Effect of Pentobarbital on Electrical Excitability of Respiratory Center in the Cat

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Abstract
In 30 cats initial anesthesia (anes.) was produced by intraperit. injn. of pentobarbital Na, 36 mg./kg. Pentob. was then admd. intraven. in amts. sufficient to cause respiratory (resp.) arrest. The resp. center was stimulated electrically with a bipolar electrode of nichrome wire and with the aid of a stereotaxic apparatus. Stimulation periods were limited to 10 sec.; recovery for 1 min. was allowed between tests. Resp. was recorded by pneumographs (thoracic and abdominal), and also at times by spirometer. After production of resp. arrest, artificial resp. was provided via tracheal cannula. Mechanical ventilation was interrupted periodically for intervals of 20 sec. to detn. the effect of stimulating the resp. center. The high susceptibility of resp. rhythmicity to the depressant action of pentob. was demonstrated early by the slowing of spontaneous breathing and the decrease in stimulus threshold for evoking sustained apneusis, and subsequently by failure of spontaneous (spont.) resp. which occurred long before the resp. center became in-excitable. One of the 1st demonstrable effects of pentob. on the resp. center was the marked reduction in amplitude of max. apneustic responses before an appreciable change occurred in the amplitude of min. responses. With progressive pentob. depression, all apneustic responses approached the level of spont. breathing. Early pentob. cumulation resulted in more marked depression of thoracic apneustic reponses, evoked by stimuli of constant strength, than of concomitant abdominal responses; a similar pattern of depression in spont. breathing was observed during this period. Variation in stimulus voltage produced direct and generally equivalent effects in thoracic and abdominal responses. In light anes., variation in stimulus frequency produced similar effects in the responses of the 2 resp. components, but thoracic activity was more labile than its abdominal counterpart; in deep anes., after resp. arrest, a reduction in stimulus frequency from 33 to 20 impulses/sec. caused the thoracic apneustic response almost to disappear whereas the abdominal response was reinforced. In 5 expts., during late pentob. cumulation when high voltage stimulating currents were required, the thoracic apneustic response was converted to an active expiratory excursion which occurred simultaneously with diaphragmatic contraction. Neurophysiological implications of these findings are discussed.

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