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Schulz R, Janssen F, Guth BD, et al. Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs. Basic Res Cardiol. 1991;86(6):534-43doi: 10.1007/BF02190703.
Schulz, R., Janssen, F., Guth, B. D., & Heusch, G. (1991). Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs. Basic research in cardiology, 86(6), 534-43. https://doi.org/10.1007/BF02190703
Schulz, R, et al. "Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs." Basic research in cardiology vol. 86,6 (1991): 534-43. doi: https://doi.org/10.1007/BF02190703
Schulz R, Janssen F, Guth BD, Heusch G. Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs. Basic Res Cardiol. 1991 Nov-Dec;86(6):534-43. doi: 10.1007/BF02190703. PMID: 1786034.
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Basic Res Cardiol. 1991 Nov-Dec;86(6):534-43. doi: 10.1007/BF02190703.

Effect of coronary hyperperfusion on regional myocardial function and oxygen consumption of stunned myocardium in pigs.

Basic research in cardiology

R Schulz, F Janssen, B D Guth, G Heusch

Affiliations

  1. Abteilung für Pathophysiologie, Zentrum für Innere Medizin, Universität Essen, FRG.

PMID: 1786034 DOI: 10.1007/BF02190703

Abstract

The "Gregg phenomenon" implies that myocardial function and oxygen consumption (MVO2) increase when coronary perfusion is enhanced within or above the autoregulatory range. We have recently demonstrated that the "Gregg phenomenon" has no significance for regional myocardial function and MVO2 in anesthetized swine in situ. There is, however, some evidence that the "Gregg phenomenon" may exist within stunned myocardium. To test whether coronary hyperperfusion increases regional myocardial function and MVO2 in stunned myocardium, in six anesthetized swine the left anterior descending coronary artery (LAD) was cannulated and perfused at constant pressure (CAP) using an extracorporal circuit. The coronary vein which parallels the LAD was cannulated to allow measurement of regional MVO2 and regional systolic wall thickening (WT%) of the anterior myocardium was assessed using sonomicrometry. Blood flow (CBF) to the LAD was increased by increasing CAP within the extracorporal circuit or by intracoronary adenosine infusion (150 micrograms/min). In normal myocardium, increasing CBF from 71.4 +/- 19.7 (SD) to 156.7 +/- 48.8 ml/min/100 g by increasing CAP from 100 +/- 10 to 190 +/- 10 mm Hg or increasing CBF from 75.1 +/- 29.1 to 189.2 +/- 45.8 ml/min/100 g by intracoronary adenosine infusion did not increase WT% (34.3 +/- 12.2% vs 32.1 +/- 10.6% and 32.3 +/- 10.7% vs 30.1 +/- 13.2%, respectively). MVO2 was not changed during enhanced CAP (6.94 +/- 1.05 vs 8.10 +/- 1.08 ml/min/100 g) and during intracoronary adenosine infusion (6.67 +/- 1.45 vs 7.30 +/- 2.23 ml/min/100 g). Twenty min of hypoperfusion followed by 30 min of reperfusion depressed WT% by 47% (p less than 0.05). However, MVO2 was only decreased by 23% (NS). In the stunned myocardium, increasing CBF from 62.1 +/- 36.4 to 157.1 +/- 60.0 ml/min by increasing CAP was not associated with an increase in WT%. MVO2, however, increased from 5.14 +/- 1.07 to 8.88 +/- 1.83 ml/min/100 g (p less than 0.05). Comparable results were achieved when CBF was increased from 60.3 +/- 28.7 to 176.9 +/- 48.5 ml/min by intracoronary adenosine infusion. WT% was unaffected, while MVO2 increased from 4.69 +/- 0.92 to 9.46 +/- 3.39 ml/min/100 g (p less than 0.05). Thus, increasing coronary perfusion within or above the autoregulatory range increases MVO2 in stunned myocardium, but without a simultaneous increase in regional myocardial function.

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