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J Thorac Cardiovasc Surg 1998;115:1047-1051
© 1998 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

Endothelial dysfunction in cerebral microcirculation duringhypothermic cardiopulmonary bypass in newborn lambs

Read at the Seventy-seventh Annual Meeting of The American Associationfor Thoracic Surgery, Washington, D.C., May 4-7, 1997.

Received for publication May 12, 1997. Revisions requested July 2, 1997. Revisions received Dec. 18, 1997. ccepted for publication Dec. 23, 1997. Address for reprints: L. Craig Wagerle, PhD, Department ofCardiothoracic Surgery, Allegheny University of the Health Sciences, Broad andVine Sts., M.S. 469, Philadelphia, PA 19102.

Objectives: Inflammatory stimuli ormechanical stresses associated with hypothermic cardiopulmonary bypass couldpotentially impair cerebrovascular function, resulting in inadequate cerebralperfusion. We hypothesize that hypothermic cardiopulmonary bypass is associatedwith endothelial or vascular smooth muscle dysfunction and associated cerebralhypoperfusion. Therefore we studied the cerebrovascular response toendothelium-dependent vasodilator, acetylcholine, endothelium-independent nitricoxide donor, sodium nitroprusside, and vasoactive amine, serotonin, in newbornlambs undergoing hypothermic cardiopulmonary bypass (nasopharygeal temperature =18° C).
Methods: Studies were performedon 13 newborn lambs equipped with a closed cranial window, allowing for directvisualization of surface pial arterioles. Six animals were studied whileundergoing hypothermic cardiopulmonary bypass, whereas seven served asnonbypass, warm (37° C) controls. Pial arteriolar caliber (range = 111to 316 µm diameter) was monitored using video microscopy.
Results: Topical application of acetylcholine caused adose-dependent increase in arteriolar diameter in the control group that wasabsent in animals undergoing hypothermic cardiopulmonary bypass. Hypothermiccardiopulmonary bypass did not alter the vasodilation in response to sodiumnitroprusside. Furthermore, the contractile response to serotonin was fullyexpressed during hypothermic cardiopulmonary bypass.
Conclusions:The specific loss of acetylcholine-induced vasodilation suggests endothelialcell dysfunction rather than impaired ability of vascular smooth muscle torespond to nitric oxide. It is speculated that loss of endothelium-dependentregulatory factors in the cerebral microcirculation during hypothermiccardiopulmonary bypass may enhance vasoconstriction, and impairedcerebrovascular function may be a basis for associated neurologic injury duringor after hypothermic cardiopulmonary bypass. (J thorac Cardiovasc Surg1998;15:1047-54)

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