Chahine R, Lasserre B, Assaad S
Institut de Physiologie, Toulouse, France.
Prostaglandins Leukot Essent Fatty Acids. 1999 Feb;60(2):101-6. doi: 10.1054/plef.1998.0014.
In this investigation, an anti-thromboxane A2 (TXA2) synthetase activity in the myocardial tissue, which can be modulated by ischemia and reperfusion, was observed. Regional ischemia was induced by 60 min occlusion of the left anterior descending coronary artery in isolated Langendorff rabbit hearts. Biosynthesis of TXA2 was carried out by using arachidonic acid (AA) as substrate, horse platelet microsomes (HPM) as the source of TXA2 synthetase and left ventricle microsomes (LVM) from ischemic and non-ischemic areas as effectors TXB2, the stable metabolite of TXA2, was determined by radioimmunoassay. Experiments carried out under the adopted conditions showed that LVM from control hearts were able to inhibit by up to 50% the biosynthesis of TXA2 from HPM. This anti-TXA2 synthetase activity was more pronounced when LVM from the non-ischemic area were used, rather then LVM from the ischemic one. A 60 min reperfusion decreased the anti-TXA2 activity. A superfused rabbit aorta strip was also used as a cascade bioassay to study the effect of LVM on the TX2-synthetase activity of HPM, and this confirmed our findings. These results suggest that the left ventricle possesses a self-defense mechanism against acute myocardial ischemia, independently from the circulation. The postulated mechanism may be initiated in the non-ischemic area.
在本研究中，观察到心肌组织中存在一种抗血栓素A2（TXA2）合成酶活性，该活性可受缺血和再灌注调节。通过在离体Langendorff兔心脏中闭塞左前降支冠状动脉60分钟诱导局部缺血。以花生四烯酸（AA）为底物，马血小板微粒体（HPM）作为TXA2合成酶的来源，缺血和非缺血区域的左心室微粒体（LVM）作为效应物进行TXA2的生物合成。通过放射免疫分析法测定TXA2的稳定代谢产物TXB2。在所采用的条件下进行的实验表明，来自对照心脏的LVM能够将HPM合成TXA2的能力抑制高达50%。当使用非缺血区域的LVM而不是缺血区域的LVM时，这种抗TXA2合成酶活性更为明显。60分钟的再灌注降低了抗TXA2活性。还使用灌注兔主动脉条作为级联生物测定法来研究LVM对HPM的TX2合成酶活性的影响，这证实了我们的发现。这些结果表明，左心室拥有一种独立于循环的针对急性心肌缺血的自我防御机制。推测的机制可能在非缺血区域启动。
