Chahine R, Chanh A P, Lasserre B, Dossou-Gbete V
Institut de Physiologie, Toulouse, France.
Prostaglandins Leukot Essent Fatty Acids. 1991 Aug;43(4):261-6. doi: 10.1016/0952-3278(91)90040-c.
The aim of the study was to determine the prostacyclin (PGI2) and thromboxane A2 (TXA2) synthetase activities of myocardial tissue and their variation during ischemia and reperfusion. Regional ischemia was induced by 10 min occlusion of the left anterior descending coronary artery in isolated Langendorff rabbit hearts. Biosynthesis of PGI2 and TXA2 were carried out by using arachidonic acid as substrate and left ventricle microsomes (LVM) from ischemic and non-ischemic areas as sources of PGI2 and TXA2 synthetase. 6-keto-PGF1 alpha and TXB2, stable metabolites of PGI2 and TXA2 respectively, were determined by radioimmunoassay. Experiments carried out under the adopted conditions showed that LVM were able to synthetise PGI2 as well as TXA2 from arachidonic acid. On the other hand, ischemia depressed both PGI2 and TXA2 synthetase activities of cardiac tissue: the depression was more pronounced on TXA2 synthetase than on PGI2 synthetase with no significant difference between ischemic and non-ischemic regions. Moreover, ischemia increased the ratio 6-keto-PGF1 alpha/TXB2 indicating therefore that it can facilitate the formation of PGI2. The post ischemic reperfusion of the heart counteracted the decrease in PGI2 synthetase induced by ischemia which returned to the normal level: reperfusion also slightly reversed the decrease in TXA2 the decrease in TXA2 synthetase. However, the diminution in TXA2 synthetase of non-ischemic myocardium was attenuated but it remained lower than the normal level. These results suggested that the whole left ventricle is affected by regional ischemia. Furthermore it appears that myocardial TXA2 synthetase is more vulnerable than PGI2 synthetase to a lack of oxygen and nutrients.
本研究的目的是测定心肌组织中前列环素（PGI2）和血栓素A2（TXA2）合成酶的活性及其在缺血和再灌注过程中的变化。通过在离体Langendorff兔心脏中闭塞左前降支冠状动脉10分钟诱导局部缺血。以花生四烯酸为底物，以缺血和非缺血区域的左心室微粒体（LVM）作为PGI2和TXA2合成酶的来源，进行PGI2和TXA2的生物合成。分别通过放射免疫测定法测定PGI2和TXA2的稳定代谢产物6-酮-PGF1α和TXB2。在所采用的条件下进行的实验表明，LVM能够从花生四烯酸合成PGI2以及TXA2。另一方面，缺血降低了心脏组织中PGI2和TXA2合成酶的活性：TXA2合成酶的降低比PGI2合成酶更明显，缺血和非缺血区域之间无显著差异。此外，缺血增加了6-酮-PGF1α/TXB2的比值，因此表明它可以促进PGI2的形成。心脏缺血后再灌注抵消了缺血诱导的PGI2合成酶的降低，使其恢复到正常水平：再灌注也略微逆转了TXA2合成酶降低导致的TXA2的降低。然而，非缺血心肌中TXA2合成酶的减少有所减轻，但仍低于正常水平。这些结果表明，整个左心室受到局部缺血的影响。此外，心肌TXA2合成酶似乎比PGI2合成酶更容易受到缺氧和营养缺乏的影响。
