摘要
目的:研究烧伤休克延迟复苏对心肌组织磷脂酶A2(PLA2)活性的影响以及维拉帕米、牛磺酸的抑制作用。方法:雄性SD大鼠造成30%体表面积的Ⅲ度烧伤,分为烧伤不复苏(B)组、早期复苏(BE)组、延迟复苏(BD)组、延迟复苏+维拉帕米(BDV)组和延迟复苏+牛磺酸(BDT)组,伤后8h取左心室肌组织匀浆后用盐酸滴定法测定PLA2活性。结果:B组心肌组织PLA2活性非常明显高于正常对照(C)组(P<0.01);BD组酶活性显著高于BE组和B组(P<0.05);BDV、BDT组酶活性显著低于BD组(P<0.05)。结论:烧伤休克延迟复苏可进一步激活心肌组织PLA2活性,维拉帕米、牛磺酸抑制PLA2活性可能是拮抗心肌缺血再灌注损伤的机制之一。
Objective: To study the effects of delayed resuscitation on the activities of PLA_2 in myocardium of severely burned rats and inhibitory roles of verapamil and taurine. Methods: Male SD rats were inflicted to 30%TBSA, full-thickness burn injury, and were classified to serve as burn with no fluid resuscitation (B) group, burn with early fluid resuscitation (BE) group, burn with delayed resuscitation (BD) group, burn with delayed resuscitation plus verapamil(BDV) and taurine(BDT) group. Gathered at 8 h postburn, the left ventricular myocardium PLA_2 activities were assayed by HCl titration after homogenation. Results: The activities of PLA_2 were very significantly higher (P<0.01) in B group compared with normal control group, and in BD group compared with BE group. Furthermore, the activities were significantly higher (P<0.05) in BD group compared with B group. Verapamil and taurine could significantly inhibit the PLA2 activities in delayed resuscitation groups (P<0.05). Conclusion: Delayed resuscitations of burn shock most severely stimulate the PLA2 in myocardium, resulting in the ischemiareperfusion injuries. Verapamil and taurine might have protection roles against the ischemiareperfusion injuries through inhibiting the PLA_2.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1998年第S1期50-52,共3页
Academic Journal of Second Military Medical University
基金
国家自然科学基金
国家自然科学基金委员会杰出人才基金
上海市卫生系统百名跨世纪优秀学科带头人培养计划资助