Oe M, Asou T, Morita S, Yasui H, Tokunaga K
Division of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Thorac Cardiovasc Surg. 1996 Aug;112(2):462-71. doi: 10.1016/S0022-5223(96)70274-X.
Protamine sulfate often causes hypotension during heparin neutralization. The concept of ventricular-arterial coupling was applied to determine whether a negative inotropic effect or a vasodilating effect of protamine was the major contributing factor to this hypotension. Thirty-five patients who underwent cardiac operations were studied during operation by measuring instantaneous left ventricular pressure and aortic flow to examine the end-systolic pressure-volume relationship. We obtained end-systolic elastance and effective arterial elastance values in a beat-to-beat fashion with a single-beat estimation method. In 28 of the 35 patients (80%), mean arterial pressure decreased more than 10 mm Hg with protamine infusion. Parameters were compared at the following three points: before a decrease in mean arterial pressure (control), at maximally decreased mean arterial pressure (maximum), and at a middle point between control and maximum values (midpoint). At both midpoint and maximum, mean arterial pressure decreased significantly (control 79.6 +/- 12.6 mm Hg, midpoint 66.5 +/- 10.8 mm Hg, maximum 52.7 +/- 9.9 mm Hg; p < 0.01). Similar changes were observed in effective arterial elastance (control 2.00 +/- 0.75 mm Hg/ml, midpoint 1.60 +/- 0.53 mm Hg/ml, maximum 1.31 +/- 0.46 mm Hg/ml; p < 0.01). Although the decrease in end-systolic elastance at midpoint (control 3.08 +/- 1.61 mm Hg/ml, midpoint 2.92 +/- 1.68 mm Hg/ml) did not reach statistical significance, end-systolic elastance significantly decreased at maximum (2.63 +/- 1.46 mm Hg/ml; p < 0.01). Continuous measurements showed that the decreases in mean arterial pressure and effective arterial elastance always preceded the depression of end-systolic elastance and that afterload reduction by vasodilating effect of protamine was the mechanism most likely to have initiated the hypotension. Delayed decrease in contractility may be ascribed to reduced coronary perfusion pressure caused by vasodilation or to a direct effect of protamine.
硫酸鱼精蛋白在中和肝素过程中常导致低血压。应用心室 - 动脉耦合的概念来确定鱼精蛋白的负性肌力作用或血管舒张作用是否是导致这种低血压的主要因素。对35例接受心脏手术的患者在手术过程中进行研究，通过测量瞬时左心室压力和主动脉血流来检查收缩末期压力 - 容积关系。我们采用单搏估计法逐搏获得收缩末期弹性和有效动脉弹性值。在35例患者中的28例（80%），输注鱼精蛋白后平均动脉压下降超过10 mmHg。在以下三个时间点比较参数：平均动脉压下降前（对照）、平均动脉压最大下降时（最大）以及对照值和最大值之间的中点（中点）。在中点和最大时，平均动脉压均显著下降（对照79.6±12.6 mmHg，中点66.5±10.8 mmHg，最大52.7±9.9 mmHg；p<0.01）。有效动脉弹性也观察到类似变化（对照2.00±0.75 mmHg/ml，中点1.60±0.53 mmHg/ml，最大1.31±0.46 mmHg/ml；p<0.01）。尽管中点时收缩末期弹性的下降（对照3.08±1.61 mmHg/ml，中点2.92±1.68 mmHg/ml）未达到统计学显著性，但在最大时收缩末期弹性显著下降（2.63±1.46 mmHg/ml；p<0.01）。连续测量表明，平均动脉压和有效动脉弹性的下降总是先于收缩末期弹性的降低，并且鱼精蛋白血管舒张作用导致的后负荷降低是最有可能引发低血压的机制。收缩力的延迟下降可能归因于血管舒张引起的冠状动脉灌注压降低或鱼精蛋白的直接作用。
