Six mongrel dogs were used to investigate the mechanism of action of fentanyl-induced bradycardia. With controlled acid-base balance and temperature, and under 1.0 to 1.2 percent endtidal halothane anesthesia, 5 and microgram/kg of IV fentanyl citrate were given sequentially 1 hour apart and heart rate (HR) followed for 60 minutes. A dose-related depression of HR followed both injections. One week later the same dogs were studied similarly, except that bilateral cervical vagotomies were performed before fentanyl was given. The decrease in HR was at most 10 percent of the decrease in HR observed in the innervated dogs. Serum fentanyl levels were comparable. The data indicate the majority of the chronotropic action of fentanyl involves vagal efferent impulses from the central nervous system.

Under halothane anesthesia five dogs were prepared with both hindlimbs isolated from the systemic circulation to allow intermittent placement on extracorporeal perfusion at constant flow. One limb of each dog was surgically denervated. In this relatively anesthetic-free preparation, graded equivalent doses of alfentanil, fentanyl, and sufentanil were infused over 30 s, and vascular resistance was measured. Increasing opioid administration caused a progressive diminution in peripheral resistance. By the high dose level, alfentanil (500 micrograms/kg), fentanyl (50 micrograms/kg), and sufentanil (6 micrograms/kg) caused equal and significant decreases of 48%, 48%, and 44% in resistance, respectively. There was no difference among the opioids in effects on resistance at equivalent dosages. Neither pretreatment with naloxone nor denervation changed the response to the narcotics. We conclude that the three synthetic opioids produce vasodilation by direct action on the peripheral vascular smooth muscle.

We studied the effects of graded exposure to hyperbaric (1,875 mm Hg) oxygen therapy in an acute stroke model prepared by unilateral carotid artery interruption in gerbils. Pentobarbital alone, superoxide dismutase alone, two periods of hyperbaric oxygen alone, and each agent combined with hyperbaric oxygen were administered to investigate possible mechanisms of protection from cerebral ischemia. Survival rates and neurologic deficit scores over 5 days in all treated groups were compared with those in a control group. Survival rates in the groups subjected to 2 (63.9±4.0%) and 4 hours (70.1 ±5.2%) of hyperbaric oxygen alone were significantly higher than in the control group (53.6 ±4.2%). The group treated with pentobarbital alone also demonstrated increased survival (69.8 ±7.0%), but the combination of therapeutic regimens offered no apparent additive protection. By 5 days there were no differences in the neurologic deficit scores of the survivors in the groups. The toxic pulmonary effects of hyperbaric oxygen were assessed in a pilot LD M study. The pressure used caused no mortality during 4 hours of exposure, and the calculated LD M was 7.26 hours. This investigation demonstrates that graded doses of hyperbaric oxygen given after the insult increase survival in a gerbil model of stroke. (Stroke 1990^21:119-123)

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Summary A new approach to the internal jugular vein is described which keeps the head and neck in the neutral