- Title
- Effects of central nervous opoid and 5-hydroxytrptamine interactions on coronary conductance regulation in the conscious dog
- Creator
- Gazibarich, G. J.; Moore, P. G.; Porges, W. L.; White, Saxon William
- Relation
- Conference of the Australasian Society of Clinical and Experimental Pharmacologists, 1983. Proceedings of the Australasian Society of Clinical and Experimental Pharmacologists Conference [presented in Clinical and Experimental Pharmacology and Physiology, Suppl. 8] (Auckland, New Zealand 19-20 May, 1983) p. 114-115
- Publisher
- Wiley-Blackwell Publishing Asia
- Resource Type
- conference paper
- Date
- 1984
- Description
- The synthetic opioid agonist, fentanyl, has been shown in our laboratory to cause a neurological mediated systemic vasoconstriction in man. This may include coronary vasconstriction since ST-segment depression on ECG may occur during fentanyl anaesthesia for a coronary artery bypass surgery. Systemic vascoconstriction induced by fentanyl in the rabbit is dependent on central nervous 5-hydroxytryptine (5HT). Therefore the present study was undertaken in the dog to examine the postulates that intravenous fentanyl causes coronary vascoconstriction which is dependent on CNS 5HT and that baroreflex gain of coronary conductance mediated through sympathetic and parasympathetic pathways is increased by fentanyl. Conscious dogs in experimental complete heart block paced at 100 beats/min were used; circumflex coronary flow was measured using a Doppler flowmeter; baroreflexes were evoked by inflation of a balloon placed in the descending thoracic aorta. Coronary haemodynamics were examined before, immediately after, and 7 days after intracisternal injection of 5,7-dihydroxytryptamine (5,7DHT). Fentanyl infusion (0.55 μg/kg per min) for 20 min in five dogs resulted in variable rises in mean aortic pressure (MAP). Circumflex coronary flow (CCF) fell or was unchanged. Circumflex coronary conductance fell in all five dogs, and baroreflex gain increased. Intracisternal 5,7DHT immeadiately evoked sustained rises in atrial rate and MAP but rises in CCC were poorly sustained. One week later, MAP was largely unaltered but there was a rise in resting CCC in three of four dogs. Baroreflex gain of CCC was reduced and fentanyl did not uniformly cause a rise in MAP or a fall in CCC as before but baroreflex gain was restored by fentanyl infusion. These data suggest that normally baroreflex gain of coronary conductance is under the influence of CNS opoid (fentanyl) and 5HT facillatory interactions.
- Subject
- fentanyl; vascoconstriction; coronary conductance; baroreflexes
- Identifier
- http://hdl.handle.net/1959.13/939024
- Identifier
- uon:12724
- Identifier
- ISSN:0305-1870
- Language
- eng
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