TY - JOUR
T1 - High-frequency ventilation attenuation of hypoxic pulmonary vasoconstriction. The role of prostacyclin
AU - Wetzel, R. C.
AU - Gordon, J. B.
AU - Gregory, T. J.
AU - Gioia, F. R.
AU - Adkinson, N Franklin
AU - Sylvester, J. T.
PY - 1985/9/19
Y1 - 1985/9/19
N2 - 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 (PI(O2)), 200 and 30 mmHg, during conventional and high-frequency ventilation in the isolated, blood-perfused lungs of 10 sheep, 5 treated with indomethacin (40 μg/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·min-1·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·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·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 F(1α) concentration in the perfusate during hypoxia was significantly greater with high-frequency ventilation (65.4 ± 8.9 pg·ml-1·min-1) than with conventional ventilation (2.8 ± 18.7 pg·ml-1·min-1). In the 5 indomethacin-treated lungs, production of 6-keto-prostaglandin F(1α) was markedly depressed, and the attenuation of the hypoxic vasoconstrictor response by high-frequency ventilation was abolished. These results demonstrate that in isolated sheep lungs, high-frequency ventilation attenuated the pulmonary vascular response to hypoxia and suggest that this attenuation could be due to enhanced prostacyclin release by the lungs.
AB - 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 (PI(O2)), 200 and 30 mmHg, during conventional and high-frequency ventilation in the isolated, blood-perfused lungs of 10 sheep, 5 treated with indomethacin (40 μg/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·min-1·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·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·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 F(1α) concentration in the perfusate during hypoxia was significantly greater with high-frequency ventilation (65.4 ± 8.9 pg·ml-1·min-1) than with conventional ventilation (2.8 ± 18.7 pg·ml-1·min-1). In the 5 indomethacin-treated lungs, production of 6-keto-prostaglandin F(1α) was markedly depressed, and the attenuation of the hypoxic vasoconstrictor response by high-frequency ventilation was abolished. These results demonstrate that in isolated sheep lungs, high-frequency ventilation attenuated the pulmonary vascular response to hypoxia and suggest that this attenuation could be due to enhanced prostacyclin release by the lungs.
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M3 - Article
C2 - 3893248
AN - SCOPUS:0021808409
SN - 0003-0805
VL - 132
SP - 99
EP - 103
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 1
ER -