Sidi Avner, Muehlschlegel Jochen D, Kirby David S, Kirby Robert R, Lobato Emilio B
Department of Anesthesiology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA.
J Cardiothorac Vasc Anesth. 2007 Jun;21(3):400-5. doi: 10.1053/j.jvca.2006.03.024. Epub 2007 Apr 5.
OBJECTIVE(S): The effects of hypertonic saline on ventricular function are controversial, whether it is increasing contractility or preload. There are no data, however, on the influence of hypertonic saline in a stunned myocardium.
This study was prospective and randomized in order to analyze the effects of hypertonic saline solution (7.5%) on myocardial function and systemic hemodynamics in a porcine model of ischemia and reperfusion.
A university teaching hospital, animal research laboratory.
Twelve adult domestic swine.
Myocardial stunning was produced by the complete occlusion of the proximal left anterior descending artery for 15 minutes followed by reperfusion. Five minutes after reperfusion, the animals were assigned to receive 4 mL/kg of hypertonic saline (n = 7) or normal saline (n = 5) over 10 minutes. Pressure-tipped catheters were placed in the left ventricular cavity and aorta. The dimensions of the left ventricle were measured with ultrasonic microcrystals. Cardiac output was measured with transit time ultrasound. Data were recorded continuously and compared before the occlusion, 5 minutes after reperfusion, and at the end of the infusion.
Compared with baseline, ventricular function was significantly depressed after left anterior descending artery occlusion. Left ventricular dP/dT and its end-systolic pressure-volume slope decreased (38% and 52%, respectively; p < 0.05), with a concomitant increase in systemic vascular resistance. The administration of hypertonic saline significantly improved left ventricular function (Emax 1,422 +/- 198 mmHg/mL, and dP/dT 3.2 +/- 0.4 mmHg/s v normal saline group values of 1,156 +/- 172 and 2.5 +/- 0.5, respectively; p < 0.05), cardiac output (2.5 +/- 0.5 v 1.84 +/- 0.4 L/min, p < 0.05), and lowered systemic vascular resistance (from 28.8 +/- 2.3 to 23.5 +/- 1.4, p < 0.05), with no significant changes with normal saline administration.
After transient myocardial ischemia, hypertonic saline administered over a short period of time acts as an inodilator by increasing contractility while simultaneously lowering systemic vascular resistance.
高渗盐水对心室功能的影响存在争议，其究竟是增强心肌收缩力还是增加前负荷尚无定论。然而，目前尚无关于高渗盐水对顿抑心肌影响的数据。
本研究为前瞻性随机研究，旨在分析高渗盐溶液（7.5%）对猪缺血再灌注模型中心肌功能和全身血流动力学的影响。
一所大学教学医院的动物研究实验室。
12只成年家猪。
通过完全阻断左前降支近端15分钟后再灌注造成心肌顿抑。再灌注5分钟后，将动物随机分为两组，一组在10分钟内接受4 mL/kg高渗盐水（n = 7），另一组接受生理盐水（n = 5）。将压力传感器导管置于左心室腔和主动脉内。用超声微晶体测量左心室尺寸。用经胸超声测量心输出量。在阻断前、再灌注5分钟时及输注结束时连续记录数据并进行比较。
与基线相比，左前降支阻断后心室功能明显降低。左心室dp/dt及其收缩末期压力-容积斜率下降（分别下降38%和52%；p < 0.05），同时全身血管阻力增加。给予高渗盐水可显著改善左心室功能（Emax为1422±198 mmHg/mL，dp/dt为3.2±0.4 mmHg/s，而生理盐水组分别为1156±172和2.5±0.5；p < 0.05）、心输出量（2.5±0.5 vs 1.84±0.4 L/min，p < 0.05），并降低全身血管阻力（从28.8±2.3降至23.5±1.4，p < 0.05），而给予生理盐水则无显著变化。
短暂心肌缺血后，短时间内给予高渗盐水可通过增强心肌收缩力同时降低全身血管阻力而起到心肌收缩性血管扩张剂的作用。
