CHANGES IN NITRIC OXIDE PRODUCTION DURING SHOCK STATE AND ISCHEMIA-REPERFUSION INJURY

应用电子自旋共振波谱技术，测定了实验性感染性休克、失血性休克和内脏缺血再灌注损伤时亚硝基血红蛋白（NO-Hb）的变化，并探讨了休克时心肌收缩力与NO-Hb产生的关系。同时观察了NO合成酶抑制剂（L-NAME，L-canavanine）和NO清除剂（carboxy-PTIO）对存活时间的影响。在大鼠实验性休克模型中，NO-Hb产生的增加与心肌收缩力的降低密切相关，并且还与休克期间对乙酰氨基酚刺激的反应降低相关。L-NAME和L-刀豆氨酸对死亡率无影响，而羧基-PTIO（自由基清除剂）可显著提高死亡率。结果提示：（1）NO-Hb主要反映诱导型NO的产生，（2）足够剂量的组成型NO的产生是治疗休克所必需的，（3）NO-Hb可作为评价休克时心肌收缩力的有用指标。

Using an electron spin resonance spectroscopy, changes in nitrosyl-hemoglobin (NO-Hb) production during experimental septic shock, hemorrhagic shock and splanchnic ischemia-reperfusion injury were measured, and the relationship between cardiac contractility and NO-Hb production during shock was evaluated. The effects of NO synthetase (L-NAME, L-canavanine) inhibitors and NO scavengers (carboxy-PTIO) on survival time were also evaluated. In experimental shock models using rats, the increase in NO-Hb production was well correlated to the decrease in cardiac contractility, and also correlated to the decrease in the response to cathecolamine stimulation during shock. L-NAME and L- canavanine did not affect the mortality ratio, however, carboxy-PTIO (radical scavenger) significantly improve the mortality. These results suggest that 1) NO-Hb detected in the study mainly indicates the production of inducible NO, 2) adequate dose of constitutive NO production was necessary for treatment of shock, 3) NO-Hb may be useful index for evaluating the cardiac contractility during shock.