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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Endothelin in the perinatal circulation.
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Endothelin in the perinatal circulation.

机译：围产期循环中的内皮素。

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During the fetal period, blood is oxygenated through the placenta, and most of the cardiac output bypasses the lung through the ductus arteriosus. At birth, pulmonary vascular resistance falls with the initiation of ventilation. Coincidentally, the ductus arteriosus constricts. Endothelin-1 (ET-1) appears to play an important role during that transition period and postnatally. ET-1 can dramatically increase resistance in the placental microcirculation and may be involved in blood flow redistribution with hypoxia. At birth, the increase in oxygen tension is important in triggering ductus vasoconstriction. It is proposed that oxygen triggers closure of the ductus arteriosus by activating a specific, cytochrome P450-linked reaction, which in turn stimulates the synthesis of ET-1. On the neonatal heart, ET-1 has a positive chronotropic but negative inotropic effect. In the newborn piglet and the fetal lamb, both term and preterm, ET-1 causes a potent, long-lasting pulmonary vasoconstriction. Furthermore, atransient dilator response has been identified, and it is ascribed to nitric oxide formation. ET receptors are abundant in the piglet pulmonary vasculature. They are predominantly of the ETA constrictor subtype, though ETB2 constrictor receptors may also be present in certain species. The dilator response is linked to the ETB1 receptor, and the number of ETB1 receptors is reduced in hypoxia-induced pulmonary hypertension. ET-1 appears to be a causative agent in the pathogenesis of hypoxia- and hyperoxia-induced pulmonary hypertension as demonstrated by reversal of hemodynamic and morphological changes with treatment with an ETA receptor antagonist. Findings are amenable to practical applications in the management of infants with pulmonary hypertension or requiring persistent patency of the ductus arteriosus.
机译：在胎儿期间，血液通过胎盘被氧化，大部分心输出量通过动脉导管绕过肺。出生时，随着通气的开始，肺血管阻力下降。巧合的是，动脉导管收缩。内皮素-1（ET-1）在该过渡时期和出生后似乎起着重要作用。 ET-1可以显着增加胎盘微循环的抵抗力，并且可能参与缺氧引起的血流重新分配。出生时，氧气紧张的增加对触发导管血管收缩很重要。有人提出，氧可以通过激活特异性的细胞色素P450连锁反应来触发动脉导管的关闭，进而刺激ET-1的合成。在新生儿心脏上，ET-1具有正变时性但具有负变力作用。在新生仔猪和胎儿羔羊中，无论是早产还是早产，ET-1都会导致强效，持久的肺血管收缩。此外，已经确定了短暂的扩张器反应，并且归因于一氧化氮的形成。 ET受体在仔猪的肺血管中丰富。它们主要是ETA收缩子亚型，尽管某些物种中也可能存在ETB2收缩子受体。扩张反应与ETB1受体相关，在缺氧引起的肺动脉高压中ETB1受体的数量减少。 ET-1似乎是由低氧和高氧血症引起的肺动脉高压发病机理的病因，这可以通过用ETA受体拮抗剂治疗逆转血流动力学和形态变化来证明。这些发现适合于在患有肺动脉高压或需要持续动脉导管未闭的婴儿的治疗中的实际应用。

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