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The Journal of Thoracic and Cardiovascular Surgery, Vol 105, 52-58, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
FW Sellke, T Shafique, FJ Schoen and RM Weintraub
Myocardial dysfunction after cardiac operations might be influenced by
altered myocardial perfusion in the postoperative period. To investigate
possible alterations in vascular reactivity, in vitro coronary
microvascular responses were examined after ischemic cardioplegia with use
of a porcine model of cardiopulmonary bypass. Since myocardial perfusion is
primarily regulated by arteries less than 200 microns in diameter, these
vascular segments were examined. After 1 hour of ischemic arrest with cold
crystalloid cardioplegia and 1 hour of reperfusion, microvessels (100 to
190 microns in diameter) were pressurized in a no-flow state,
preconstricted by 30% to 60% of the baseline diameter with acetylcholine,
and examined with video microscopic imaging and electronic dimension
analysis. Endothelium- dependent relaxations to bradykinin (55% +/- 13%
versus 99% +/- 1% = maximum relaxation of the preconstricted diameter in
cardioplegia- reperfusion vessels versus control vessels, respectively; p
< 0.05) and the calcium ionophore A 23187 (33% +/- 6% versus 90% +/- 4%;
p < 0.05) were markedly impaired while endothelium-independent
relaxation to sodium nitroprusside was similar to control value. After 1
hour of ischemic cardioplegia without reperfusion, endothelium-dependent
relaxation was only slightly affected. Transmission electron microscopy
showed minimal endothelial damage after ischemic cardioplegia and
reperfusion. These findings have important implications regarding coronary
spasm and cardiac dysfunction after cardiac operations.
ARTICLES
Impaired endothelium-dependent coronary microvascular relaxation after cold potassium cardioplegia and reperfusion
Department of Surgery, Beth Israel Hospital, Boston, MA 02215.
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