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采用微循环实验方法,研究一氧化氮(NO)、一氧化碳(CO)对大鼠软脑膜和提睾肌微血管急性缺氧反应的影响。结果显示,内源CO生成阻断剂ZnPPⅨ对软脑膜血管的基础管径及缺氧脑微动脉扩张反应均无影响,10~(-4)mol/L ZnPPⅨ可使提睾肌微动脉收缩(7.55±3.55)％,并可使提睾肌微动脉缺氧收缩反应由(10.84±3.07)％增强至(15.48±4.94)％。10~(-4)mol/L内源NO生成阻断剂L-NNA使脑和提睾肌微动脉基础口径分别缩小(7.94±1.99)％和(10.75±3.90)％,并可使脑微动脉缺氧扩张反应由(28.16±13.20)％减弱至(20.35±8.35)％;却对提睾肌微动脉缺氧收缩反应无显著影响。而外源给CO使基础脑和提睾肌微动脉收缩,并使其缺氧反应减弱。外源给NO可轻微扩张脑微动脉和提睾肌微动脉,但对其缺氧反应无影响。
The effects of nitric oxide (NO) and carbon monoxide (CO) on the acute hypoxia in the pia mater and cremasteric myocytes of rats were studied by using microcirculation method. The results showed that the endogenous CO production blocker ZnPPⅨ had no effect on the basic diameter of pial vessels and the dilation response of hypoxic cerebral arterioles. 10 ~ (-4) mol / L ZnPPⅨ could cause the contraction of the cremasteric arterioles 7.55 ± 3.55)%, and could increase the anaerobic contraction response of cremasteric myocytes from (10.84 ± 3.07)% to (15.48 ± 4.94)%. L-NNA, a blocker of endogenous NO at a concentration of 10 -4 mol / L, reduced the basilar caliber of cerebral and cremasteric arteries by (7.94 ± 1.99)% and (10.75 ± 3.90)%, respectively, Arterial hypoxia dilatation response decreased from (28.16 ± 13.20)% to (20.35 ± 8.35)%, but had no significant effect on the anoxia and contractile responses of the cremasteric arteries. The exogenous CO to the basal brain and cremasteric arterioles shrink, and make its hypoxic response weakened. Exogenous to NO can slightly dilate cerebral arterioles and cremasteric arterioles, but had no effect on their hypoxia response.