Aj. Liedtke et al., MYOCARDIAL-FUNCTION AND METABOLISM IN PIG HEARTS AFTER RELIEF FROM CHRONIC PARTIAL CORONARY STENOSIS, American journal of physiology. Heart and circulatory physiology, 36(4), 1994, pp. 80001312-80001319
Metabolic behavior was compared during acute extracorporeal reperfusio
n 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 i
n RCS hearts was induced in the left anterior descending (LAD) artery
by partial inflation of a hydraulic occluder to restrict LAD peak phas
ic velocity by similar to 50%. Regional mechanical shortening was decr
eased in RCS compared with Sham hearts after 4 days of chronic coronar
y stenosis [diminished systolic shortening (P < 0.066) with systolic e
xpansion (P < 0.015)] but was comparable to Sham hearts after relief f
rom stenosis. At analogous workloads (left ventricular pressure and he
art rate) during reperfusion, metabolic behavior was distinctive betwe
en groups. Specifically, compared with Sham hearts, myocardial O-2 con
sumption was selectively increased in RCS hearts (+49 Delta%, P < 0.02
6) as was fatty acid oxidation estimated from (CO2)-C-14 production fr
om [U-C-14]palmitate (+60 Delta%, P < 0.061) and exogenous glucose uti
lization measured from the release of (H2O)-H-3 from [5-H-3]glucose (517 Delta%, P < 0.025). At the conclusion of the studies, triphenyltet
razolium chloride staining showed no gross evidence of macroinfarction
in RCS or Sham hearts, and there was an essentially unremarkable hist
ological survey of anterior myocardium for microscopic necrosis in eit
her 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 remov
al of chronic partial coronary stenosis. The increase in use of glucos
e substrate is of interest and may indicate loss of allosteric regulat
ion by fatty acids or its intermediates upon rate-limiting enzymes in
the glycolytic cascade.