Background Endogenous hydrogen sulfide is a new neuromodulator which takes part in the regulation of central nervous system physiology and diseases. Whether endogenous hydrogen sulfide in the central nervous system re...Background Endogenous hydrogen sulfide is a new neuromodulator which takes part in the regulation of central nervous system physiology and diseases. Whether endogenous hydrogen sulfide in the central nervous system regulates cardiovascular activity is not known. In the present study, we observed the hemodynamic changes of hydrogen sulfide or its precursor by intracerebroventricular injection, and investigate the possible roles of endogenous digitalis like factors and sympathetic activity in the regulation. Methods Ninety-four Sprague-Dawley rats underwent a right cerebroventricular puncture, then the hydrogen sulfide saturation buffer or its precursor injected by intrcerebroventricular catheter. A heperin-filled catheter was inserted into the right femoral artery or into the left ventricle, and changes of blood pressure or cardiac function recorded by a Powerlab/4S instrument. Phentolamine or metoprolol were pre-injected to observe the possible role in autonomic nerve activity. After rats were sacrificed, plasma was collected and endogenous digitalis-like factors were measured with a commercial radioimmunoassay kit. The aortic, cardiac sarcolemmal vesicles were isolated and the activity of Na＋-K＋-ATPase was measured as ouabain-sensitive ATP hydrolysis under maximal velocity conditions by measuring the release of inorganic phosphate from ATP. Unpaired Student＇s ttest for two groups or analysis of variances （ANOVA） for multiple groups were used to compare the differences of the changes. Results Intracerebroventricular injection of hydrogen sulfide induced a transient hypotension, then dramatic hypertenive effects in a dose-dependent manner. Bolus injection of L-cysteine or beta-mercaptopyruvate also increased mean arterial pressure （P 〈0.01）, whereas hydroxylamine-a cystathionine beta synthase inhibitor decreased the arterial pressure （P 〈0.01）. Hydrogen sulfide and L-cysteine increased mean arterial pressure, left ventricular develop pressure and left-ventricle maximal rate of systolic and di展开更多
目的研究大鼠慢性心衰(HF)急性加重模型方法学。方法 SD大鼠麻醉后,测定术前左室缩短分数(FS),结扎冠状动脉前降支(假手术组只穿线不结扎),8周后,测定术后FS,选取FS较术前下降50%以上的大鼠作为HF模型鼠,按FS心衰程度随机分为3组,每组1...目的研究大鼠慢性心衰(HF)急性加重模型方法学。方法 SD大鼠麻醉后,测定术前左室缩短分数(FS),结扎冠状动脉前降支(假手术组只穿线不结扎),8周后,测定术后FS,选取FS较术前下降50%以上的大鼠作为HF模型鼠,按FS心衰程度随机分为3组,每组10只。采用生理盐水作为容量负荷方式,按容量负荷程度分为轻度(1 m L/kg,即HF+轻度负荷组)、中度(2 m L/kg,即HF+中度负荷组)、重度(3 m L/kg,即HF+重度负荷组)3种模式,输注速度1 m L/min。假手术组同重度负荷模式。测定左室压最大上升/下降速率(±LVdp/dtmax)、左室舒张末期压(LVEDP)、中心静脉压(CVP)、呼吸频率(RR)、心率(HR)并对数据进行统计学处理。结果 HF大鼠给予不同容量负荷,+LVdp/dtmax出现不同程度降低,轻、中、重负荷心脏收缩功能恶化百分率分别可达40%、80%、100%;随着负荷加重,RR减低率逐渐增多,重度负荷可达到100%;轻、中、重度负荷HR降低幅度最大可达3.5%、7.5%、8.4%,CVP升高幅度分别最大可达23.7%、31.1%、51.5%;LVEDP升高幅度分别最大可达2.5、5.7、10.3 mm Hg。与假手术组比较,中、重负荷组负荷后一段时间内±LVdp/dtmax、LVEDP、CVP、RR、HR差异显著(P<0.05、0.01、0.001)。结论容量负荷法在一定程度上,可以使大鼠慢性心衰具备部分急性加重的特征。展开更多
基金This work was supported by the Major State Basic Research Development Program of China （No. 30890042） the National Natural Science Foundation of China （No. 30971084 and No. 30821001） and the Educational Bureau of Hubei Province （No. Q20092403 and No. B20082405）.
