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机构地区:[1]湖北民族学院医学院药理教研室,湖北恩施445000
出 处:《辽宁中医杂志》2007年第11期1643-1645,共3页Liaoning Journal of Traditional Chinese Medicine
基 金:湖北省卫生厅科研基金资助(JXIB120)
摘 要:目的:观察对家兔灌胃给予复方丹参后,其含药血清对大鼠离体灌流心脏内外源性自由基所致心肌损伤的保护作用。方法:家兔每日2次灌胃给予复方丹参5mL/kg,连续3天,末次给药后60min取血,分离血清。将含药血清加到Langendorff法灌流的离体心脏,记录左室内压(LVP)、左室内压最大上升速率(+dp/dmt ax)、左室舒张末压(LVEDP)、心率(HR),定时收集冠脉流出液测定冠脉流量(CF)和肌酸激酶(CK)活性,再灌结束时测定心肌组织中丙二醛(MDA)含量。结果:以含0.25μmol/L 1,1-二苯基-2-三硝基苯肼(DPPH)或0.06μmol/L次黄嘌呤(HX)和2.0μ/L黄嘌呤氧化酶(XO)的K-H液灌流心脏10min,可显著降低LVP、+dp/dtm ax,升高LVEDP,增加CK和MDA释放;预先用含药血清灌流心脏10min,可显著改善DPPH或HX+XO所致心功能损伤,减少CK和MDA释放。结论:含复方丹参血清对DP-PH或HX+XO诱导内外源性自由基所致心肌损伤具有明显保护作用。Objective: To investigate the protective effects of Compound Danshen on myocardial injury induced by endogenous and exogenous free radical in isolated rat hearts. Methods: The experiment was accomplished by serum pharmacology. All rabbits were treated with Compound Danshen via gastric garage twice dally for three days consecutively. After this treatment, 60 min after the last dosing the blood was taken and the serum was separated. The herbal medicines serum was added to the isolated rat hearts perfused in a Langendorff model. Left ventricular pressure (LVP) ,the frist derivative of LVP ( + dp/dtmax) ,left ventricular end - diastolic pressure ( LVEDP ) and heart rate ( HR ) were recorded. Coronary flow (CF) in coronary effluent were measured by timed collection of coronary effluent. At the end of the reperfusion , the content of malondialdahycle ( MDA ) in cardiac tissue was measured. Results : Perfusion with 1,1 - diphenyl - 2 - picryl - hydrazyl ( DPPH 0.25μmol/L ) or hypoxanthine (HX 0.06 μmol/L ) and xanthine oxidase ( XO 0.2μ/L ) for 10 min caused a marked decrease in LVP and + dp/dtmax, and an increase in LVEDP , the release of CK and the content of MDA. Pretreatment with herbal medicines serum for 10 min produced a significant improvement of cardiac function injury induced by DPPH or HX + XO and a decrease in the release of CK and the content of MDA. Conclusion : Compound Danshen have marked protectively effects on myecardiac injury induced by endogenous and exogenous free radical which were produced by DPPH or HX + XO.
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