心肌缺血／再灌注对球结膜微循环的影响以及一氧化氮的调节作用

对照观察兔急性心肌缺血／再灌注时球结膜微循环的变化，测定动物血浆中内皮舒张因子／一氧化氮（ＥＤＲＦ／ＮＯ）、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１α（６－Ｋｅｔｏ－ＰＧＦ１α）、超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）的浓度变化，并用光镜和电镜对缺血／再灌注心肌组织作形态学观察。结果发现：（１）兔心肌缺血／再灌注后球结膜微循环异常；表现为Ａ３、Ａ４微动脉血管管径缩小，毛细血管交换距离增大。（２）血浆中ＥＤＲＦ／ＮＯ水平降低；（３）血浆ＴＸＢ２、ＭＤＡ水平升高，ＳＯＤ、６－Ｋｅｔｏ－ＰＧＦ１α下降；（４）光镜下：缺血区心肌组织细胞肿胀变性。电镜下：内皮细胞肿胀，部分毛细血管腔内有红细胞、白细胞附壁阻塞，线粒体肿胀，糖原颗粒减少。结果提示：心肌在较短时间缺血后再灌注（缺血３０ｍｉｎ再灌注３０ｍｉｎ）后就可产生组织损伤，这可能与血管内皮受损，ＥＤＲＦ／ＮＯ合成释放减少，缩血管物质ＴＸＡ２升高，血小板、白细胞粘附、聚集在血管内皮上，氧自由基产生过多等有关。上述因素共同作用导致缺血／再灌注心肌微循环功能障碍进而引起组织形态改变。

Changes of Bulbar Conjunctival Microcirculation by Ischemia/Reperfusion and Modulation of Nitric Oxide

The bulbar conjunctival microcirculation was observed in rabbits with acute myocardial ischemia/reperfusion. Simultaneously, plasma levels EDRF/NO, TXB 2, 6 Keto PGF 1α , SOD(superoxide dismutase) and MDA(Malondialdehyde) were determined. With light microscopy and electron microscopy, morphologic observation on myocardial tissues was performed. Results: (1)The diameter of arterioles(A 3,A 4) turned small, but capillary diffusion diameter became large. (2)Plasma levels of EDRF/NO, 6 Keto PGF 1α and SOD decreased. (3)Myocardial tissue tense contractioning, lumen of capillary closing, leukocytes adhered on wall of capillary, mitochondria, endothelial cell swelling. Results indicated that ultrastructure injury occurred after ischemia/reperfusion. The possible reason is ischemia/reperfusion result in enthothelial cell damage. When the endothelium was abnormal, vasoconstrictive mediator increased, meanwhile OFR(oxide free radical) was released in large quantity. Furthermore, myocardial microcirculation dysfunction and pathologic changes happened.