Stewart J M, Patel M B, Wang J, Ochoa M, Gewitz M, Loud A V, Anversa P, Hintze T H
Department of Physiology, New York Medical College, Valhalla 10595.
Am J Physiol. 1992 Feb;262(2 Pt 2):H331-9. doi: 10.1152/ajpheart.1992.262.2.H331.
Elevated plasma catecholamine levels may cause both myocardial hypertrophy and tissue damage. To determine whether the left ventricle from dogs with chronic norepinephrine infusion can sustain additional functional loads, we altered ventricular preload or afterload and determined both global and left ventricular (LV) wall function. Dogs were instrumented to measure LV wall function, LV internal base diameter, and LV pressures and were allowed to fully recover. Preload was altered by volume loading and afterload by injection of phenylephrine. Osmotic infusion pumps were implanted to continuously release norepinephrine at 0.5 micrograms.kg-1.min-1 for 28 days, and the volume loading and phenylephrine were repeated on days 14 and 28. Heart rate decreased, whereas there were no differences in mean arterial pressure, maximum first derivative of LV pressure (dP/dt), LV dP/dt/developed pressure of 40 mmHg, LV dP/dt/end-diastolic circumference, slope of the pressure-diameter relation, peak systolic wall stress, LV/end-diastolic diameter, or LV/end-systolic diameter during norepinephrine infusion. Diastolic and systolic wall thickness and chamber weights were increased (P less than 0.05). Indexes of diastolic function, including end-diastolic pressure, end-diastolic pressure-end-diastolic diameter relationship, maximum negative dP/dt, and the time constant (tau) were unchanged after chronic norepinephrine infusion, although maximum end-diastolic pressure during volume loading was increased from 17.7 +/- 2.0 to 21.7 +/- 1.0 mmHg. Chronic norepinephrine infusion did not alter tau, and tau increased equivalently with phenylephrine injection in both normal (36 +/- 1 to 62 +/- 5 ms) dogs and in those chronically infused with norepinephrine (36 +/- 1 to 56 +/- 5 ms).(ABSTRACT TRUNCATED AT 250 WORDS)
血浆儿茶酚胺水平升高可能导致心肌肥大和组织损伤。为了确定慢性输注去甲肾上腺素的犬的左心室是否能够承受额外的功能负荷,我们改变了心室前负荷或后负荷,并测定了整体和左心室(LV)壁功能。给犬安装仪器以测量LV壁功能、LV基部内径和LV压力,并使其充分恢复。通过容量负荷改变前负荷,通过注射去氧肾上腺素改变后负荷。植入渗透式输注泵以0.5微克·千克⁻¹·分钟⁻¹的速度持续释放去甲肾上腺素28天,在第14天和第28天重复进行容量负荷和去氧肾上腺素注射。心率下降,而去甲肾上腺素输注期间平均动脉压、LV压力的最大一阶导数(dP/dt)、LV dP/dt/40 mmHg的发展压力、LV dP/dt/舒张末期周长、压力-直径关系斜率、收缩期峰值壁应力、LV/舒张末期直径或LV/收缩末期直径无差异。舒张期和收缩期壁厚以及心室重量增加(P<0.05)。慢性输注去甲肾上腺素后,舒张功能指标,包括舒张末期压力、舒张末期压力-舒张末期直径关系、最大负向dP/dt和时间常数(tau)未改变,尽管容量负荷期间的最大舒张末期压力从17.7±2.0 mmHg增加到21.7±1.0 mmHg。慢性输注去甲肾上腺素未改变tau,在正常犬(36±1至62±5毫秒)和慢性输注去甲肾上腺素的犬(36±1至56±5毫秒)中,tau随去氧肾上腺素注射等效增加。(摘要截短于250字)