磷酸肌酸治疗心肌缺血性损伤的疗效分析

目的探究磷酸肌酸治疗心肌缺血性损伤的疗效。方法选取2017年1月至2018年4月我院收治的心肌缺血性损伤者共50例,根据治疗方法分为实验组与对照组,各组例数为25例,实验组采用常规治疗联合磷酸肌酸,对照组采用常规治疗,观察两组患者治疗效果、不同时间段肌磷酸肌酸激酶、磷酸肌酸激酶同工酶。结果主动脉开发后1 h、5 h、24 h实验组肌磷酸肌酸激酶水平低于对照组;主动脉开发后1 h、5 h、24 h实验组磷酸肌酸激酶同工酶低于对照组,P<0.05。结论辅以磷酸肌酸治疗心肌缺血性损伤利于改善心肌酶谱,值得推广。

电针“委中”对布比卡因致大鼠腰多裂肌损伤后形态学及CK、IL-17表达的影响

目的:观察电针"委中"穴对布比卡因(bupivacaine,BPVC)致大鼠腰多裂肌损伤后组织形态学及磷酸肌酸激酶(CK)、白介素17(IL-17)表达水平的影响。方法:将32只雄性SD大鼠随机分为对照组、模型组、电针委中组和电针肾俞组,每组8只。模型组、电针委中组和电针肾俞组采用0.5%BPVC肌内注射制备多裂肌损伤模型;对照组采用同样的方法注射0.9%Na Cl溶液。电针委中组、电针肾俞穴分别电针"委中"与"肾俞"穴,选用疏密波,频率2 Hz/10 Hz,电流强度1~2 m A,持续20 min;对照组与模型组不进行针刺干预。电针干预14 d后,通过苏木精-伊红(HE)染色和马松三色染色法(Masson)观察多裂肌炎细胞计数、瘢痕面积和肌纤维横截面积的变化。通过酶联免疫吸附法(ELISA)检测血清CK活性和IL-17的含量,并用免疫组化法检测多裂肌损伤部位的IL-17表达。结果:干预后,模型组、电针委中组和电针肾俞组的炎细胞计数、瘢痕面积明显高于对照组(均P<0.01),肌纤维横截面积明显减少(均P<0.01);电针委中组和电针肾俞组炎细胞计数、瘢痕面积均少于模型组(均P<0.01),肌纤维横截面积大于模型组(P<0.01,P<0.05)。干预后,模型组、电针委中组和电针肾俞组多裂肌损伤局部的IL-17表达、血清IL-17含量及CK活性均明显高于对照组(均P<0.01);电针委中组和电针肾俞组多裂肌中IL-17的表达、血清IL-17含量及CK活性均低于模型组(P<0.01,P<0.05);与电针肾俞组比较,电针委中组下调IL-17的趋势更明显(P<0.01)。结论:电针"委中"穴可通过下调血清CK和白介素-17的过度表达,减轻炎性反应,促进多裂肌的良性修复。

Association of the phosphatidylinositol signal pathway with prolonged myocardial ischemia

OBJECTIVE: To study the changes in activity of phosphatidylinositol 4 kinase (PI 4 kinase), phosphatidylinositol 4 phosphate 5 kinase (PIP 5 kinase) and protein kinase C (PKC) during myocardial ischemia and elucidate the relationship between phosphatidylinositol signal pathways and prolonged myocardial ischemia. METHODS: In vivo an ischemic rat model was used. Activity of PI 4 kinase, PIP 5 kinase and PKC were measured at different times in postischemic heart cells using isotope analysis. RESULTS: The activity of PI kinase, PIP kinase and PKC in the myocardium increased to peak at 1 hour postischemia, with activities 6.1, 3.0 and 4.0 fold over control levels, respectively. Their activities declined to normal levels with time. CONCLUSION: The phosphatidylinositol signal pathway is involved in prolonged myocardial ischemia, but its mechanism needs further study.