Lung Perfusion with Angiotensins I and II
Lung Perfusion with Angiotensins I and II
复制标题
用血管紧张素 I 和 II 进行肺灌注
DOI：
10.1161/01.res.28.5.559
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发表时间：
1971
影响因子：
20.1
通讯作者：
P. Khairallah
中科院分区：
文献类型：
--
作者：
R. K. Trker;M. Yamamoto;F. Bumpus;P. Khairallah
血管紧张素I或II在Krebs9溶液中灌注离体大鼠和豚鼠肺可导致肽活性明显丧失。血管紧张素辅助因子不能预防这种情况。除了在通过肺部时转化为八肽外，血管紧张素I释放出一种不同于血清素、肾上腺素、去甲肾上腺素和前列腺素e1和f2 α的致肌物质。这种物质不是我检测的血管紧张素碎片之一。反复暴露于含有血管紧张素1的肺灌注液后，兔主动脉的反应性降低。由于多次直接暴露于Krebs9溶液中的这种肽和代谢片段并没有产生这种效果，因此假设这是由肺部释放的物质引起的。
Perfusion of isolated rat and guinea pig lungs with angiotensin I or II in Krebs9 solution results in significant losses of peptide activity. This was not prevented by angiotensin cofactor. In addition to being converted to the octapeptide during passage through the lung, angiotensin I released a myotropic substance which is different from serotonin, epinephrine, norepinephrine, and prostaglandin E 1 and F 2α . This substance was not one of the several fragments of angiotensin I tested. There was a decreased responsiveness of rabbit aorta following repeated exposure to lung perfusate containing angiotensin I. Since repeated direct exposure to this peptide and metabolic fragments in Krebs9 solution did not produce this effect, it was assumed to be caused by a substance released from the lungs.