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AIM To establish a new bioassay method for estimating the rat angiotensin Ⅰ converting engyme (ACE) activity in vivo by using ramipril (Ram), a ACE inhibitor. METHODS The change in mean arterial pressure induced by angioteuasin Ⅰ (AngⅠ) or bradykinin (BK) was measured before and 1, 24, 48 h after pretreatment with Ram (0 05,0 1 mg?kg -1 ,iv). The ACE activity was expressed by the pressor effect (%)of AngⅠ or the depressor effect (%) of BK. RESULTS The pressor effects of AngⅠ or the supernatant fraction of heart tissue homogenate containing AngⅠ were siginificantly reduced 1 h and 24 h after pretreatment with Ram, but not 48 h after pretreatment with Ram. In comparison of the depressor response of BK vs pressor response of AngⅠ 1 h after pretreatment with Ram,it was shown that the depressor effect of BK is more sensitive than the pressor effect of AngⅠ( P
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AIM: To observe the protective effects of shenmai injection on myocardial injury induced by 1,1-dipheyl-2-picryl hydrazyl (DPPH)free radic al in isolated rabbit hearts. METHODS: The isolated rabbit hear ts were perfused in a Langendorff model. Left ventricular pressure (LVP), the fi rst derivative of LVP (+dp/dt max ), left v entricular end-diastolic pressur e (LVEDP) and heart rate (HR) were recorded. Coronary flow (CF) and the activity of creatine kinase (CK) in coronary effluent were measured by timed collection of coronary effluent. RESULTS: Perfusion with DPPH ( 0.25 ?mol?L -1 ) for 10 min caused a significant impairment of cardiac functi on, as shown by a decrease in LVP, +dp/dt ma x and HR and an increase in LV EDP as well as the increased release of CK. After perfusion with DPPH ( 0.25 ?mol?L -1 ) for 10 min, treatment with shenmai injection (1320 or 1 160) for 10 min produced a significant improvement of cardiac function and a d ecrease in the release of CK. CONCLUSION: Shenmai injection prot ects against myocardial injury induced by DDPH free radical in isolated rabbit h earts.
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Objective To observe the delayed cardioprotective effect of the extract of Gingkgo biloba leaves(EGb761)and its possible mechanisms in rats.Methods Myocardial ischemia-reperfusion(I/R)injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts.Heart rate(HR),coronary flow(CF),left ventricular pressure(LVP),and its first derivatives(+dp/dtmax)were recorded,and the releasing content of creatine kinase(CK),contents of malondialdehyde(MDA)and nitric oxide(NO)in myocardial tissues were measured.Results Single ig EGb761(50 or 100 mg/kg)at 24 h before I/R were done could significantly attenuate the damage of cardiac function(LVP and +dp/dtmax)and the lowering of NO level in myocardial tissues,and inhibit the increasing in CK release and MDA level induced by I/R in myocardial tissues.The delayed cardioprotective effects of EGb761 were markedly inhibited by pretreatment with L-NAME(5 mg/kg),an inhibitor of NO synthase,or HMR1883(3 mg/kg),an antagonist of sarcolemmal ATP-sensitive potassium channels(sarcKATP).Conclusion Pretreatment with EGb761 could protect against I/R-induced myocardial injury in rats,and the delayed cardioprotection of EGb761 may be related to increasing in NO production and opening of sarcKATP.
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OBJECTIVE:To study the protctive effect of ginkgo biloba extractEGBon the kindey in the case of is?chemia-reperfusion injury.METHODS:The model of renal ischemia-reperfusion injury in male rats was made by ligation of left renal artery for40min and3h of reperfusion.The rats with pretreatment were fed with EGB at different doses prior to operation.The content of malonadialdihydeMDA,the activity of superoxide dismutaseSODin renal cortex and the levels of blood urea nitrogenBUN,creatinineCrin plasma were measured.The pathological changes of renal tissues were observed by electron microscope.RESULTS:After ischemia-reperfusion,the activity of SOD in renal cortex was decreased,however,the content of MDA in renal cortex and the levels of BUN,Cr in plasma were increased.Pathological changes induced by ischemia-reperfusion in renal tissues were observed clearly.The pretreatment of rats with EGB significantly prevented reduction of SOD activity and increase of MDA content in renal cortex,decreased elevation of concentration of BUN and Cr in plas?ma.Pathological changes of proximal tubular cells in rat kidneys induced by ischemia-reperfusion were also prevented by the pretreatment with EGB.CONCLUSION:EGB can protect rats from renal injuries caused by ischemia-reperfusion.The mechanism of protective effects of EGB may be related to preserving the activity of SOD and alleviating lipid peroxidation.