Karliner J S, LeWinter M M, Mahler F, Engler R, O'Rourke R A
J Clin Invest. 1977 Sep;60(3):511-21. doi: 10.1172/JCI108803.
We studied the effects of acute pharmacologic and hemodynamic interventions on isovolumic left ventricular relaxation in 19 conscious dogs using micromanometer tip catheters. Isoproterenol (11 studies) augmented peak rate of rise of left ventricular pressure [(+) dP/dt] by 1,275+/-227 (SE) mm Hg/s (P < 0.001) and dP/dt at an isopressure point of 35 mm Hg during isovolumic relaxation [(-) dP/dt(35)] by 435+/-80 mm Hg/s (P < 0.001). Peak (-) dP/dt decreased by 467+/-89 mm Hg/s (P < 0.002). The time constant, T, derived from the logarithmic fall of pressure during isovolumic relaxation, shortened from 20+/-2.8 to 14.9+/-1.8 ms (P < 0.003). Calcium (11 studies) increased peak (+) dP/dt and (-) dP/dt(35) (both P < 0.0001); peak (-) dP/dt was unchanged. T shortened from 20.4+/-1.8 to 17.3+/-1.5 ms (P < 0.002). Volume (13 studies) did not affect either dP/dt or T. Phenylephrine (13 studies) augmented peak (-) dP/dt, but reduced (-) dP/dt(35) (both P < 0.01); T lengthened from 22.1+/-1.5 to 32.5+/-1.5 ms (P < 0.01). In 15 studies, rapid atrial pacing increased peak (+) dP/dt and (-) dP/dt(35) (both P < 0.01). In the first post-pacing beat, peak (-) dP/dt and (-) dP/dt(35) decreased (both P < 0.01), although peak (+) dP/dt increased further. T paralleled values of (-) dP/dt(35). In five dogs, beta adrenergic blockade had no significant effect on any variable after calcium, volume, or phenylephrine infusion or during or after atrial pacing when the pre-and post-propranolol states were compared. We conclude that positive inotropic interventions augment both left ventricular contraction and relaxation. The changes in isovolumic relaxation are independent of alterations in sympathetic tone produced by beta-adrenergic blockade. Peak (-) dP/dt may not be a valid measure of left ventricular relaxation rate during acute alterations in inotropic state or afterload.
我们使用微测压尖端导管研究了19只清醒犬急性药物和血流动力学干预对左心室等容舒张的影响。异丙肾上腺素（11项研究）使左心室压力上升的峰值速率[(+) dP/dt]增加了1275±227（标准误）mmHg/s（P<0.001），并使等容舒张期间35mmHg等压点处的dP/dt[(-) dP/dt(35)]增加了435±80mmHg/s（P<0.001）。峰值(-) dP/dt下降了467±89mmHg/s（P<0.002）。等容舒张期间压力对数下降得出的时间常数T从20±2.8ms缩短至14.9±1.8ms（P<0.003）。钙剂（11项研究）使峰值(+) dP/dt和(-) dP/dt(35)均增加（均为P<0.0001）；峰值(-) dP/dt未改变。T从20.4±1.8ms缩短至17.3±1.5ms（P<0.002）。容量（13项研究）对dP/dt或T均无影响。去氧肾上腺素（13项研究）使峰值(-) dP/dt增加，但使(-) dP/dt(35)降低（均为P<0.01）；T从22.1±1.5ms延长至32.5±1.5ms（P<0.01）。在15项研究中，快速心房起搏使峰值(+) dP/dt和(-) dP/dt(35)均增加（均为P<0.01）。在起搏后的第一个搏动中，峰值(-) dP/dt和(-) dP/dt(35)降低（均为P<0.01），尽管峰值(+) dP/dt进一步增加。T与(-) dP/dt(35)的值平行。在5只犬中，在输注钙剂、容量或去氧肾上腺素后，或在心房起搏期间及之后，当比较普萘洛尔给药前后的状态时，β肾上腺素能阻滞剂对任何变量均无显著影响。我们得出结论，正性肌力干预可增强左心室收缩和舒张。等容舒张的变化与β肾上腺素能阻滞剂引起的交感神经张力改变无关。在急性变力状态或后负荷改变期间，峰值(-) dP/dt可能不是左心室舒张速率的有效测量指标。
