Respiratory reflexes in response to nasal administration of halothane to anesthetized, spontaneously breathing dogs

Tatsushi Mutoh Laboratory of Veterinary Surgery, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.
present address is the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616.

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Arata Kanamaru Laboratory of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.

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Hirokazu Tsubone Laboratory of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.

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Ryohei Nishimura Laboratory of Veterinary Surgery, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.

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Nobuo Sasaki Laboratory of Veterinary Surgery, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.

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Abstract

Objective—To characterize and determine the sensory innervation of respiratory reflexes elicited by nasal administration of halothane to dogs.

Animals—10 healthy Beagles.

Procedure—Dogs underwent permanent tracheostomy and, 2 to 3 weeks later, were anesthetized with thiopental and α-chloralose administered IV. The nasal passages were functionally isolated so that halothane could be administered to the nasal passages while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of halothane at concentrations of 1.25, 1.75, and 2.5 times the minimum alveolar concentration (MAC), and 5% (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of 5% halothane were also recorded following transection of the infraorbital nerve, transection of the caudal nasal nerve, and nasal administration of lidocaine.

Results—Nasal administration of halothane induced an inhibition of breathing characterized by a dosedependent increase in expiratory time and a resultant decrease in expired volume per unit time. Effects were noticeable immediately after the onset of halothane administration and lasted until its cessation. Reflex responses to halothane administration were attenuated by transection of the caudal nasal nerve and by nasal administration of lidocaine, but transection of the infraorbital nerve had no effect.

Conclusions and Clinical Relevance—Nasal administration of halothane at concentrations generally used for mask induction of anesthesia induces reflex inhibition of breathing. Afferent fibers in the caudal nasal nerve appear to play an important role in the reflex inhibition of breathing induced by halothane administration. (Am J Vet Res 2000;61:260–267)

Abstract

Objective—To characterize and determine the sensory innervation of respiratory reflexes elicited by nasal administration of halothane to dogs.

Animals—10 healthy Beagles.

Procedure—Dogs underwent permanent tracheostomy and, 2 to 3 weeks later, were anesthetized with thiopental and α-chloralose administered IV. The nasal passages were functionally isolated so that halothane could be administered to the nasal passages while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of halothane at concentrations of 1.25, 1.75, and 2.5 times the minimum alveolar concentration (MAC), and 5% (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of 5% halothane were also recorded following transection of the infraorbital nerve, transection of the caudal nasal nerve, and nasal administration of lidocaine.

Results—Nasal administration of halothane induced an inhibition of breathing characterized by a dosedependent increase in expiratory time and a resultant decrease in expired volume per unit time. Effects were noticeable immediately after the onset of halothane administration and lasted until its cessation. Reflex responses to halothane administration were attenuated by transection of the caudal nasal nerve and by nasal administration of lidocaine, but transection of the infraorbital nerve had no effect.

Conclusions and Clinical Relevance—Nasal administration of halothane at concentrations generally used for mask induction of anesthesia induces reflex inhibition of breathing. Afferent fibers in the caudal nasal nerve appear to play an important role in the reflex inhibition of breathing induced by halothane administration. (Am J Vet Res 2000;61:260–267)

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