Circulation, Vol 85, 699-707, Copyright © 1992 by American Heart Association
SE Downing and V Chen
BACKGROUND. Recovery from prolonged low-flow ischemia was studied in
isolated, isovolumically beating neonatal piglet hearts (n = 11) and
compared with controls (n = 5). METHODS AND RESULTS. Hearts were perfused
with red blood cell-enhanced Krebs-Henseleit buffer with physiological
oxygen-carrying capacity. Left ventricular mechanical function was assessed
with a fluid-filled balloon. Measurements of peak systolic pressure,
pressure-rate product (PRP), and +dP/dtmax were obtained at various filling
pressures. Myocardial oxygen delivery and metabolism (MVO2) and lactate
uptake were measured at 30-minute intervals. Control data were obtained
with coronary flow (CF) set at 2 ml.min-1.g-1. CF was then reduced to 0.2
ml.min-1.g-1 for 2 hours. Thereafter, reperfusion was instituted at control
levels. Hearts not subjected to ischemia were studied at identical time
intervals. In these, function remained at greater than 80% after more than
3.5 hours of study. Reduction of CF to 10% was accompanied by an abrupt
diminution in function (pressure-rate product) and MVO2 to 20% of control
and by lactate release. These measures remained constant for the full 2
hours of ischemia. Incremental return of CF caused a lockstep increase in
mechanical function and metabolism. At 30 minutes of reperfusion, PRP was
78% of time-matched controls (p = 0.05), and dP/dtmax did not differ.
Increasing calcium to 5 mmol/l returned PRP (and dP/dtmax) to preischemia
levels. Myocardial ATP and creatine phosphate concentrations were identical
in both groups, although glycogen was lower in the ischemic hearts.
CONCLUSIONS. Acute hibernation is associated with protection of the in
vitro heart from prolonged normothermic ischemia. Systolic function was
only modestly lower, and velocity (dP/dtmax) did not differ from control
hearts. The minimal "stunning" was fully reversible with calcium.
ARTICLES
Acute hibernation and reperfusion of the ischemic heart
Department of Pathology, Yale University School of Medicine, New Haven, Conn. 06510.
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