Kien N D, Kramer G C
Department of Anesthesiology, University of California, Davis 95616.
Braz J Med Biol Res. 1989;22(2):245-8.
The present study was undertaken to examine cardiovascular function before and after either intravenous or intra-arterial infusion of hypertonic saline (7.5% NaCl) in halothane-anesthetized dogs. A high-fidelity micromanometer and ultrasonic dimension transducers were implanted to measure pressure and wall motion of the left ventricle (LV). Cardiac output (CO) was measured using an electromagnetic flowmeter and thermodilution. The slope (Ees) of the linear regression of the LV pressure-diameter relationship was used as an index of cardiac contractility. Intravenous infusion of hypertonic saline (3 ml/kg) increased mean arterial pressure (MAP, 104 +/- 6 to 116 +/- 6 mmHg), heart rate (HR, 124 +/- 21 to 140 +/- 13 bpm), CO (3.2 +/- 0.9 to 4.2 +/- 0.5 l/m) and Ees (11.6 +/- 2.1 to 14.8 +/- 1.9 mmHg/mm). Systemic vascular resistance (SVR) fell by 18%. The above responses were similar whether infusion was intravenous or intra-arterial into innervated or denervated hind limbs. While nerve blockade at T-4 (xylocaine) attenuated the changes in CO and SVR and completely prevented the tachycardia, the inotropic response remained intact. These studies suggest that the cardiac effects of hypertonic saline infusion are not mediated by pulmonary or peripheral osmoreceptors and the increased contractility may result from a direct myocardial effect of increased osmolality.
本研究旨在检测在氟烷麻醉的犬中静脉或动脉输注高渗盐水（7.5%氯化钠）前后的心血管功能。植入高保真微测压计和超声尺寸换能器以测量左心室（LV）的压力和壁运动。使用电磁流量计和热稀释法测量心输出量（CO）。LV压力-直径关系的线性回归斜率（Ees）用作心脏收缩力指标。静脉输注高渗盐水（3 ml/kg）可使平均动脉压（MAP，从104±6 mmHg升至116±6 mmHg）、心率（HR，从124±21次/分钟升至140±13次/分钟）、CO（从3.2±0.9 l/m升至4.2±0.5 l/m）和Ees（从11.6±2.1 mmHg/mm升至14.8±1.9 mmHg/mm）升高。全身血管阻力（SVR）下降18%。无论输注是静脉内还是动脉内进入有神经支配或去神经支配的后肢，上述反应均相似。虽然T-4水平的神经阻滞（利多卡因）减弱了CO和SVR的变化并完全防止了心动过速，但正性肌力反应仍保持不变。这些研究表明，高渗盐水输注的心脏效应不是由肺或外周渗透压感受器介导的，收缩性增加可能是由于渗透压升高对心肌的直接作用所致。
