ACUTE EFFECTS OF PARTIAL COMPRESSION OF DUCTUS-ARTERIOSUS ON FETAL PULMONARY CIRCULATION
ACUTE EFFECTS OF PARTIAL COMPRESSION OF DUCTUS-ARTERIOSUS ON FETAL PULMONARY CIRCULATION
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DOI:
10.1152/ajpheart.1989.257.2.h626
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发表时间:
1989-08-01
影响因子:
--
通讯作者:
ACCURSO, FJ
中科院分区:
文献类型:
--
作者:
ABMAN, SH;ACCURSO, FJ
To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 .+-. 1 to 60 .+-. 1 mmHg (mean .+-. SE) and left pulmonary artery blood flow from 65 .+-. 6 to 151 .+-. 11 ml/min at 30 min (P < 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P < 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate(P < 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 .+-. 0.27 (control) to 1.59 .+-. 0.21 ml .cntdot. min-1 .cntdot. mmHg-1 during the postcompression period (P < 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P < 0.001). We conclude that the hemodynamic response to partial compression of the ductus arteriosus is time dependent, with the initial rise of pulmonary blood flow partially mediated by the local release of a vasodilating cyclooxygenase product. Mechanisms contributing to subsequent elevations of pulmonary vascular resistance, changes in the pressure-flow relationship, and attenuation of the vasodilation response after acute hypertension are not yet known.