短时间缺血再灌注后前列腺素合成的心外膜与心内膜“镜中”变化。

Eicosanoids Pub Date : 1992-01-01
B Rabinowitz, M Arad, E Elazar, R Klein, Y Har Zahav
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引用次数: 0

摘要

心脏缺血和再灌注与冠状静脉流出物中前列腺素水平升高有关。本研究采用体内-体外技术研究心脏组织PGE2和PGF2 α新生生成的区域变化。犬心内膜和心外膜外植体分别在体内诱导5 min局部缺血或5 min缺血+ 10 min再灌注后孵育(n = 10和6)。与非缺血区相比,缺血导致心内膜前列腺素合成显著增加,但心外膜前列腺素合成没有增加:PGF2 α为7.6 +/- 0.7 vs 4.5 +/- 0.5 pg/mg / h (P < 0.001), PGF2 α为8.8 +/- 1.2 vs 6.8 +/- 1.2 pg/mg / h (P < 0.01)。再灌注后,正常心肌的PGE2高于病变心内膜(5.8 +/- 0.6 vs 4.4 +/- 0.5 pg/mg / h, P < 0.05)。再灌注心外膜发生相反的变化:与“正常”区域相比,再灌注心外膜PGE2分别为8.2 + 0.9和4.9 +/- 0.7 pg/mg / h (P < 0.01), PGF2 α为11.1 +/- 0.9和6.0 +/- 0.6 pg/mg / h (P < 0.001)。我们的研究结果表明,左心室壁对缺血和再灌注的二十烷类反应是不均匀的。在心内膜与心外膜之间以及损伤区与正常区之间可见镜内改变。
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Epicardial versus endocardial "in mirror" changes in prostaglandin synthesis after short periods of ischemia and reperfusion.

Cardiac ischemia and reperfusion are associated with increased prostaglandin levels in the coronary venous effluent. This study implemented an in vivo-in vitro technique to investigate regional alterations in heart tissue PGE2 and PGF2 alpha de novo production. Canine endocardial and epicardial explants were incubated following 5 min regional ischemia, or 5 min ischemia with 10 min reperfusion, induced in vivo in two groups of animals (n = 10 and 6, respectively). Ischemia produced a significant upsurge in endocardial but not in epicardial prostaglandin synthesis as compared with the non-ischemic zone: 7.6 +/- 0.7 versus 4.5 +/- 0.5 pg/mg tissue per h in PGE2 (P < 0.001) and 8.8 +/- 1.2 versus 6.8 +/- 1.2 pg/mg per h PGF2 alpha (P < 0.01). Following reperfusion, PGE2 was higher in the apparently normal than in the affected endocardium (5.8 +/- 0.6 versus 4.4 +/- 0.5 pg/mg per h, P < 0.05). Opposite changes occurred in the reperfused epicardium: 8.2 + 0.9 versus 4.9 +/- 0.7 pg/mg per h PGE2 (P < 0.01) and 11.1 +/- 0.9 versus 6.0 +/- 0.6 pg/mg per h PGF2 alpha (P < 0.001), for the reperfused as compared to the "normal" region, respectively. Our findings imply that the left ventricular wall is not homogeneous in its eicosanoid response to ischemia and reperfusion. "In mirror" changes were found between endocardium end epicardium and between the injured and the apparently normal regions.

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