Epicardial versus endocardial "in mirror" changes in prostaglandin synthesis after short periods of ischemia and reperfusion.
Epicardial versus endocardial "in mirror" changes in prostaglandin synthesis after short periods of ischemia and reperfusion.
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短暂缺血和再灌注后，心外膜与心内膜前列腺素合成的“镜像”变化。
DOI：
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发表时间：
1992
期刊：
影响因子：
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通讯作者：
Y. Har Zahav
中科院分区：
文献类型：
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作者：
B. Rabinowitz;M. Arad;E. Elazar;R. Klein;Y. Har Zahav
心脏缺血和再灌注与冠状静脉流出液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PGE 2和PGF 2 α从头产生的区域变化。在两组动物（分别为n = 10和6）中，在体内诱导5 min局部缺血或5 min缺血伴10 min再灌注后孵育犬心内膜和心外膜外植体。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显著增加：PGE 2为7.6 +/- 0.7 vs 4.5 +/- 0.5 pg/mg组织/h（P < 0.001），PGF 2 α为8.8 +/-1.2 vs 6.8 +/- 1.2 pg/mg组织/h（P < 0.01）。再灌注后，明显正常的心内膜中的PGE 2高于受影响的心内膜（5.8 +/- 0.6 vs 4.4 +/- 0.5 pg/mg/h，P < 0.05）。在再灌注的心外膜中发生了相反的变化：与“正常”区域相比，再灌注区域的PGE 2分别为8.2 ± 0.9和4.9 ± 0.7 pg/mg/h（P < 0.01），PGF 2 α分别为11.1 ± 0.9和6.0 ± 0.6 pg/mg/h（P < 0.001）。我们的研究结果表明，左心室壁是不均匀的类花生酸反应缺血和再灌注。心内膜与心外膜之间及损伤区与表面正常区之间存在“镜像”改变。
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.