Mechanisms of coronary vasoconstriction induced by high arterial oxygen tension
Mechanisms of coronary vasoconstriction induced by high arterial oxygen tension
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DOI：
10.1152/ajpheart.1997.272.1.h67
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发表时间：
1997-01-01
影响因子：
4.8
通讯作者：
Vicaut, E
中科院分区：
文献类型：
--
作者：
Mouren, S;Souktani, R;Vicaut, E
在用红细胞悬液灌流的离体兔心脏上，我们研究了内皮细胞和几种物质在高动脉血氧分压(PaO2)引起的冠脉血管收缩中的作用。将Krebs-Henseleit缓冲液中的红细胞充氧，以获得对照和高PaO2灌流液。通过降低高PaO2灌流液中的血红蛋白浓度，使两种灌流液中的动脉氧含量保持恒定。冠脉血流量保持恒定，供氧不会随着PaO2的升高而变化。因此，灌流压力的增加反映了冠状动脉阻力的增加。吲哚美辛、去甲二氢愈创木酸、N-G-硝基-L-精氨酸、超氧化物歧化酶和过氧化氢酶不影响高PaO_2引起的冠脉收缩，但可被内皮损伤或克罗卡林所阻断。这些结果表明：1)内皮细胞参与了高PaO_2引起的冠脉收缩；2)这种作用不依赖于环氧合酶或脂氧合酶产物、一氧化氮或自由基；3)关闭ATP敏感的K+通道介导了这种收缩。
In isolated rabbit hearts perfused with suspension of red blood cells, we investigated the role of the endothelium and of several substances in the coronary vasoconstriction induced by a high arterial blood oxygen tension (Pa-O2). Red blood cells in Krebs-Henseleit buffer were oxygenated to obtain control and high-Pa-O2 perfusates. Arterial oxygen content was kept constant in both perfusates by reducing hemoglobin concentration in the high-Pa-O2 perfusate. Coronary blood flow was kept constant so that oxygen supply would not vary with the rise in Pa-O2. Increases in perfusion pressure therefore reflected increased coronary resistance. The high Pa-O2-induced coronary vasoconstriction was not affected by administration of indomethacin, nordihydroguaiaretic acid, N-G-nitro-L-arginine, or superoxide dismutase and catalase but was abolished after endothelium damage or by cromakalim. These results demonstrate that 1) the endothelium contributes to the high Pa-O2-induced coronary vasoconstriction; 2) this effect is independent of cyclooxygenase or lipoxygenase products, nitric oxide, or free radicals; and 3) the closure of ATP-sensitive K+ channels mediates this vasoconstriction.