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Nitrous Oxide and the Baroreceptor Reflexes in the Dog
Author(s) -
Bagshaw R. J.,
Cox R. H.
Publication year - 1982
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1982.tb01721.x
Subject(s) - medicine , baroreceptor , halothane , nitrous oxide , anesthesia , carotid sinus , reflex , vascular resistance , cardiac output , hemodynamics , blood pressure , cardiology , heart rate
The effects were studied of 67 % nitrous oxide on the baroreceptor control of systemic haemodynamics in the dog. Nitrous oxide was added to end‐tidal halothane concentrations of about 0.9% (H2) together with halothane levels approximately 25 % above (H3) and below (H1) the H2 concentration. Baroreceptor function was assessed by brachiocephalic artery occlusion (BCO) or perfusion of the isolated carotid sinuses. In the intact animal, nitrous oxide significantly increased mean arterial pressure only at the H2 level (P<0.001). At the closed loop operating point of the carotid sinus reflex (CSR), for all halothane levels, nitrous oxide decreased cardiar output and stroke volume, increased systemic vascuIar resistance and central venous pressure with no effect upon mran arterial pressure. The operating point gain of the CSR was significantly depressed by nitrous oxide at the H1 and H3 levels (P<0.05). The C sr operating characteristics were significantly modified by N 2 O in a manner which depended upon the underlying concentration of halothane.