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Department of Veterans Affairs, Western New York Health Care System, and Departments of Medicine and Physiology, University at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York 14214
We sought to identify mechanisms for chronic
dysfunction in hibernating myocardium. Pigs were instrumented with a
left anterior descending artery stenosis for 3 mo. Angiography
demonstrated high-grade stenoses and hibernating myocardium with
1) severe anterior hypokinesis
(P < 0.001 vs. shams),
2) reduced subendocardial perfusion
[0.73 ± 0.05 (SE) vs. 1.01 ± 0.06 ml · min
1 · g1
in normal, P < 0.001], and
3) critically reduced adenosine flow (1.0 ± 0.17 vs. 3.84 ± 0.26 ml · min1 · g1
in normal, P < 0.001). Histology did
not reveal necrosis. Northern blot analysis of hibernating myocardium
demonstrated regional downregulation in mRNAs for sarcoplasmic
reticulum (SR) proteins phospholamban (0.76 ± 0.08 vs. 1.07 ± 0.06, P < 0.02) and SR
Ca2+-ATPase (0.83 ± 0.06 vs.
1.02 ± 0.06, P < 0.05)
with no change in calsequestrin (1.08 ± 0.06 vs. 0.96 ± 0.05, P = not significant). Heat shock protein (HSP)-70 mRNA was regionally induced in hibernating myocardium (2.4 ± 0.3 vs. 1.0 ± 0.11, P < 0.01). Directionally similar
changes were confirmed by Western blot analysis of respective proteins.
Our results indicate that hibernating myocardium exhibits a molecular
phenotype that on a regional basis is similar to end-stage ischemic
cardiomyopathy. This supports the hypothesis that SR dysfunction from
reversible ischemia may be an early defect in the progression
of left ventricular dysfunction.
coronary flow; myocardial ischemia; calcium regulatory proteins; sarcoplasmic reticulum
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