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The Journal of Thoracic and Cardiovascular Surgery, Vol 88, 748-753, Copyright © 1984 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
C Aren, C Blomstrand, C Wikkelso and K Radegran
High-dose prostacyclin treatment during cardiopulmonary bypass reduces
platelet activation and possibly postoperative blood loss. A side- effect
is arterial hypotension. We studied the incidence of cerebral complications
in 79 patients requiring coronary bypass. Only patients without known
cerebrovascular disease were studied. Thirty-nine patients received
prostacyclin 50 ng/kg/min during cardiopulmonary bypass and 40 patients
served as controls. Mean arterial blood pressure in the group given
prostacyclin was below 30 mm Hg during the first 30 minutes of bypass but
remained above 60 mm Hg in the control group. Postoperative neurological
examination revealed transient cerebral dysfunction in six control patients
and two prostacyclin-treated patients. Investigation of cerebrospinal fluid
showed signs of blood- brain barrier damage in 12 control and seven
prostacyclin-treated patients. Cytologic changes in cerebrospinal fluid
consistent with brain tissue damage occurred in two control patients but in
no patient given prostacyclin. Myelin basic protein and adenylate kinase in
cerebrospinal fluid were assayed as being markers of brain damage. Myelin
basic protein was within the normal range in all patients. Adenylate kinase
was moderately increased (greater than 0.035 U/L) in five of 15 control
patients and six of 13 prostacyclin-treated patients. We conclude that
treatment with prostacyclin 50 ng/kg/min during cardiopulmonary bypass does
not increase the risk of postoperative cerebral damage.
ARTICLES
Hypotension induced by prostacyclin treatment during cardiopulmonary bypass does not increase the risk of cerebral complications
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