Parrillo J E, Burch C, Shelhamer J H, Parker M M, Natanson C, Schuette W
J Clin Invest. 1985 Oct;76(4):1539-53. doi: 10.1172/JCI112135.
We have previously described a subpopulation of patients with septic shock who had a reversible depression of radionuclide-determined left ventricular ejection fraction (EF). To investigate the mechanism of this myocardial depression, an in vitro model of mammalian myocardial cell performance was established employing primary spontaneously beating rat myocardial cells. The contraction of a single cardiac cell was quantitated by recording the changes in area occupied by the cell during contraction and relaxation. In 20 septic shock patients during the acute phase, the mean left ventricular EF was decreased (mean = 0.33, normal mean = 0.50), and serum obtained during this acute phase induced a mean (+/- standard error of the mean) 33 +/- 4% decrease in extent and 25 +/- 4% decrease in velocity of myocardial cell shortening during contraction (P less than 0.001). In contrast, serum obtained from 11 of these same patients before shock (n = 2) or after recovery (n = 9) of the left ventricular EF (mean = 0.50) showed a return toward normal in extent and velocity of shortening (P less than 0.001). Sera from 17 critically ill nonseptic patients, from 10 patients with structural heart disease as a cause for a depressed EF, and from 12 healthy laboratory personnel, induced no significant changes in in vitro myocardial cell performance. In 20 patients during the acute phase of septic shock, the decreased EF in vivo demonstrated a significant correlation (r = +0.52, P less than 0.01) with a decrease in the extent of myocardial cell shortening in vitro. The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substance in producing the reversible cardiomyopathy seen during septic shock in humans.
我们之前曾描述过脓毒性休克患者的一个亚群，他们的放射性核素测定的左心室射血分数（EF）出现可逆性降低。为了研究这种心肌抑制的机制，我们利用原代自发搏动的大鼠心肌细胞建立了一个哺乳动物心肌细胞功能的体外模型。通过记录单个心肌细胞在收缩和舒张过程中所占面积的变化来定量其收缩情况。在20例脓毒性休克急性期患者中，平均左心室EF降低（平均值 = 0.33，正常平均值 = 0.50），在此急性期获得的血清导致心肌细胞收缩时缩短程度平均降低（平均值±平均标准误差）33±4%，缩短速度平均降低25±4%（P < 0.001）。相比之下，从这些患者中的11例在休克前（n = 2）或左心室EF恢复后（n = 9）获得的血清（平均值 = 0.50）显示缩短程度和速度恢复正常（P < 0.001）。来自17例重症非脓毒症患者、10例因结构性心脏病导致EF降低的患者以及12名健康实验室人员的血清，均未引起体外心肌细胞功能的显著变化。在20例脓毒性休克急性期患者中，体内EF降低与体外心肌细胞缩短程度降低呈显著相关性（r = +0.52，P < 0.01）。左心室EF降低与这种血清心肌抑制物质之间的定量和时间相关性表明，这种抑制物质在人类脓毒性休克期间出现的可逆性心肌病的发生中具有病理生理作用。
