原发性高血压患者心功能特征100例分析

背景:高血压患者心功能常有不同程度损害,不同分期高血压患者心功能损害程度有何差异?目的:观察高血压不同分期患者的心功能,并与健康者相应指标进行对照.设计:病例-对照,对比观察.单位:解放军沈阳军区总医院特诊科.对象:选择2002-10/2003-05解放军沈阳军区总医院内科住院原发性高血压患者100例.其中高血压Ⅰ期30例,高血压Ⅱ期40例,高血压Ⅲ期30例.选择同期本院健康体检者30人为对照.纳入对象均知情同意.方法:纳入对象心功能测定采用XJS-Ⅰ型心功能检测仪.患者取仰卧位,按四电极法放置电极.于呼气末屏气,同步描记Ⅰ导联心电图、心音图、心导纳微分图、颈动脉搏动图.通过微机处理显示各种指标.检测指标为:心率,排血前时间,左室排血时间,排血前时间/左室排血时间,电机械延迟时间,等容收缩时间,等容收缩时间/左室排血时间,脉搏波传递时间,每搏量,心排血量,心脏指数,心肌收缩强度指数,总外周阻力,血管顺应性.主要观察指标:不同分期高血压患者与健康者心功能状况比较.结果:原发性高血压患者100例和健康者30人均进入结果分析.[1]排血前时间、等容收缩时间、总外周阻力、排血前时间/左室排血时间和等容收缩时间/左室排血时间:高血压患者明显大于或长于健康者(P＜0.01),Ⅱ,Ⅲ期高血压患者明显高于或长于Ⅰ期高血压患者(P＜0.01).[2]每搏量、心排血量、心肌收缩强度指数、血管顺应性、脉搏波传递时间、心脏指数:高血压患者明显低于或短于健康者(P＜0.01),Ⅱ,Ⅲ期高血压患者明显低于或短于Ⅰ期高血压患者(P＜0.01).在上述指标中,Ⅲ期高血压患者血管总外周阻力明显高于Ⅱ期高血压患者(P＜0.05),血管顺应性明显低于Ⅱ期高血压患者(P＜0.05).结论:高血压患者心功能较健康者明显下降,随着高血压病情发展,心功能进一步下降.

高压氧辅助治疗青年人心肌缺血398例

Background: Main causes of youth myocardial ischemia are smoking and hypercholesterolemia, which leads to disorder of collateral circulation, increase of cardiac accidence and coronary atherosclerosis. Hypoxia is easy to happen because thick of sclerotic vessels wall nearly reaches the maximal diffuse distance in this tissue. CO in cigarettes can lead to hypoxia and myocardial ischemia. After use of hyperbaric oxygen, blood fat decrease, incidence of coronary atherosclerosis decreases apparently. And it promotes myocardial hypoxia and metabolism, increases myocardial contraction and promotes heart function, thereby decrease incidence of angina, myocardial infarction and sudden death.

Aim:To explore the effects of benactyzine (BEN) on the action potential and contractile force in guinea pig papillary muscles.Methods:Conventional microelectrode technique was used to record the fast action potentials (FAP) and slow action potentials (SAP) of guinea pig papillary muscles.Results:Benactyzine 5,10,50 μmol·L-1 suppressed the maximal upstroke velocity (vmax) of FAP and contractile force (Fc) concentration-dependently while prolonged the action potential duration at 50%,90% repolarization (APD50,APD90) and effective refractory period (ERP) of FAP.The suppression on the vmax was frequency-dependent.Benactyzine 5,10,50μmol·L-1 lengthened the APD50,APD90 of SAP induced by isoprenaline or histamine when perfused with KCl 22 mmol·L-1 Tyrode's solution.The vmax of the SAP was not decreased by benactyzine 5,10 μmol·L-1 but by 50 μmol·L-1.The effects on the SAP were antagonized by elevation of the extracellular calcium from 2.0 to 5.6 mmol·L-1.The effects of benactyzine on SAP elicited by tetrodotoxin resembled that by isoprenaline or histamine except the more pronounced suppression on vmax and action potential amplitude (APA).The persistent rapid spontaneous activity and triggered tachyarrhythmia induced by ouabain were also abolished immediately by benactyzine 5 μmol·L-1.Conclusion:Benactyzine can inhibit Na+,K+,Ca2+ transmembrane movement and intracellular Ca2+ mobilization in the myocardium,and this may be the electrophysiological basis of its effects against experimental arrhythmias.

Objective: To examine the function change of myocardial calcium transports and determined what role the change plays in cardiac dysfunction after severe burn injury in rats.Methods: The contraction and relaxation properties of the left ventricle (LV) were studied in the isolated hearts preparations of Wistar rats at 3, 8, and 24 h after a 30%TBSA (total body surface area) full-thickness burn. The calcium transport function of the sarcoplasmic reticulum (SR) was measured by the millipore filtration technique.Results: The maximal rate of LV pressure (± dp/dtmax) of the burn group was significantly lower than that of the control group (P ＜ 0.01). In addition, the calciumdependent ATPase activity and the coupling ratio of SR were also markedly depressed.Conclusions: It indicates that the decrease in the SR calcium transport function is one of the important mechanisms for the cardiac contractile dysfunction after severe burn injury.