A new role of NO on the accelerating effect of oxygen supply to tissue

采用双点光度计法观察大鼠肝窦单侧、无支肝窦，研究硝酸甘油对微循环氧释放的影响。硝酸甘油显著增加血窦内红细胞的氧释放量。血窦单位长度血红蛋白氧饱和度差异明显增强，而红细胞速度、血红蛋白（Hb）浓度、进入血窦的氧合血红蛋白以及激光组织血流仪测量的肝局部血流量无明显变化。在离体肝脏灌注无hb含氧缓冲液后，肝氧消耗没有变化。脱硝异山梨酯也有类似的效果，但效果较慢。这些结果表明硝酸甘油和硝酸异山梨酯可以促进红细胞的氧释放，但不会显著增加组织血流量。体外实验表明，硝酸甘油处理后大鼠血液中O2亲和力明显降低。它含有单独与Hb亚基结合的NO。可能是器官循环过程中NO血红素铁近端组氨酸键断裂或拉伸导致O2亲和力降低，而肺内O2亲和力通过恢复该键而恢复。当细胞因子在炎症等事件中诱导血管系统NO合成酶时，这些结果应该是有效的。

The effect of nitroglycerin on oxygen (O2) release in microcirculation was investingated by examining single, unbranched hepatic sinusoids of rats using dual-spot microspectroscopy. Nitroglycerin significantly increased O2 selease from erythrocytes flowing in the sinusoids. Differences in O2 saturation of hemoglobin per unit length of the sinusoid were significantly enhanced, while there were no significant changes in erythrocyte velocity, hemoglobin (Hb) concentration, and oxyhemoglobin flow into the sinusoids, as well as regional hepatic blood flow measured with a laser tissue blood flow meter. No change was noted for hepatic O2 consumption measured in isolated liver perfused with Hb-free oxygenated buffer. Isosorbide denitrate showed a similar but slower effect. These findings suggest that nitroglycerin and isosorbide dinitrate enhance O2 release from erythrocytes without significantly increasing tissue blood flow. In vitro study revealed O2 affinity was significantly decreased in blood taken from rats treated with nitroglycerin. It contained NO bound to Hb a subunit alone. It is possible that breaking or stretching of the NO heme iron-proximal histidine bond during organ circulation triggered the decrease in O2 affinity, while the O2 affinity was recovered in lung by restoring the bond. These results should operate when cytokines induce NO synthase in vascular system during such events as inflammation.