Beneficial effects of low-flow perfusion resumed early after zero-flow ischemia on myocardial energy metabolism and mechanical function: 31P-NMR study in the isolated perfused rat heart.
Effects of low-flow perfusion after zero-flow ischemia on myocardial mechanical function and energy metabolism were studied with 31P nuclear magnetic resonance spectroscopy, using isolated perfused rat hearts. After control perfusion, hearts were randomly divided into five experimental groups: Groups I and II were subjected to zero-flow ischemia of 40 and 60 min, respectively. In groups III-V the perfusion was resumed at a rate of 0.1 ml/min after 40 (group III), 30 (group IV) and 20 (group V)-min of zero-flow ischemia in order to compare the effects of low-flow perfusion with those of persistent zero-flow. After these interventions all the hearts were perfused for 40 min at a normal flow rate. Compared with the hearts exposed to total ischemia of 60 min, the preservation of high energy phosphate compounds (HEP) was better in groups with early low-flow perfusion; Creatine phosphate (CrP) levels, which had decreased rapidly after induction of zero-flow ischemia, increased gradually after initiation of the low-flow perfusion and reached significantly higher levels at the end of ischemic period in groups IV and V than in group II (p less than 0.05). The decrease in adenosine triphosphate (ATP) was likewise significantly suppressed by low-flow perfusion (groups IV and V greater than group II). Restoration of CrP levels after complete reperfusion was also significantly greater in group V than in group II. The recovery of ATP after complete reperfusion was also much better in group V being comparable to those in group I, although the total duration of ischemia was longer in group V than in group I. These results indicate the beneficial effects of low-flow perfusion on the preservation during ischemia and recovery after reperfusion of myocardial HEP.
Matsubara
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First Department of Internal Medicine, Niigata University School of Medicine, Japan.
D000255:Adenosine Triphosphate / Q000097:blood; D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010710:Phosphates / Q000097:blood; D010725:Phosphocreatine / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains
D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate