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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Different laryngeal responses during respiratory arrest produced by hypoxia withdrawal, thiopentone, ketamine, and lidocaine in cats.

The changes in laryngeal resistance (LR) during respiratory arrest produced by withdrawal of hypoxia stimulation and administration of various respiratory depressants were studied in 14 spontaneously breathing, anesthetized cats (11 cats with alpha-chloralose and three cats with halothane). Withdrawal of hypoxia stimulation caused a transient respiratory arrest with no central inspiratory activity, during which a considerable increase in LR was observed to a level higher than the fixed resistance after muscle paralysis [LR(fix)]. Intravenous injection of thiopentone, ketamine, and lidocaine all caused a transient respiratory arrest. However, the effects on the laryngeal function and the central inspiratory activity were different for each agent. Both thiopentone and ketamine induced an inspiratory apneusis pattern in phrenic nerve discharge, and lidocaine caused a silence of phrenic nerve activity. Thiopentone relaxed the larynx, and LR during thiopentone-induced respiratory arrest was almost equal to LR(fix). Ketamine maintained a dilatation of the larynx, and LR during ketamine-induced respiratory arrest was lower than LR(fix). Lidocaine caused a constriction of the larynx and LR greatly increased, leading frequently to laryngospasm. These results indicate that hypoxia withdrawal, thiopentone, ketamine, and lidocaine all cause different effects on the central inspiratory activity, and that the central respiratory depression produced by these methods is not accompanied by a uniform depression of laryngeal function.[1]

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