儿茶酚胺类药物对脓毒性休克大鼠心肌的影响

目的 :利用生化指标和形态学方法研究儿茶酚胺类药物对脓毒性休克大鼠心脏的影响与机制。方法 :用盲肠结扎穿孔术 (CL P)制成大鼠的脓毒性休克模型。采用多巴酚丁胺 (DB)、去甲肾上腺素 (NE)及两者最小剂量联合应用以纠正血压。动物随机分为假手术对照组、CL P对照组、CL P+DB组、CL P+NE组、CL P+DB+NE组 ,每组各 8只大鼠。心肌损害程度应用血清心肌钙蛋白 I(c Tn I)和肌酸激酶 (CK)浓度来表达 ,用光镜与电镜检查心肌组织形态学变化。结果 :脓毒性休克大鼠 c Tn I升高 (P<0 .0 5 ) ,儿茶酚胺类药物浓度不影响 c Tn I的水平 ;但 CK总量水平在儿茶酚胺治疗组升高 (P均 <0 .0 5 ) ;心肌组织形态学检查与 c Tn I的结果相符合。结论 :脓毒性休克心肌损害由缺血引起 ,没有明确的证据显示儿茶酚胺类药物能加重心肌损害。

Influence of catecholamines on myocardium in experimental septic shock

Objective: To study the influence of catecholamine on myocardium in rats with septic shock and its mechanism by biochemical and pathophysiological methods to evaluate the underlying pathophysiologic mechanism of myocardial damage and the influence of catecholamine on the myocardial injury. Methods: Septic shock was replicated in rats by cecal ligation and puncture (CLP). Dobutamine(DB), norepinephrine(NE) and combination of DB and NE were used in the lowest dose. The rats were randomly divided into sham operations, CLP control group, CLP+DB group, CLP+NE group and CLP+DB+NE group, 8 rats in each group. Troponin I (cTnI) and total creatine kinase (CK) were measured, and myocardial tissue was examined under light microscopy and electron microscopy. Results: An significantly increased cTnI level was found in CLP septic shock rats, compared with sham rats(P<0.05). In the present study, the use of DB or NE alone, or the combination of the two drugs, was not found to influence the cTnI levels. But, the total CK levels in catecholamine-treated group were significantly increased(P<0.05). There was no statistically significant correlation between cTnI and CK levels. Morphological study confirmed the results of cTnI. Findings that were common in the myocardium of CLP septic shock rats included extracellular and intracellular edema as well as mitrochondrial injury. However, no conclusive evidence was found for the influence of catecholamine on myocardial damage. Conclusion: No evidence of the influence of catecholamine on myocardial damage is found. Pathological study suggests that myocardial injury is the result of ischemia.