Levin D L, Mills L J, Parkey M, Garriott J, Campbell W
J Pediatr. 1979 Apr;94(4):647-50. doi: 10.1016/s0022-3476(79)80043-8.
The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in the fetal pulmonary to systemic arterial mean blood pressure difference across the ductus arteriosus rising significantly, presumably secondary to constriction of the ductus arteriosus. The pressure difference was due to pulmonary arterial hypertension, and not due to a fall in systemic arterial mean blood pressure. Fetal arterial blood gas tensions and pH values were normal throughout. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of PGE1 into the fetal inferior vena cava. Indomethacin was present in fetal blood, and maternal plasma prostaglandin levels were suppressed. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus and fetal pulmonary arterial hypertension which, if severe, may cause rapid fetal death. It is possible that this mechanism may be one cause of persistent pulmonary hypertension or tricuspid insufficiency or both in the newborn infant.
给怀孕的母羊口服或静脉注射前列腺素合成酶抑制剂吲哚美辛。这导致胎儿动脉导管两端的肺循环与体循环动脉平均血压差显著升高，推测这是动脉导管收缩的继发结果。该血压差是由于肺动脉高压引起的，而非体循环动脉平均血压下降所致。整个过程中胎儿动脉血气张力和pH值均正常。在五项实验中，通过向胎儿下腔静脉注射PGE1，血压差可迅速但暂时逆转。胎儿血液中存在吲哚美辛，且母体血浆前列腺素水平受到抑制。孕期使用吲哚美辛会导致胎儿动脉导管收缩和胎儿肺动脉高压，若情况严重，可能导致胎儿迅速死亡。这种机制有可能是新生儿持续性肺动脉高压或三尖瓣关闭不全或两者兼有的一个原因。
