患者病情重,病死率高,呼吸道感染所致脓毒症比例高,血小板计数和血清白蛋白降低结合APACHEⅡ评分增高可能与不良预后有关。
Objective: To observe the effect of Huanglian jiedu decoction( HLJDT) on the changes of the motilin( MTL) and vasoactive intestinal peptide( VIP) in the acute stage of cerebral infarction rats. Methods:Models of middle cerebral artery occlusion( MCAo) as cerebral infarction were made,they were divided into cerebral infarction group,HLJDT routine dose group,high dose group,cimetidine group,sham operation group randomly,another rats were chosen as the normal control group. Rats were given sodiun chloride,HLJDT routine dose,HLJDT high dose,cimetidine,sodiun chloride respectively. On the forth day and the seventh day,inferior vena venous blood samples were collected to detect MTL and VIP concentrations by radioimmunoassay. Results:On the 4th and 7th day,plasma MTL and VIP of cerebral infarction group and still higher than those of the normal group and sham operation group,those in HLJDT high dose group were lowered obviously( P 0. 01); on the 4th day,compared with HLJDT routine dose group,the MTL level of HLJDT high dose group has significant difference( P 0. 01),and there was also significant in level of VIP( P 0. 05); The 7th day,MTL and VIP of HLJDT routine dose group were lower than those on the 4th day( P 0. 05). Concultion: HLJDT can effectively regulate the expression of MTL and VIP,and the efficacy were dose- related.