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Vasodilation and Mechanism of Action of HSYA on Porcine Coronary Artery

Author: ZhangDongHui
Tutor: WangZuo
School: Lanzhou University
Course: Pharmacy
Keywords: HSYA A Coronary Vasodilation
CLC: R285.5
Type: Master's thesis
Year: 2011
Downloads: 42
Quote: 0
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Abstract


OBJECTIVE: Coronary artery disease research is an important cardiovascular target organ of coronary atherosclerosis can lead to myocardial ischemia and hypoxia or necrosis, is a common pathological basis of cardiovascular disease , so the effect of the drug on coronary cardiovascular drug development a major focus . This study of chalcones , traditional blood circulation drugs safflower highest concentrations of water-soluble monomer composition - HSYA A contraction of isolated porcine coronary blood vessels, and discuss its possible role mechanism for the biological activity of safflower research and application of reference. Methods: Porcine coronary artery rings as materials, experimental methods of vascular function in vitro testing HSYA A vasoactive effect. Results: HSYA A on porcine coronary artery rings resting tension of no effect , but the pre-contracted vessels in a concentration -dependent vasodilation , maximal relaxation effect was 124.22 ± 6.25%, corresponding pD2 value of 2.91 ± 0.23; HSYA can KCl dose-response curve down, concentration dependent . Removal of endothelium , with the nitric oxide synthase inhibitor L-NNA, guanylate cyclase inhibitor methylene blue , β -blocker propranolol , β1 and β2 receptor inhibitor receptor antagonist atenolol ICI 118551 pretreatment, could significantly weaken the role HSYA induced vasodilation ; prostaglandin synthetase inhibitor indomethacin , K channel blocker TEA, Gly, BaCl2 after pretreatment vasodilation can not be blocked. Conclusion : Based on endothelium-dependent and non -dependent factors research , drug discovery vasodilatory activity is the result of the combined effects of multiple pathways , mainly through endothelial -NO-cGMP pathway and β- adrenergic receptor -cAMP pathway , factor and vascular smooth muscle relaxation and release of prostaglandin I2 potassium channels unrelated , but can block the vascular smooth muscle voltage-dependent calcium channels.

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