Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs.
Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs.
复制标题
清醒狗前列腺素合成抑制后的肺升压反应。
DOI：
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发表时间：
1982
期刊：
影响因子：
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通讯作者：
J. Reeves
中科院分区：
文献类型：
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作者：
B. Walker;N. Voelkel;J. Reeves
最近的研究表明，血管扩张剂三尖杉酯碱是由离体大鼠肺持续产生的。我们推测这些血管扩张剂可能有助于维持正常的低肺动脉压。在清醒的狗中，在给予甲氨酰（2 mg/kg iv，随后以2 mg/kg输注）之前和之后30至60 min测量肺压和心输出量。kg-1 . h-1）或结构上不同的抑制剂RO-20-5720（1 mg/kg iv，随后以1 mg . kg-1 . h-1）。在抑制之前和之后，通过吸入10%O2使动物缺氧。进行时间对照实验，其中仅施用盐水媒介物。甲氨蝶呤或RO-20-5720导致平均肺动脉压和总肺阻力增加。心输出量和体循环压未受影响。观察到的轻度低氧性肺动脉升压反应不受甲氨蝶呤的影响。动物呼吸30%的氧气，以抵消丹佛的海拔高度也表现出增加肺压力和阻力时，给予meclutamate。它的结论是，内源性血管扩张剂的肾上腺素可能有助于正常的，低血管张力的肺循环。
Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO-20-5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO-20-5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.