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为探讨急性低氧时 Starling 效应对左室搏血效率的影响,在12条麻醉开胸狗上进行了实验。给狗依次吸入氧分压为84、64、52mmHg 的氧氮混合气体和纯氮气造成急性低氧。我们将心泵急性低氧反应分为稳态调节、剧烈动员和衰竭三个阶段。在Starling 效应开始持续发动以前,心泵处于稳态调节阶段、左室舒张期末直径(LVEDD)、在室压力(LVP)、每搏输出量(SV)、每搏外功(W)、与每搏外功功率峰值(N_(max))等稳定于对照水平,略有波动。搏血效率指数(I_(BEE)=SV/N_(max))也稳定于对照水平。稳态调节阶段持续时间的长短与心泵能耐受低氧的程度和时间呈正相关(r=0.83,P<0.001)。在剧烈动员阶段,左室舒张期末直径进行性地迅速增大,从对照时的 51.55±1.09mm(M±SE)增至54.60±1.63mm(P<0.01)。同时,LVP、SV、W、N_(max)等泵功能指标也明显上升,形成一个显著高于对照值的峰(各指标与对照相比,均P<0.01)。此时,搏血效率指数仍维持于对照水平(P>0.05)。此结果表明;剧烈动员阶段时 Starlins效应的发动和维持,并未降低搏血效率,有利于心泵功能代偿。
To investigate the effect of Starling effect on LV ejection fraction during acute hypoxia, experiments were performed on 12 anesthetized thoracotomic dogs. Inhaled oxygen to the dog partial pressure of 84,64,52 mmHg of oxygen and nitrogen mixed gas and pure nitrogen caused by acute hypoxia. We will heart pump acute hypoxia response divided into steady-state regulation, severe mobilization and failure of three stages. Prior to the onset of Starling, the cardiac pump was in steady-state regulation with LVEDD, LVP, SV, and stroke per beat (W) The peak value of external power (N_ (max)) is stable at the control level with a slight fluctuation. The stroke efficiency index (I_ (BEE) = SV / N_ (max)) also stabilized at the control level. The duration of the steady-state regulation phase was positively correlated with the extent and duration of cardiorespiratory hypoxia (r = 0.83, P <0.001). During the intense mobilization phase, the diameter of the left ventricular end diastolic increased rapidly progressively from 51.55 ± 1.09mm (M ± SE) to 54.60 ± 1.63mm (P <0.01) at the time of control. At the same time, the indexes of LVP, SV, W, Nmax and other pump functions also increased obviously, forming a peak which was significantly higher than the control value (all P <0.01 compared with the control). At this point, stroke blood efficiency index remained at the control level (P> 0.05). This result indicates that the initiation and maintenance of Starlins effect during the intense mobilization phase did not reduce the stroke blood efficiency, which is in favor of cardiac pump compensation.