Self-protection by cardiac myocytes against hypoxia and hyperoxia
Self-protection by cardiac myocytes against hypoxia and hyperoxia
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DOI：
10.1161/01.res.85.8.690
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发表时间：
1999-10-15
影响因子：
20.1
通讯作者：
Samuel, JL
中科院分区：
文献类型：
--
作者：
Winegrad, S;Henrion, D;Samuel, JL
心肌必须在其能量供应和做功之间保持持续的平衡。实现这种平衡的一个重要机制是通过心肌细胞和心肌血管系统之间的化学信号进行的串扰。这已经通过在不同浓度的氧气中孵育分离的心肌细胞，然后在分离的主动脉环和小阻力动脉上测定血管活性物质的条件培养基来证明。随着氧浓度增加到6%以上，心肌细胞产生越来越多的血管紧张素I，血管紧张素I被血管转化为血管紧张素II。血管紧张素II刺激血管内皮细胞分泌内皮素并增加血管张力。低于6%的氧气，心肌细胞分泌腺苷，其直接作用于血管平滑肌以阻断α-肾上腺素能激动剂的作用并降低血管张力。在一个完整的心脏，这两个调节系统的净效应将是维持心肌细胞的氧浓度在一个狭窄的范围内。通过充当氧传感器，心肌细胞根据肌细胞的需要调节血管张力，并减少缺氧和活性氧物质的广泛形成的潜在问题。
Cardiac muscle must maintain a continuous balance between its energy supply and work performed. An important mechanism involved in achievement of this balance is cross talk via chemical signals between cardiac myocytes and the cardiac muscle vascular system. This has been demonstrated by incubating isolated cardiac myocytes in different concentrations of oxygen and then assaying the conditioned media for vasoactive substances on isolated aortic rings and small-resistance arteries. With increasing oxygen concentrations above 6%, cardiac myocytes produce increasing amounts of angiotensin I, which is converted to angiotensin II by the blood vessel. The angiotensin II stimulates vascular endothelial cells to secrete endothelin and increase vascular tone. Below 6% oxygen, cardiac myocytes secrete adenosine, which acts directly on vascular smooth muscle to block the effect of alpha-adrenergic agonists and reduce vascular tone. In an intact heart, the net effect of these 2 regulatory systems would be the maintenance of oxygen concentration within a narrow range at the cardiac myocytes. By acting as oxygen sensors, cardiac myocytes modulate vascular tone according to the needs of the myocytes and reduce potential problems of hypoxia and extensive formation of reactive oxygen species.