Hypoxia-induced pulmonary vasoconstriction: effects of fentanyl following different routes of administration.
Recent investigations have revealed that intravenous anesthetics, including fentanyl, do not reduce the pulmonary vasoconstrictor response to alveolar hypoxia. In contrast, the response is markedly reduced or abolished by inhalation anesthetics. Recent investigations have demonstrated that the route of administration is of importance. Halothane, which inhibits the response when administered via the airways, behaves more like an intravenous anesthetic following administration via the blood stream, provided the alveolar concentration has been kept low (Bjertnaes et al. 1977). It was therefore a distinct possibility that the lack of any damping effect of fentanyl on the response could be due to the route of administration rather than to a different pharmacological property. We have tested this hypothesis by introducing fentanyl in nebulized form via the airways in one group of isolated rat lungs, and via the blood stream in another group. We found, however, no effect of fentanyl on the pulmonary vasoconstrictor response to hypoxia, regardless of the route of administration. Plasma concentrations of fentanyl were determined by radioimmunoassay and compared with those encountered in anesthetic practice.
D000769:Anesthesia, Inhalation; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D005283:Fentanyl / Q000008:administration & dosage* / Q000097:blood / Q000494:pharmacology; D000860:Hypoxia; D007269:Injections, Intra-Arterial; D011312:Pressure; D011651:Pulmonary Artery / Q000187:drug effects; D011863:Radioimmunoassay; D051381:Rats; D012119:Respiration / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
D005283:Fentanyl