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The Journal of Thoracic and Cardiovascular Surgery, Vol 106, 479-486, Copyright © 1993 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
T Shafique, RG Johnson, HB Dai, RM Weintraub and FW Sellke
Pulmonary vascular resistance is frequently elevated after cardiac
operations in which cardiopulmonary bypass is used. In our study of the
possible contribution of altered pulmonary microvascular reactivity to this
condition, sheep were heparinized, cannulated via the aorta and right
atrium, and placed on total cardiopulmonary bypass. After 90 minutes of
total cardiopulmonary bypass and pulmonary arterial occlusion, the sheep
were removed from cardiopulmonary bypass, and their lungs were perfused
normally for 60 minutes. Noninstrumented animals were used as controls. To
evaluate the effect of 90 minutes of extracorporeal circulation without
reduced pulmonary perfusion, we studied additional sheep after they
underwent right heart bypass with a pump-oxygenator. Pulmonary
microarterial vessels (130 to 230 microns in diameter) from each group were
examined in vitro in a pressurized (20 mm Hg), no-flow state with video
microscopic imaging and electronic dimension analysis. After
preconstriction of vessels with the thromboxane A2 analog U46619 by 30% to
40% of the baseline diameter, vasoactive drugs were applied extraluminally.
Serotonin caused control microvessels to dilate. In the presence of the
nitric oxide synthetase inhibitor NG-methyl-L-arginine, this was converted
to a significant contractile response. Acetylcholine alone had minimal
effect on control vessels. However, in the presence of the cyclooxygenase
inhibitor indomethacin, acetylcholine caused a significant relaxation
response. After total cardiopulmonary bypass and pulmonary reperfusion,
pulmonary microvessels contracted significantly when exposed to
acetylcholine and serotonin, compared with respective control responses.
Both these contractile responses were inhibited in the presence of
indomethacin. Endothelium-independent responses to sodium nitroprusside and
U46619 and dilation responses to adenosine were not altered after
cardiopulmonary bypass. Extracorporeal circulation with continued pulmonary
arterial perfusion (right heart bypass group) had no effect on
microvascular responses. In conclusion, total cardiopulmonary bypass with
associated reduced pulmonary perfusion causes significant alterations of
endothelium-dependent pulmonary microvascular responses because of the
increased release of a constrictor prostanoid substance and possibly
because of reduced release of endothelium-derived relaxing factor.
ARTICLES
Altered pulmonary microvascular reactivity after total cardiopulmonary bypass
Department of Surgery, Charles A. Dana Research Laboratory, Beth Israel Hospital, Boston, MA 02215.
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