摘要
为探讨NO-样松驰因子(NO-LRF)在休克中的效应及其病理生理意义,本工作在大鼠止血带休克(ToS)模型上发现离体灌流的主动脉环对去甲肾上腺素的反应性降低,组织cGMP含量增加。用NO前体L-精氨酸(L-Arg)或NO合成阻断剂L-NNA,可溶性乌苷酸环化酶抑制剂亚甲蓝灌流,分别增强或减轻ToS动物主动脉的上述变化,而且这些药物的作用不受血管内皮是否存在的影响。实验结果提示非内皮细胞源的NO-LRF是引起ToS动物血管低反应性的因素之一。体内实验表明 L-Arg治疗缓解,而L-NNA恶化ToS病程,提示NO-LRF可能参与机体的适应保护机制。
On tourniquet shock (ToS) rat model, it was found that the reactivity of iso-lated perfused aortic ring to noradrenaline was decreased, while the cGMP contentof the aortic tissue was increased. These ToS-induced changes could be potenti-ated or attenuated respectively by perfusion with NO-precursor, L-arginine, or NO-synthesis inhibitor L-NNA independent of the presence of vascular endothelium.Guanylate cyclase inhibitor, methylene blue, could also attenuate the aortic rea-ctivity. All these results suggest that the aortic musculature can produce a NO-LRF factor capable of lowering the vascular reactivity of the ToS animals. ThatL-argine can ameliorate while L-NNA can exacerbate TOS, suggest that NO-LRF do play an adaptive role in the protective mechanism of the organism dur-ing ToS.
出处
《生理学报》
CAS
CSCD
北大核心
1992年第6期576-582,共7页
Acta Physiologica Sinica
关键词
一氧化氮
环化磷酸乌苷
休克
nitric oxide
cGMP
tourniquet shock
aorta
endothelium
