摘要
观察了急性缺氧和慢性间断性缺氧兔心肌血流量、心肌组织中腺苷和cGMP含量的变化及N ̄ω-NO3-L-精氨酸(L-NA)阻断一氧化氮(NO)生成后的影响。结果表明,急性缺氧兔心肌血流量增加,心肌组织中腺苷和cGMP含量增高;静脉输入L-NA后,心肌血流量减少,同时心肌组织中cGMP含量降低,腺苷含量进一步增高。慢性缺氧免心肌血流量无明显变化,红细胞压积(Hct)增高;抑制NO合成后,右室心肌血流量减少,左室心肌血流量无明显变化。说明NO和腺苷均参与急性缺氧时冠状血管扩张机制;NO参与慢性缺氧兔心肌血管基础张力调节。
To investigate the roles of nitric oxide(NO)and adenosine in regulation of myocardial bloodflow(MBF) during hypoxia,the changes of M BF,the myocardial adenosine and cGMP contentsand the effect of Nω-nitro-L-arginine(L-NA) were obServed.The results were as follows:(1)Acute hypoxia caused increase in left and right ventricular M BF, myocardial adenosine andcGMP contents. After administration of L-NA(i.v.0.5% L-NA 0.3ml / min×20min),the leftand right ventricular M BF and myocardial cGMP content were reduced signiflcantly.(2)lntermittent hypobaric hypoxia for 4 weeks did not lead to signiflcant change in the left and rightventricular MBF,the myocardial cGMP and adenosine contents. However,hematocrit and MBFshowed negative correlation during hypoxia. After treatment with L-NA(i.v,0.5 % L-NA0.3ml/min×20min)right ventricular MBF decreased,while the left ventricular MBF remainedunchanged.These results suggest that NO and adenosine may be involved in the regulation ofacute hypoxic M BF and NO may play a certain role in the maintenance of basal coronaryvascular tone in the chronic hypoxic rabbits.
出处
《中国应用生理学杂志》
CAS
CSCD
1996年第2期170-173,共4页
Chinese Journal of Applied Physiology
基金
中国科学院低氧生理开放实验室资助