Horton J W
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031.
Circ Shock. 1989 May;28(1):23-35.
Isolated coronary-perfused guinea pig hearts were used to determine if in vivo hemorrhagic shock (mean arterial blood pressure, 32.8 +/- 2.3 mmHg for 2 hr) alters intrinsic contractile function of the left ventricle. Compared to control hearts, shocked hearts developed significantly less left ventricular pressure (control: 64.7 +/- 3.3; shock: 34.1 +/- 3.1 mmHg, P less than .001) and +dP/dt max (control: 1,429 +/- 187; shock: 894 +/- 119 mmHg/sec, P less than .038) and -dP/dt max (control: 1,416 +/- 176; shock: 808 +/- 94 mmHg/sec, P less than .011) at a left ventricular end-diastolic pressure of 10 mmHg. Increasing left ventricular end-diastolic pressure from 0 to 20 mmHg, electrical pacing at control heart rate, and increased coronary flow rate failed to restore shock-induced cardiac dysfunction. Left ventricular function curves calculated from shocked hearts were shifted downward and to the right of values obtained from control hearts (P = .001). Furthermore, left ventricular performance in shocked hearts remained depressed as extracellular calcium concentration was increased from 1 to 8 mM. While calcium increased left ventricular pressure, +dP/dt max, and -dP/dt max in a dose-dependent manner in both control and shocked hearts, all indices of contractile performance were consistently less in shocked hearts than those measured in control hearts at each calcium concentration. Our data suggest that cardiac depression is a feature of hemorrhagic shock.
