Cheng C P, Freeman G L, Santamore W P, Constantinescu M S, Little W C
Section of Cardiology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.
Circ Res. 1990 Mar;66(3):814-23. doi: 10.1161/01.res.66.3.814.
We investigated left ventricular (LV) early diastolic filling in 10 normal conscious dogs that had been previously instrumented to measure LV and left atrial (LA) pressures and three orthogonal LV internal dimensions. LV volume was calculated as a general ellipsoid. The pressure within a passive structure increases as it is filled. If myocardial relaxation is rapid enough to substantially aid LV diastolic filling, it may overcome this effect and cause LV pressure to fall despite an increase in volume. Thus, we defined the amount of LV filling that occurred while LV pressure was falling as relaxation filling, which is a measure of the importance of LV relaxation during early diastolic filling. The time constant of relaxation (T) was derived from the exponential fall of LV pressure during isovolumic relaxation. While LV pressure was falling early in diastole (the relaxation filling period), all three LV diameters increased. Autonomic blockade with hexamethonium (5 mg/kg) and atropine (0.1 mg/kg) reduced relaxation filling from 21 +/- 6% (mean +/- SD) to 12 +/- 3% of the stroke volume (p less than 0.01). The mean LA pressure also was significantly decreased (from 12 +/- 2 to 10 +/- 5 mm Hg, p less than 0.05), while the duration of the relaxation filling period and T were unchanged. Positive inotropic stimulation with dobutamine (10 micrograms/kg/min) shortened T without changing LA pressure. The maximum LA-LV pressure gradient, dV/dtmax, and relaxation filling all increased. Augmented preload produced by dextran infusion (500 ml/10 min) caused an increase in LA pressure (from 11 +/- 3 to 21 +/- 8 mm Hg, p less than 0.05) without altering T. This also increased the maximum LA-LV pressure gradient, dV/dtmax, and relaxation filling. Augmented afterload produced by methoxamine (10 mg/3 min i.v.) significantly increased LA pressure (from 9 +/- 4 to 15 +/- 10 mm Hg, p less than 0.05) and lengthened T (from 35 +/- 4 to 50 +/- 7 msec, p less than 0.05) and the duration of relaxation filling (from 36 +/- 5 to 44 +/- 9 msec, p less than 0.01) without altering the maximum LA-LV pressure gradient, dV/dtmax, or LV relaxation filling. Incremental changes in heart rate induced by atrial pacing (from 100-180 beats/min) resulted in progressive decreases in the time constant of LV relaxation and the duration of relaxation filling. The LA pressure was also decreased. There was no corresponding increase in the amount of active LV filling until the heart rate reached 180 beats/min. During all these interventions, T correlated with the duration of LV relaxation filling (r = 0.99. p less than 0.05). The amount of relaxation filling and dV/dtmax both correlated with the maximum LA-LV pressure gradient.(ABSTRACT TRUNCATED AT 400 WORDS)
我们对10只正常清醒犬的左心室（LV）早期舒张期充盈情况进行了研究，这些犬此前已植入仪器用于测量左心室和左心房（LA）压力以及三个相互垂直的左心室内径。左心室容积按一般椭球体计算。被动结构内的压力会随着其充盈而升高。如果心肌舒张足够迅速，能对左心室舒张期充盈起到显著辅助作用，那么尽管容积增加，它也可能克服这种压力升高的影响，使左心室压力下降。因此，我们将左心室压力下降时发生的左心室充盈量定义为舒张期充盈，这是衡量左心室舒张在早期舒张期充盈过程中重要性的一个指标。舒张时间常数（T）由等容舒张期左心室压力的指数下降得出。在舒张早期左心室压力下降时（舒张期充盈期），左心室的三个直径均增大。用六甲铵（5毫克/千克）和阿托品（0.1毫克/千克）进行自主神经阻断后，舒张期充盈量从每搏量的21±6%（平均值±标准差）降至12±3%（P<0.01）。平均左心房压力也显著降低（从12±2降至10±5毫米汞柱，P<0.05），而舒张期充盈期的持续时间和T值未变。用多巴酚丁胺（10微克/千克/分钟）进行正性肌力刺激可缩短T值，而不改变左心房压力。最大左心房 - 左心室压力梯度、dV/dtmax和舒张期充盈量均增加。右旋糖酐输注（500毫升/10分钟）产生的前负荷增加导致左心房压力升高（从11±3升至21±8毫米汞柱，P<0.05），而不改变T值。这也增加了最大左心房 - 左心室压力梯度、dV/dtmax和舒张期充盈量。甲氧明（10毫克/3分钟静脉注射）产生的后负荷增加显著升高了左心房压力（从9±4升至15±10毫米汞柱，P<0.05），延长了T值（从35±4升至50±7毫秒，P<0.05）以及舒张期充盈的持续时间（从36±5升至44±9毫秒，P<0.01），而未改变最大左心房 - 左心室压力梯度、dV/dtmax或左心室舒张期充盈量。心房起搏引起的心率逐渐增加（从100 - 180次/分钟）导致左心室舒张时间常数和舒张期充盈持续时间逐渐缩短。左心房压力也降低。直到心率达到180次/分钟时，左心室主动充盈量才相应增加。在所有这些干预过程中，T值与左心室舒张期充盈持续时间相关（r = 0.99，P<0.05）。舒张期充盈量和dV/dtmax均与最大左心房 - 左心室压力梯度相关。（摘要截选至400字）
