PHARMACOLOGIC AND HEMODYNAMIC INFLUENCES ON RATE OF ISOVOLUMIC LEFT-VENTRICULAR RELAXATION IN NORMAL CONSCIOUS DOG
PHARMACOLOGIC AND HEMODYNAMIC INFLUENCES ON RATE OF ISOVOLUMIC LEFT-VENTRICULAR RELAXATION IN NORMAL CONSCIOUS DOG
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DOI：
10.1172/jci108803
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发表时间：
1977-01-01
影响因子：
15.9
通讯作者：
OROURKE, RA
中科院分区：
文献类型：
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作者：
KARLINER, JS;LEWINTER, MM;OROURKE, RA
应用微量压力针尖导管，观察急性药物干预和血流动力学干预对19只清醒犬等容左室舒张功能的影响。异丙肾上腺素(11项研究)使左室压峰值上升速率[(+)dp/dt[压力随时间变化]]增加1275。+-。227(SE)mm Hg/S(P<；0.001)和等压点35 mm Hg时的dp/dt[(-)dp/dt35]435+-。80毫米汞/S(P<；0.001)。峰(-)dp/dt下降467.+-。89毫米汞/S(P<；0.002)。从等容松弛过程中压力的对数下降得到的时间常数T，从20。+-缩短。2.8至14.9+-1.8ms(P<；0.003)。CA(11项研究)增加峰(+)dp/dt和(-)dp/dt 35(P均为0.0001)，峰(-)dp/dt不变。T由20.4.+-缩短。1.8至17.3。+-。1.5ms(P<；0.002)。容量(13项研究)不影响dp/dt或T.苯肾上腺素(13项研究)增加峰(-)dp/dt，但降低(-)dp/dt35(均P<；0.01)；T从22.1+-延长。1.5至32.5+-1.5ms(P<；0.01)。在15项研究中，快速心房起搏增加了峰值(+)dp/dt和(-)dp/dt35(P均<0.01)。起搏后第1次，峰(-)dp/dt和(-)dp/dt35降低(均P<0.01)，峰(+)dp/dt进一步升高。T(-)dp/dt35的平行值。在5只狗中，β-肾上腺素能受体阻滞剂在钙容量或注射苯肾上腺素后或在心房起搏过程中或之后比较心得安前后状态时，对任何变量都没有显著影响。正性肌力干预可能同时增强左心室收缩和松弛。等容松弛的变化与β-肾上腺素能受体阻滞剂产生的交感神经张力的变化无关。峰(-)dp/dt可能不是后负荷变力状态急性变化时左室舒张速率的有效量度。
The effects of acute pharmacologic and hemodynamic interventions were examined 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 [change in pressure with time]] by 1275 .+-. 227 (SE) mm Hg/s (P < 0.001) and dP/dt at an isopressure point of 35 mm Hg during isovolumic relaxation [(-) dP/dt35] 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). Ca (11 studies) increased peak (+) dP/dt and (-) dP/dt35 (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/dt35 (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/dt35 (both P < 0.01). In the 1st post-pacing beat, peak (-) dP/dt and (-) dP/dt35 decreased (both P < 0.01), although peak (+) dP/dt increased further. T paralleled values of (-) dP/dt35. In 5 dogs, .beta.-adrenergic blockade had no significant effect on any variable after Ca volume, or phenylephrine infusion or during or after atrial pacing when the pre- and post-propranolol states were compared. Positive inotropic interventions probably 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 of afterload.