ABSTRACT
AIM: To study the role and the mechani sm of heme oxygenas/endogenous carbon monoxide on nitric oxide synthase/nitric oxide system in rats with pulmo nary hypertension induced by hypoxic hypercapnia. METHODS: Spr ague-Dawley rats w ere randomly divided into three groups: control group (A group),hypoxic hypercap n ic group (B group), hypoxic hypercapnia+hemin group (C group). Blood CO concentr at ion (COHb%),NO concentration,HO-1 activity, iNOS, cNOS in blood serum and lung h omogenate were measured, respectively. RESULTS: ① mPAP and RV /(LV+S) of B g roup were significantly higher than those of A and C group( P
ABSTRACT
AIMTo study the protective effects of EA against cer ebral ischemia-reperfusion injury. METHODSAcute cerebral ischemia w as produced by the occlusion of bilateral common carotid arteries of mice .The s urvival time in 12 h of the mice was observed, and the mortalities in 2 h, 6 h, 12 h were recorded. Pulsinelli four-vessel occlusion method was used to make ce rebral ischemia-reperfusion model of rats. The EEG and the reappearing time of righting reflex were recorded and the activity of GSH-Px,LDH,NOS in the brain w as tested. Researching the iNOS expression in hippocampiwith immunocytochemistry method and measure the mean optical density. RESULTSEA can decrease the mortalities and prolong the survival t ime in 12 h of the mice. EA can promote the recovery of the EEG and the RR after cerebral ischemia-reperfusion operation in rats and enhance the activities of the GSH-Px LDH, reduce the activity of the NOS. EA also inhibits the expression of iNOS and reduce it's value of mean optical density in hippocampi of the rat s. CONCLUSIONEA has protective effects against cerebral ischemai-r eperfusion injury.