Effects of high frequency oscillatory ventilation compared to conventional ventilation upon pulmonary vascular prostanoid production in neonatal piglets.
In order to investigate the possibility that high-frequency oscillatory ventilation (HFO) might preferentially stimulate intrapulmonary prostacyclin (PGI2) synthesis thereby decreasing pulmonary vascular smooth muscle tone, we determined pulmonary prostacyclin and thromboxane production in neonatal piglets ventilated by conventional means and by HFO (8 Hz). There was no detectable release of prostacyclin or thromboxane into blood passing through the lungs (i.e., pulmonary arterial concentrations were greater than aortic concentrations) during ventilation by conventional means or during HFO. Furthermore, there were no differences between the two modes of ventilation in cardiac output, systemic or pulmonary vascular resistance, or pulmonary vascular response to hypoxia/hypercapnia. We conclude that HFO does not stimulate pulmonary prostacyclin production and does not affect pulmonary vascular resistance or the pulmonary vasoconstriction associated with alveolar hypoxia/hypercapnia when compared to conventional ventilation in anesthetized newborn piglets.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis / Q000097:blood; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis* / Q000097:blood; D006935:Hypercapnia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D008168:Lung / Q000378:metabolism*; D012123:Pulmonary Ventilation; D012119:Respiration; D012121:Respiration, Artificial / Q000295:instrumentation; D013552:Swine; D013928:Thromboxane A2 / Q000096:biosynthesis / Q000097:blood; D013929:Thromboxane B2 / Q000096:biosynthesis / Q000097:blood; D013931:Thromboxanes / Q000096:biosynthesis* / Q000097:blood
D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol