Tang W C, Weil M H, Gazmuri R J, Bisera J, Rackow E C
Department of Medicine, University of Health Sciences, Chicago Medical School, North Chicago, IL 60064.
Crit Care Med. 1991 Feb;19(2):218-24. doi: 10.1097/00003246-199102000-00018.
Striking increases in PCO2 of the myocardium have recently been documented during cardiac arrest. The purpose of the present study was to investigate selective effects of hypercarbia as distinct from acidosis on left ventricular contractile function and oxygen utilization. An isolated, spontaneously beating rat heart preparation was utilized. The perfusate was equilibrated with gases containing 5%, 10%, 20%, and 30% CO2. In a subset of experiments, the [H+] was adjusted independently of PCO2 by decreasing the concentration of HCO3-.
When the PCO2 of the perfusate was progressively increased from 36 to 146 torr (4.8 to 29.5 kPa), the left ventricular systolic pressure (LVSP) generated by the isolated heart and the maximum rate of pressure change in the left ventricle (dP/dt) were decreased to 20% of their control values. However, comparable acidosis in the absence of hypercarbia produced only minimal decreases in the LVSP or dP/dt such that contractility remained at greater than or equal to 88%. Increases in the perfusate PCO2 but not in the perfusate H+ were highly correlated with decreases in both myocardial contractility and oxygen consumption (r2 = .88).
Hypercarbia rather than acidosis accounts for decreased contractility and oxygen utilization in the isolated perfused rat heart.
最近有文献记载,心脏骤停期间心肌的二氧化碳分压(PCO₂)显著升高。本研究的目的是探究高碳酸血症相对于酸中毒对左心室收缩功能和氧利用的选择性影响。使用了离体的、自主搏动的大鼠心脏标本。灌注液用含5%、10%、20%和30%二氧化碳的气体进行平衡。在一部分实验中,通过降低碳酸氢根(HCO₃⁻)浓度独立于PCO₂来调节氢离子浓度([H⁺])。
当灌注液的PCO₂从36托(4.8千帕)逐渐升高至146托(29.5千帕)时,离体心脏产生的左心室收缩压(LVSP)和左心室压力变化最大速率(dP/dt)降至对照值的20%。然而,在不存在高碳酸血症的情况下,类似的酸中毒仅使LVSP或dP/dt有极小的降低,收缩性仍保持在大于或等于88%。灌注液PCO₂的升高而非灌注液H⁺的升高与心肌收缩性和氧消耗的降低高度相关(r² = 0.88)。
在离体灌注的大鼠心脏中,导致收缩性和氧利用降低的是高碳酸血症而非酸中毒。