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The Journal of Thoracic and Cardiovascular Surgery, Vol 106, 959-967, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
AC Cave, A Manche, NW Derias and DJ Hearse
Clinically, it is well established that cardiopulmonary bypass results in
pulmonary dysfunction. Using a recently developed preparation for
cardiopulmonary bypass in the rabbit, we have been able to mimic a similar,
but more severe, condition. We found that, despite normal histologic
structure of the myocardium, hearts could not be weaned from bypass because
of a serious increase in pulmonary vascular resistance. Histologic studies
of the lungs showed severe intravascular neutrophil aggregation and marked
vasoconstriction. To identify the nature and origin of the mediator
responsible for the changes in the pulmonary vasculature, we subjected
groups of rabbits (n = 4 per group) to bypass with cooling to 18 degrees C,
circulatory arrest for 1 hour, and rewarming on bypass to 33 degrees C.
Pulmonary vascular resistance was measured at the same temperature before
and after bypass. Four groups were studied: group I were untreated
controls; group II received the cyclooxygenase inhibitor, indomethacin (0.2
mg/kg intravenously), before operation; group III received the thromboxane
A2 synthetase inhibitor, Dazmegral (5 mg/kg intravenously), before
operation together with the thromboxane A2 receptor blocker GR 32191B (2
mg/kg per 30 minutes intravenously); and group IV were treated with mustine
hydrochloride (1.75 mg/kg intravenously) 3 days before the experiment to
deplete the neutrophils by 90%. During circulatory arrest, the heart was
protected with an initial infusion (10 ml at 4 degrees C over 1 minute) of
St. Thomas' Hospital cardioplegic solution. At the end of the experiment,
the heart and lungs were histologically examined. In the control group, a
significant increase (+395% when compared with the value recorded before
bypass) in pulmonary vascular resistance was observed after bypass.
However, in none of the treated groups did pulmonary vascular resistance
increase significantly (percentage changes in groups II, III, and IV were
-24%, 0%, and +33%, respectively). Pulmonary histologic characteristics
were normal in all treated groups, and all animals were successfully weaned
from bypass. These results indicate that the increase in pulmonary vascular
resistance that arises as a consequence of bypass in rabbits is primarily a
result of the production of thromboxane A2, a process in which the
neutrophil plays a pivotal role.
ARTICLES
Thromboxane A2 mediates pulmonary hypertension after cardiopulmonary bypass in the rabbit
Department of Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, England.
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