High-frequency ventilation attenuation of hypoxic pulmonary vasoconstriction. The role of prostacyclin.
High-frequency ventilation attenuation of hypoxic pulmonary vasoconstriction. The role of prostacyclin.
复制标题
缺氧肺血管收缩的高频通气衰减。
DOI：
--
复制
发表时间：
1985
期刊：
影响因子：
--
通讯作者：
J. Sylvester
中科院分区：
文献类型：
--
作者：
Randall C. Wetzel;John B. Gordon;T. Gregory;F. Gioia;N. F. Adamson;J. Sylvester
In order to determine the effects of high-frequency ventilation on the pulmonary vascular response to hypoxia, we assessed pulmonary vascular resistance at 2 levels of inspired oxygen tension (PlO2), 200 and 30 mmHg, during conventional and high-frequency ventilation in the isolated, blood-perfused lungs of 10 sheep, 5 treated with indomethacin (40 micrograms/ml of perfusate) and 5 untreated. Resistance was assessed by measuring pulmonary artery pressure-flow curves generated over a wide range of flows (20 to 140 ml X min-1 X kg body wt-1). Conventional ventilation was provided by an animal ventilator at a rate of 10 min-1 and a tidal volume of 10 ml X kg body wt-1. High-frequency ventilation was provided by a flow interrupter at a rate of 1,200 min-1 and a tidal volume less than 1.5 ml X kg body wt-1. In the 5 untreated lungs, the normoxic pressure-flow curve was unaltered by high-frequency ventilation, but the hypoxic pulmonary vasoconstrictor response was significantly attenuated. Furthermore, the net rate of change of 6-keto-prostaglandin F1 alpha concentration in the perfusate during hypoxia was significantly greater with high-frequency ventilation (65.4 +/- 8.9 pg X ml-1 X min-1) than with conventional ventilation (2.8 +/- 18.7 pg X ml-1 X min-1). In the 5 indomethacin-treated lungs, production of 6-keto-prostaglandin F1 alpha was markedly depressed, and the attenuation of the hypoxic vasoconstrictor response by high-frequency ventilation was abolished.(ABSTRACT TRUNCATED AT 250 WORDS)
