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The Annals of Thoracic Surgery, Vol 55, 977-985, Copyright © 1993 by The Society of Thoracic Surgeons
FW Sellke, T Shafique, RG Johnson, HB Dai, PF Banitt, FJ Schoen and RM Weintraub
Alterations of vascular reactivity may be a cause of reduced myocardial
perfusion after cardioplegic arrest. The effects of blood and albumin
cardioplegia on endothelium-dependent coronary microvascular function and
ultrastructure were examined after cardiopulmonary bypass, ischemic arrest,
and reperfusion. During cardiopulmonary bypass, porcine hearts were
arrested with either blood, albumin-crystalloid, or crystalloid
cardioplegia for 1 hour, followed with reperfusion for 1 hour.
Noninstrumented pigs were used as controls. Coronary microarterial vessels
(90 to 190 microns in diameter) were studied in a pressurized, no-flow
state with video microscopic imaging and electronic dimension analysis.
Ischemic arrest with crystalloid cardioplegia markedly reduced
endothelium-dependent relaxations to the adenine nucleotide adenosine
diphosphate and the calcium ionophore A23187. Enhanced contractile
responses were observed to the platelet-derived vasoactive substance
serotonin and to the thromboxane A2 analogue U46619. Indomethacin corrected
the enhanced contractile responses to serotonin, indicating the enhanced
release of a constrictor prostanoid substance. Indomethacin had no effect
on the impaired relaxations to adenosine diphosphate or A23187.
Endothelium-dependent relaxations to adenosine diphosphate, serotonin, and
A23187 were significantly preserved with either blood or
albumin-crystalloid cardioplegia, whereas contractile responses to U46619
were normal. Endothelium-independent relaxation to nitroprusside was
similar in all groups, indicating normal smooth muscle responsiveness.
Electron microscopy revealed minimal alterations of vascular morphology of
vessels in both crystalloid and blood cardioplegia groups.(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Blood and albumin cardioplegia preserve endothelium-dependent microvascular responses
Department of Surgery, Beth Israel Hospital, Boston, MA 02215.
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