摘要
本实验采用同时测定血清磷脂酶Ａ２（ＰＬＡ２）和脂质过氧化代谢终产物丙二醛（ＭＤＡ）的方法，动态观察两者在犬肠缺血性休克中的作用及促甲状腺素释放激素（ＴＲＨ）对它们的影响。结果显示：休克后，血清ＰＬＡ＿２活性和血清ＭＤＡ含量均明显升高，与平均动脉压呈显著负相关。而两者间则存在显著正相关关系，两者协同参与了肠缺血性休克的发生发展过程。静脉注射ＴＲＨ能有效地抑制血清ＰＬＡ。活性升高和明显地降低血清ＭＤＡ含量，这可能是ＴＲＨ抗休克机理的一个重要因素。
By testing serum phospholipase A2 (PLA2)activity and serum malondialdehyde(MDA)coneentration simuItaneously、the role of them in dogs intestinal ischemia shockand the effects of thyrotropin-releasing hormone(TRH)on them were studied The model ofshock was created by occluding both Superior mesenteric artery and vein(SMAv)for a 240min period and releasing SMA.V. The TRH-treated dogs(n=5)were given TRH(total 5mg/kg)iv at 30min before releasing SMA,V,and the control dogs(n=5)received salineequivalent.The resuIts showed that serum PLA2 cativity and serum MDA concentrationwere increased significantly after shock and were correlated with decrease of mean artery pressure(P<0.01).While there was a definite positive correlation between serum MDA coneentrationand serum PLA2 activity,which suggested that both PLA2 and LPO are involved in thepathophysiological changes of intestinal ischemia shock coordinately.Serum PLA2 activity ofthe TRH-treated dogs increased also,but was lower than that ofthe control dogs after treatment(P<0.01 or <0.001).Serum MDA of the TRH-treated dogs did not increase and was lowerthan that of the control dogs after treatment(P<0.05 or < 0.00 1).These results suggestedthat one important factor of the antishock mechanisnis of TRH in canine intestinal ischemiashock might be its effective suppression of serum PLA2 activity and alleviation oflipoperoxidation danlage.
出处
《中国病理生理杂志》
CSCD
北大核心
1996年第4期392-395,共4页
Chinese Journal of Pathophysiology
关键词
丙二醛
磷酶类
肠缺血性休克
TRH
Dogs.Malondialdehyde.phosnholinases.Shock.ThvrotroDin releasing hormone
