The Journal of Thoracic and Cardiovascular Surgery, Vol 88, 49-56, Copyright © 1984 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Reperfusion of inflow-limited myocardium following hypothermic potassium-induced cardioplegia
WR Chitwood Jr, RC Hill and AS Wechsler
Previous studies have shown that transmural reperfusion patterns may be
markedly abnormal following periods of ischemia. The present study was done
to elucidate the effects of hypothermic potassium cardioplegia on
pressure-flow characteristics during reperfusion of myocardial regions with
chronically compromised arterial inflow. Prior to cardiopulmonary bypass
studies. Ameroid constrictors were placed on the circumflex coronary artery
of 10 adult dogs to create a myocardial region subserved by
inflow-restricting collaterals. Subsequently, during cardiopulmonary bypass
at 80 mm Hg, 10 minutes of ischemic arrest was induced with hypothermic
potassium cardioplegia (15 degrees C, pH 7.4, potassium chloride 25 mEq/L).
Transmural myocardial flow was measured in normal and collateral-dependent
regions during control conditions and at 1, 5, and 10 minutes of
reperfusion. Also, retrograde circumflex pressures were monitored as an
additional index of perfusion of the collateral regions. A normal
endocardial/epicardial flow ratio was maintained in the normal regions at
1, 5, and 10 minutes of reperfusion. In contrast, a marked decrease in
endocardial/epicardial flow ratio occurred transiently in the collateral
regions at 1 minute of reperfusion (0.28 +/- 0.05). Simultaneously,
retrograde circumflex pressures fell from 55 +/- 3.5 mm Hg to 42 +/- 3.0 mm
Hg (p less than 0.001). By 5 minutes of reperfusion, retrograde circumflex
pressure, mean flow, and transmural endocardial/epicardial ratios returned
to normal in collateral regions. These data suggest that, even with optimal
myocardial protection, changes in transmural flow occur very early during
reperfusion and are exaggerated in inflow-restricted myocardial regions.
Mechanisms responsible for these changes may include refilling of
epicardial vessels emptied during the cross-clamp period or an early
epicardial hyperemic response. Despite these alterations, normal transmural
flow patterns are reestablished rapidly. Thus, when detailed attention is
paid to adequate myocardial protection, abnormal reperfusion
characteristics are obviated, and this is particularly important in
myocardium supplied by inflow-compromised coronary vessels.
