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J Thorac Cardiovasc Surg 1996;112:8-13
© 1996 Mosby, Inc.
SURGERY FOR CONGENITAL HEART DISEASE |
Supported in part by National Research Service Award NIH HL07819-02, SCOR HL-17670, and the Harold and Linda Plemmons Cardiac Surgical Research Foundation.
Received for publication June 14, 1995 Revisions requested June 14, 1995; revisions received Dec. 26, 1995 Accepted for publication Dec. 26, 1995. Address for reprints: James E. Lowe, MD, Department of Surgery, Box 3954, Duke University Medical Center, Durham, NC 27710.
Abstract
The effect of chronic hypoxia on neonatal myocardial metabolism remains undefined. With a new neonatal piglet model, we determined changes in myocardial metabolism during global ischemia after chronic hypoxia. Five-day-old piglets (N = 30) were randomly assigned to two groups and exposed to an atmosphere of 8% oxygen or to room air for 28 days before they were killed. Left ventricular myocardium was then analyzed at control and at 15-minute intervals during 60 minutes of global normothermic ischemia to determine high-energy phosphate levels, glycogen stores, and lactate accumulation. Time to peak ischemic myocardial contracture was measured with intramyocardial needle-tipped Millar catheters as a marker of the onset of irreversible ischemic injury. Results showed an initially greater level of myocardial adenosine triphosphate in the hypoxic group (27 ± 1.2 vs 19 ± 1.8µmol/gm dry wt, p = 0.001) and a delay in adenosine triphosphate depletion during 60 minutes of global ischemia compared with the control group. Initial energy charge ratios (
adenosine diphosphate + adenosine triphosphate/adenosine monophosphate + adenosine diphosphate + adenosine triphosphate) were also greater in the hypoxic group (0.96 ± 0.01 vs 0.81 ± 0.04, p = 0.01) and remained so throughout global ischemia. Initial glycogen stores were greater in the hypoxic group (273 ± 13.3 vs 215 ± 14.7µmol/gm dry weight, p = 0.02) when compared with the control group. Lactate levels in the hypoxic group were initially higher (19.1 ± 6.4 vs 8.9 ± 3.1µmol/gm dry weight, p = 0.001) compared with control levels and remained elevated throughout 60 minutes of ischemia. Time to peak ischemic contracture was prolonged in the hypoxic group (69.5 ± 1.8 vs 48.9 ± 1.4 minutes, p = 0.001) compared with the controls group. These data show that chronic hypoxia results in significant myocardial metabolic adaptive changes, which in turn result in an improved tolerance to severe normothermic ischemia. These beneficial effects are associated with elevated baseline glycogen storage levels and an accelerated rate of anaerobic glycolysis during ischemia. (J THORAC CARDIOVASC SURG 1996;112:8-13)
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