TY - JOUR
T1 - Mechanism of elevated left ventricular end-diastolic pressure after ischemic arrest and reperfusion
AU - Schaff, H. V.
AU - Gott, V. L.
AU - Goldman, R. A.
PY - 1981
Y1 - 1981
N2 - The effects of ischemic arrest and reperfusion on isovolumic end-diastolic pressure, diastolic pressure-volume curves, and indices of ventricular relaxation and contractility were studied in an isolated feline heart preparation. In hearts subjected to 60 min of normothermic (37°C) ischemic arrest, isovolumic developed pressure, and dP/dt(max) during reperfusion returned to only approximately 60% of prearrest control levels. Isovolumic end-diastolic pressure (P(ed)) increased 37.0 ± 4.3 mmHg and the time constant of ventricular relaxation was prolonged. Hearts maintained at 27°C hypothermia during the 60-min ischemic period demonstrated improved contractile performance (~ 100% of control), less elevation of P(ed) (21.4 ± 4.5 mmHg), and no significant increase in the time constant of relaxation. In both groups of hearts, postarrest end-diastolic pressure-volume curves were shifted up and to the left, whereas indices of ventricular stiffness and muscle stiffness remained unchanged. These data suggest that the rise in isovolumic end-diastolic pressure observed after 1 h of ischemic arrest and reperfusion is the result of an upward and to the left shift of the entire diastolic pressure-volume relationship of the left ventricle. This shift does not appear to be related to diminished contractile performance or incomplete relaxation. Furthermore, the shift is not due to a change in muscle compliance, but to a reduction in the unstressed volume of the ventricle, which most likely results from myocardial contracture and edema.
AB - The effects of ischemic arrest and reperfusion on isovolumic end-diastolic pressure, diastolic pressure-volume curves, and indices of ventricular relaxation and contractility were studied in an isolated feline heart preparation. In hearts subjected to 60 min of normothermic (37°C) ischemic arrest, isovolumic developed pressure, and dP/dt(max) during reperfusion returned to only approximately 60% of prearrest control levels. Isovolumic end-diastolic pressure (P(ed)) increased 37.0 ± 4.3 mmHg and the time constant of ventricular relaxation was prolonged. Hearts maintained at 27°C hypothermia during the 60-min ischemic period demonstrated improved contractile performance (~ 100% of control), less elevation of P(ed) (21.4 ± 4.5 mmHg), and no significant increase in the time constant of relaxation. In both groups of hearts, postarrest end-diastolic pressure-volume curves were shifted up and to the left, whereas indices of ventricular stiffness and muscle stiffness remained unchanged. These data suggest that the rise in isovolumic end-diastolic pressure observed after 1 h of ischemic arrest and reperfusion is the result of an upward and to the left shift of the entire diastolic pressure-volume relationship of the left ventricle. This shift does not appear to be related to diminished contractile performance or incomplete relaxation. Furthermore, the shift is not due to a change in muscle compliance, but to a reduction in the unstressed volume of the ventricle, which most likely results from myocardial contracture and edema.
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U2 - 10.1152/ajpheart.1981.240.2.h300
DO - 10.1152/ajpheart.1981.240.2.h300
M3 - Article
C2 - 7468824
AN - SCOPUS:0019532524
SN - 0363-6135
VL - 9
SP - H300-H307
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 2
ER -