Lin H, McGrath J J
Department of Physiology, Texas Tech University Health Sciences Center, Lubbock 79430.
Drug Chem Toxicol. 1988;11(4):371-85. doi: 10.3109/01480548809018109.
The vasodilator effects of carbon monoxide (CO) were studied in an isolated perfused rat thoracic aorta preparation. Thoracic aortas from male Sprague-Dawley laboratory rats were dissected free of surrounding tissue, cannulated proximally, and tethered to in situ length. The vessels were perfused with oxygenated Krebs-Henseleit (KH) solution at 37 degrees C in a constant flow system with a circumferentially-applied, pulsatile (300/min), basal "systolic" pressure of 100 mm Hg. Aortas were precontracted with high-potassium (K+) or norepinephrine (NE). Changes in perfusion pressure were indicative of changes in vascular resistance induced by the test gas mixtures. Oxygen (O2) content of the perfusate was kept constant, while CO and nitrogen (N2) were altered. CO (2.5, 5 and 10%) dilated both K+-contracted and NE-contracted aortas in a dose-dependent manner. A significant vasodilation in response to 5% CO (24.5% of maximal), but not to 5% N2, was obtained in the K+-contracted aortas. After the endothelium was removed chemically, the aortas continued to dilate in response to CO. These results suggest that CO has a direct vasorelaxant effect on vascular smooth muscle which is nonspecific and is not endothelium-dependent.
在离体灌注大鼠胸主动脉标本中研究了一氧化碳（CO）的血管舒张作用。从雄性斯普拉格-道利实验室大鼠分离出胸主动脉，去除周围组织，在近端插管，并固定至原位长度。血管在恒流系统中用37℃的含氧 Krebs-Henseleit（KH）溶液灌注，施加周向搏动性（300次/分钟）基础“收缩压”100 mmHg。主动脉先用高钾（K+）或去甲肾上腺素（NE）预收缩。灌注压力的变化表明测试气体混合物引起的血管阻力变化。灌注液中的氧（O2）含量保持恒定，而CO和氮（N2）则发生改变。CO（2.5%、5%和10%）以剂量依赖方式使K+预收缩和NE预收缩的主动脉均扩张。在K+预收缩的主动脉中，对5% CO（最大扩张的24.5%）有显著血管舒张反应，但对5% N2无反应。化学去除内皮后，主动脉对CO仍有舒张反应。这些结果表明，CO对血管平滑肌有直接的血管舒张作用，该作用是非特异性的且不依赖于内皮。
