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Objective:To observe the affection of angiotensin Ⅱ antagonists on the cultured subtype 2 receptor of angiotensin II transfected aortic vascular smooth muscle cells of rat.Methods:After transfected the plasmid that contained the cDNA of subtype 2 receptor of angiotensin II into cultured rat vascular smooth muscle cells, the cells were divided into three groups：cells of group 1 were treated with angiotensinⅡ,cells of group 2 were treated with angiotensinⅡand losartan,cells of group 3 were treated with angiotensinⅡ and PD123319 .After experiments，the expression of PCNA, NOS and the cell number was tested, respectively.Results：After treated with Losartan，the cell number of group 2 was(4.17±0.15)×105，the OD value of PCNA was 0.202 6±0.007 6，both of which were less than that of cells of group 3；the OD value of NOS of cells was more in group 2(0.027 5±0.002 1 ) than that in group 3 (0.016 9±0.002 0) (P＜0.01).Conclusions:It suggests that when being activated,subtype 2 receptor of angiotensin Ⅱ could inhibit the proliferation of vascular smooth muscle cells and antagonist the effect of subtype 1 receptor of angiotensin Ⅱ,such an effect may be related to the activation of NOS.
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AIM and METHODS: The protective effects of multi-enzyme Ⅱ was studied on cultured endothelial cells which was injuried by hyperlipidemia serum. RESULTS: Hyperlipidemia serum increased ICAM-1 expression on the surface of endothelial cells, and decreased NO- 2 release significantly (P
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AIM: The effects of BDM on isolated rat heart in cold cardioplegia were studied METHODS: Rat heart were subjected to cold cardioplegia at 4℃ for 8, 18 and 24 h Then each heart was perfused (90 cm H 2O) in Langendorff model at 37℃ for 40 min In the high K + group( n =24) the hearts were preserved in St Thomas cardioplegic solution, in BDM group( n =24) hearts were preserved in K-H solution with BDM 30 mmoL/L RESULTS: After 18 h, heart rate and the coronary flow in BDM group were significantly higher than in high K + group( P
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The effects of prostaglandin E_2 on hemodynamics and cardial function in normal rabbits and on cardioprotection in experimental acute myocardial infarction rabbits were investigated. To determine the action of prostaglandin E_2 in normal rabbits (n = 10), we measured arterial systolic pressure (ASP), arterial diastolic pressure (ADP), mean arterial pressure (MAP), heart rate (HR), left ventricular ejection time (LVET), +dp/dt max, -dp/dt max, Vc_E-50, T time after injected prostaglandin E_2 (1?g/min/kg). The results showed that ASP, ADP, MAP were decreased. HR, Vc_E-50, LVET were unchanged. To determine the effects of prostaglandin E_2 on the cardioprotection in acute myocardial infarction in rabbits (n=8), left ventricular systolic pressure (LVEP), +dp/dt max,-dp/dt max, ST of ECG, infarct size were also measured by us. The results showed that +dp/dt max, -dp/dt max were higher than control (n=9), ST lower than control, LVSP and infarct size were unchanged. Thus, prostaglandin E_2 could relax vascular smooth muscle, reduce laod of heart, decrease myocardial oxygen demands, maintain cardiac function during acute myocardial infarction.
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AIM To compare the protective effects of norepinephrine preconditioning(NEPC)and ischemic preconditioning(IPC)on myocardial ischemic/reperfused injury in rats in vivo . METHODS Rats were divided into control, ischemia/ reperfusion, classic IPC and NEPC groups. After 20 min reperfusion, several indexes including cardiac function indexes, MDA were tested, the myocardial ultrastr ucture and the injury reaction of catalase observed. RESULTS Both IPC and NEPC could protect myocardial ultra structure, ameliorate left heart function, decrease cardiac MDA content and protect the activity of catalase. CONCLUSION Extra micro norepinephrine preconditioning as a non injury method can mimic the protective effects of classic IPC and shows its clinical values.