Abe H, Holt W, Watters T A, Wu S, Parmley W W, Schiller N, Higgins C, Wikman-Coffelt J
Department of Medicine (Cardiology), University of California, San Francisco 94143.
Am Heart J. 1988 Aug;116(2 Pt 1):447-54. doi: 10.1016/0002-8703(88)90617-5.
Isovolumic perfused rat hearts containing an intraventricular balloon were used to assess the effects of incremental balloon volumes on developed pressure, oxygen consumption, coronary flow, phosphorylation potential obtained by P-31 nuclear magnetic resonance, wall thickness obtained by two-dimensional echocardiography, and diastolic wall stress. Three phases in developed pressure were noted: (1) volumes from 0 to 150 microliter resulted in a continuous increase in developed pressure; (2) with volumes from 150 to 250 microliter, developed pressure remained constant whereas developed (systolic) and diastolic wall stress rose sharply; and (3) with volumes from 250 to 400 microliter, developed pressure fell whereas developed (systolic) and diastolic wall stress continued to rise. The ln [(PCr)/(Pi)] was in synchrony with oxygen consumption at 0 and 50 microliter balloon volumes, and then diverged at volumes greater than 100 microliter. Oxygen consumption increased from 0 to 50 microliter, was constant from 50 to 250 microliter balloon volume, and then declined. The ln [(PCr)/(Pi)] fell precipitously at balloon volumes greater than 100 microliter, most likely limited by oxygen consumption. Coronary flow did not change significantly until 250 microliter or more of water was added to the balloon, and then it started to decline. Volumes greater than 100 microliter result in overstretch of myofibers, as observed by the precipitous decline in ln [(PCr)/(Pi)], and the steep increase in diastolic wall stress. With excessive volume loading, the drop in phosphorylation potential, ln [(PCr)/(Pi)], appears to contribute to the decrease in developed pressure.
舒张末压、耗氧量、冠状动脉血流量、通过磷-31核磁共振获得的磷酸化电位、通过二维超声心动图获得的心室壁厚度以及舒张期壁应力。观察到舒张末压有三个阶段:(1)容积从0至150微升时,舒张末压持续升高;(2)容积从150至250微升时,舒张末压保持恒定,而舒张期(收缩期)和舒张期壁应力急剧上升;(3)容积从250至400微升时,舒张末压下降,而舒张期(收缩期)和舒张期壁应力继续上升。在球囊容积为0和50微升时,ln[(磷酸肌酸)/(无机磷酸)]与耗氧量同步,然后在容积大于100微升时出现差异。耗氧量从0至50微升增加,在球囊容积为50至250微升时保持恒定,然后下降。在球囊容积大于100微升时,ln[(磷酸肌酸)/(无机磷酸)]急剧下降,很可能受耗氧量限制。直到向球囊内加入250微升或更多的水时,冠状动脉血流量才出现显著变化,然后开始下降。如ln[(磷酸肌酸)/(无机磷酸)]的急剧下降以及舒张期壁应力的急剧增加所示,容积大于100微升会导致肌纤维过度拉伸。在容量负荷过大时,磷酸化电位ln[(磷酸肌酸)/(无机磷酸)]的下降似乎是舒张末压降低的原因。