• D W Blake and P I Korner.
• J. Auton. Nerv. Syst. 1982 Mar 1;5(2):145-54.

AbstractThe changes in baroreceptor-heart rate reflex properties and in hemodynamics produced by light ketamine anesthesia were studied in one group of rabbits before and after infracollicular decerebration and those produced by althesin anesthesia in another group. Ketamine produced marked depression of baroreceptor reflex-mediated vagal effects on heart rate which was of similar magnitude in intact and pontine decerebrate rabbits; this indicates that its action was largely at or below the pons. Althesin produced much less vagal depression than ketamine in the intact rabbit but in pontine rabbits the depression was greatly enhanced. The smaller vagal depression in the intact rabbit appears to be due to a facilitatory effect through a suprapontine pathway by Althesin which partially masks its depressant effect below the pons. In the intact rabbit ketamine produced a greater rise in blood pressure than Althesin anesthesia for 1 h; the greater pressor response was due to a transient rise in total peripheral resistance (TPR) and a sustained rise in cardiac output. The difference in the blood pressure responses was mainly due to differences in action of the two anesthetics at or below the pons and only the transient rise in TPR during ketamine anesthesia was mediated through a suprapontine pathway.

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