Vengen O A, Ellingsen O, Ilebekk A
Institute for Experimental Medical Research, Ullevaal Hospital, University of Oslo, Norway.
Am J Physiol. 1988 Aug;255(2 Pt 2):H228-35. doi: 10.1152/ajpheart.1988.255.2.H228.
To study whether right atrial contraction can forward blood into the pulmonary artery during diastole, blood volume was expanded in anesthetized open-chest pigs until mean right atrial pressure was 13-20 mmHg (range). In the control situation, blood flow in the pulmonary artery was only observed during ventricular systole. Forward diastolic pulmonary artery flow, coinciding with right atrial contraction, was observed when diastolic pulmonary artery pressure was reduced during selectively increased left-side contractility, during bradycardia after propranolol injection (0.5 mg/kg body wt iv), and during the prolonged diastolic interval after spontaneously occurring atrial extrasystoles. The prolongation of the diastolic interval in all three series caused the diastolic pulmonary artery pressure to decline and the filling of the right atrium to increase, thus further stimulating the right atrial Frank-Starling mechanism. The diastolic blood flow in the pulmonary artery constituted 11% of the stroke volume during increased left-side inotropic stimulation, 8% during bradycardia, and 6% in beats preceded by a prolonged diastolic interval. Thus, in the normal heart, blood can be ejected into the pulmonary artery during right atrial contraction.
为研究右心房收缩在舒张期是否能将血液泵入肺动脉,对麻醉开胸猪进行血容量扩充,直至平均右心房压力达到13 - 20 mmHg(范围)。在对照情况下,仅在心室收缩期观察到肺动脉内的血流。当在选择性增加左侧心肌收缩力时、注射普萘洛尔(0.5 mg/kg体重,静脉注射)后出现心动过缓时以及自发性房性早搏后舒张期延长时,舒张压肺动脉压力降低,观察到与右心房收缩同时出现的舒张期肺动脉正向血流。在所有这三种情况下,舒张期的延长导致舒张压肺动脉压力下降以及右心房充盈增加,从而进一步刺激右心房的Frank - Starling机制。在左侧心肌收缩力增强刺激时,肺动脉舒张期血流占每搏输出量的11%,心动过缓时占8%,舒张期延长后的搏动中占6%。因此,在正常心脏中,右心房收缩时血液可被泵入肺动脉。