Yerebakan Can, Klopsch Christian, Niefeldt Sabine, Zeisig Vilia, Vollmar Brigitte, Liebold Andreas, Sandica Eugen, Steinhoff Gustav
Department of Cardiac Surgery, Medical Faculty, University of Rostock, Schillingallee 35, 18057 Rostock, Germany.
Interact Cardiovasc Thorac Surg. 2010 Apr;10(4):519-25. doi: 10.1510/icvts.2009.221234. Epub 2010 Jan 20.
We aimed to determine the response of the right ventricle (RV) to surgically induced pressure and volume overload in both acute and chronic settings. Four-month-old sheep were operated via left anterior thoracotomy. Pressure overload of the RV was established by banding of the pulmonary trunk. Volume overload was induced by the implantation of a transannular patch to the right ventricular outflow tract. Right ventricular function was obtained with conductance catheters before and after surgery as well as three months postoperatively. Acute pressure overload resulted in an increase of end-systolic volume (ESV) (P=0.002) and end-diastolic volume (EDV) (P=0.004), increments in contractile indexes [maximal slope of systolic pressure increment (dP/dt(max)), P=0.002; slope of end-systolic pressure volume relation (Ees), P=0.002; preload recruitable stroke work (PRSW), P=0.002] and an acceleration of early diastole [relaxation time (tau), P=0.012; maximal slope of diastolic pressure decrement (dP/dt(min)), P=0.002]. Acute volume overload revealed better contractility and more prominent increases in preload (ESV, EDV; both P=0.008). Three months postoperatively, pressure overloaded hearts demonstrated superior systolic (Ees, P=0.022; PRSW, P=0.013) and diastolic reserves (dP/dt(min), P=0.013; slope of end-diastolic pressure volume relation (Eed), P=0.005; P(20), P=0.003) than volume overloaded hearts. Acute pressure overload leads to enhanced contractility of the RV as a result of the Anrep effect and the Frank-Starling mechanism whereas volume overload institutes only the latter. The chronically pressure overloaded RV exposes more contractile and elastic reserves than the chronically volume overloaded RV under stress conditions.
我们旨在确定右心室（RV）在急性和慢性情况下对手术诱导的压力和容量超负荷的反应。对4月龄绵羊行左前开胸手术。通过结扎肺动脉主干建立右心室压力超负荷。通过在右心室流出道植入跨瓣环补片诱导容量超负荷。在手术前、后以及术后3个月用导管测量右心室功能。急性压力超负荷导致收缩末期容积（ESV）增加（P=0.002）和舒张末期容积（EDV）增加（P=0.004），收缩指数增加[收缩压上升最大斜率（dP/dt(max)），P=0.002；收缩末期压力-容积关系斜率（Ees），P=0.002；可招募前负荷搏功（PRSW），P=0.002]，舒张早期加速[舒张时间（tau），P=0.012；舒张压下降最大斜率（dP/dt(min)），P=0.002]。急性容量超负荷显示出更好的收缩性，前负荷增加更显著（ESV、EDV；均P=0.008）。术后3个月，压力超负荷心脏的收缩储备（Ees，P=0.022；PRSW，P=0.013）和舒张储备（dP/dt(min)，P=0.013；舒张末期压力-容积关系斜率（Eed），P=0.005；P(20)，P=0.003）优于容量超负荷心脏。急性压力超负荷由于Anrep效应和Frank-Starling机制导致右心室收缩性增强，而容量超负荷仅激活后者。在应激条件下，长期压力超负荷的右心室比长期容量超负荷的右心室表现出更多的收缩和弹性储备。