文摘Background Endogenous hydrogen sulfide is a new neuromodulator which takes part in the regulation of central nervous system physiology and diseases. Whether endogenous hydrogen sulfide in the central nervous system regulates cardiovascular activity is not known. In the present study, we observed the hemodynamic changes of hydrogen sulfide or its precursor by intracerebroventricular injection, and investigate the possible roles of endogenous digitalis like factors and sympathetic activity in the regulation. Methods Ninety-four Sprague-Dawley rats underwent a right cerebroventricular puncture, then the hydrogen sulfide saturation buffer or its precursor injected by intrcerebroventricular catheter. A heperin-filled catheter was inserted into the right femoral artery or into the left ventricle, and changes of blood pressure or cardiac function recorded by a Powerlab/4S instrument. Phentolamine or metoprolol were pre-injected to observe the possible role in autonomic nerve activity. After rats were sacrificed, plasma was collected and endogenous digitalis-like factors were measured with a commercial radioimmunoassay kit. The aortic, cardiac sarcolemmal vesicles were isolated and the activity of Na＋-K＋-ATPase was measured as ouabain-sensitive ATP hydrolysis under maximal velocity conditions by measuring the release of inorganic phosphate from ATP. Unpaired Student＇s ttest for two groups or analysis of variances （ANOVA） for multiple groups were used to compare the differences of the changes. Results Intracerebroventricular injection of hydrogen sulfide induced a transient hypotension, then dramatic hypertenive effects in a dose-dependent manner. Bolus injection of L-cysteine or beta-mercaptopyruvate also increased mean arterial pressure （P 〈0.01）, whereas hydroxylamine-a cystathionine beta synthase inhibitor decreased the arterial pressure （P 〈0.01）. Hydrogen sulfide and L-cysteine increased mean arterial pressure, left ventricular develop pressure and left-ventricle maximal rate of systolic and di
文摘目的研究大鼠慢性心衰(HF)急性加重模型方法学。方法 SD大鼠麻醉后,测定术前左室缩短分数(FS),结扎冠状动脉前降支(假手术组只穿线不结扎),8周后,测定术后FS,选取FS较术前下降50%以上的大鼠作为HF模型鼠,按FS心衰程度随机分为3组,每组10只。采用生理盐水作为容量负荷方式,按容量负荷程度分为轻度(1 m L/kg,即HF+轻度负荷组)、中度(2 m L/kg,即HF+中度负荷组)、重度(3 m L/kg,即HF+重度负荷组)3种模式,输注速度1 m L/min。假手术组同重度负荷模式。测定左室压最大上升/下降速率(±LVdp/dtmax)、左室舒张末期压(LVEDP)、中心静脉压(CVP)、呼吸频率(RR)、心率(HR)并对数据进行统计学处理。结果 HF大鼠给予不同容量负荷,+LVdp/dtmax出现不同程度降低,轻、中、重负荷心脏收缩功能恶化百分率分别可达40%、80%、100%;随着负荷加重,RR减低率逐渐增多,重度负荷可达到100%;轻、中、重度负荷HR降低幅度最大可达3.5%、7.5%、8.4%,CVP升高幅度分别最大可达23.7%、31.1%、51.5%;LVEDP升高幅度分别最大可达2.5、5.7、10.3 mm Hg。与假手术组比较,中、重负荷组负荷后一段时间内±LVdp/dtmax、LVEDP、CVP、RR、HR差异显著(P<0.05、0.01、0.001)。结论容量负荷法在一定程度上,可以使大鼠慢性心衰具备部分急性加重的特征。
