Myocardial function and metabolism in pig hearts after relief from chronic partial coronary stenosis
Liedtke, A.J.; Renstrom, B.; Nellis, S.H.; Subramanian, R.
American Journal of Physiology 267(4 Pt 2): H1312-H1319
1994
ISSN/ISBN: 0002-9513 PMID: 7943376 Document Number: 426143
Metabolic behavior was compared during acute extracorporeal reperfusion after removal of a chronic 4-day partial coronary stenosis in eight pig hearts (RCS group) and during comparable extracorporeal perfusion in seven chronically prepared hearts (Sham group). Coronary stenosis in RCS hearts was induced in the left anterior descending (LAD) artery by partial inflation of a hydraulic occluder to restrict LAD peak phasic velocity by apprx 50%. Regional mechanical shortening was decreased in RCS compared with Sham hearts after 4 days of chronic coronary stenosis (diminished systolic shortening (P lt 0.066) with systolic expansion (P lt 0.015)) but was comparable to Sham hearts after relief from stenosis. At analogous workloads (left ventricular pressure and heart rate) during reperfusion, metabolic behavior was distinctive between groups. Specifically, compared with Sham hearts, myocardial O-2 consumption was selectively increased in RCS hearts (+49-DELTA%, P lt 0.026) as was fatty acid oxidation estimated from 14CO-2 production from (U-14C)palmitate (+60-DELTA%, P lt 0.061) and exogenous glucose utilization measured from the release of 3H-2O from (5-3H)glucose (+517-DELTA%, P lt 0.025). At the conclusion of the studies, triphenyltetrazolium chloride staining showed no gross evidence of macroinfarction in RCS or Sham hearts, and there was an essentially unremarkable histological survey of anterior myocardium for microscopic necrosis in either group. The level of O-2 consumption and preservation of preferred fatty acid utilization indicate that metabolism remains or regains its aerobic pattern of activity in early recovery immediately after removal of chronic partial coronary stenosis. The increase in use of glucose substrate is of interest and may indicate loss of allosteric regulation by fatty acids or its intermediates upon rate-limiting enzymes in the glycolytic cascade.