目的利用在体大鼠心肌缺血再灌注模型观察Bayk8644对大鼠心功能的影响。方法将18只大鼠随机分为3组:假手术组(sham组)、Bay k8644组(B组)和二甲基亚枫组(D组),分别在缺血30 m in时静脉持续泵入生理盐水、Bay k8644和二甲基亚枫,于缺血前...目的利用在体大鼠心肌缺血再灌注模型观察Bayk8644对大鼠心功能的影响。方法将18只大鼠随机分为3组:假手术组(sham组)、Bay k8644组(B组)和二甲基亚枫组(D组),分别在缺血30 m in时静脉持续泵入生理盐水、Bay k8644和二甲基亚枫,于缺血前,缺血5、20、40 m in以及再灌注5、30、60、90 m in时,分别测定心率(HR)、左心室收缩峰压(LVSP)、左心室舒张末压(LVEDP)、左心室压力变化最大速率(±dp/dtm ax),以评价心脏功能。结果缺血后HR变化不显著,LVSP和+dp/dtm ax降低(与缺血前和sham组比较差异有显著性P<0.05),LVEDP升高,-dp/dtm ax降低;再灌注时B组HR逐渐减慢,D组逐渐增快,两组比较差异无显著性(P>0.05);LVSP和+dp/dtm ax进行性升高,LVEDP升高,-dp/dtm ax降低,各时间点两组比较差异无显著性(P>0.05)。结论持续静脉注射Bay k8644(2μg.kg-1.m in-1)不影响缺血再灌注损伤大鼠的心脏功能。展开更多
Objective To study the central role of ginkgolide B （BN52021） in regulating cardiovascular function of nerve center by examining the effects of ginkgolide B on the electrical activity of rat paraventricular nucleus ...Objective To study the central role of ginkgolide B （BN52021） in regulating cardiovascular function of nerve center by examining the effects of ginkgolide B on the electrical activity of rat paraventricular nucleus （PVN） neurons in hypothalamic slice preparation and to elucidate the mechanism involved. Methods Extracellular single-unit discharge recording technique. Results （1） In response to the application of ginkgolide t3 （0.1, 1, 10 μmol/L; n = 27） into the perfusate for 2 rain, the spontaneous discharge rates （SDR） of 26 （26/27, 96.30%） neurons were significantly decreased in a dose-dependent manner. （2） Pretreatment with L-glutamate （L-Glu, 0.2 mmol/L） led to a marked increase in the SDR of all 8 （100%） neurons in an epileptiform pattern. The increased discharges were suppressed significantly after ginkgolide B （1 μmol/L） was applied into the perfusate for 2 min. （3） In 8 neurons, perfusion of the selective L-type calcium channel agonist, Bay K 8644 （0.1 μmol/L）, induced a significant increase in the discharge rates of 8 （8/8, 100%） neurons, while ginkgolide B （1μmol/L） applied into the perfusate, could inhibit the discharges of 8 （100%） neurons. （4） In 8 neurons, the broad potassium channels blocker, tetraethylammonium （TEA, 1 mmol/L） completely blocked the inhibitory effect of ginkgolide B （1 μmol/L）. Conclusion These results suggest that ginkgolide B can inhibit the electrical activity of paraventricular neurons. The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and potentially concerned with delayed rectifier potassium channel （KDR）.展开更多
文摘Objective To study the central role of ginkgolide B （BN52021） in regulating cardiovascular function of nerve center by examining the effects of ginkgolide B on the electrical activity of rat paraventricular nucleus （PVN） neurons in hypothalamic slice preparation and to elucidate the mechanism involved. Methods Extracellular single-unit discharge recording technique. Results （1） In response to the application of ginkgolide t3 （0.1, 1, 10 μmol/L; n = 27） into the perfusate for 2 rain, the spontaneous discharge rates （SDR） of 26 （26/27, 96.30%） neurons were significantly decreased in a dose-dependent manner. （2） Pretreatment with L-glutamate （L-Glu, 0.2 mmol/L） led to a marked increase in the SDR of all 8 （100%） neurons in an epileptiform pattern. The increased discharges were suppressed significantly after ginkgolide B （1 μmol/L） was applied into the perfusate for 2 min. （3） In 8 neurons, perfusion of the selective L-type calcium channel agonist, Bay K 8644 （0.1 μmol/L）, induced a significant increase in the discharge rates of 8 （8/8, 100%） neurons, while ginkgolide B （1μmol/L） applied into the perfusate, could inhibit the discharges of 8 （100%） neurons. （4） In 8 neurons, the broad potassium channels blocker, tetraethylammonium （TEA, 1 mmol/L） completely blocked the inhibitory effect of ginkgolide B （1 μmol/L）. Conclusion These results suggest that ginkgolide B can inhibit the electrical activity of paraventricular neurons. The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and potentially concerned with delayed rectifier potassium channel （KDR）.
