Fentanyl is a commonly used narcotic that has wide applications in general anesthesia and critical care settings. We have previously shown that fentanyl, an opioid agonist, when administered to canines (1) blocked b-adrenergic hemodynamic responses to epinephrine and isoproterenol and (2) did not effect the a-adrenergic effects of epinephrine or phenylephrine. Our proposal is to extend these studies to define the mechanism of fentanyl-catecholamine interactions by performing similar studies in canines with pertussis toxin, an inhibitor of G-protein signaling. These studies have implications for understanding the mechanism that accounts for altered hemodynamic responses due to fentanyl in anesthesia and in critically ill patients.
