Abstract
The mechanism for the bronchodilator properties of halothane was investigated in the dog. In 18 dogs without premedication, administration of 0.5 to 3.0% halothane in oxygen caused a reduction in pulmonary resistance and increase in compliance. Increase of halothane arterial blood levels from 15 to 30 mg/100 ml caused a decrease in pulmonary resistance of 40%, a rise in compliance of 24% and a decrease of respiratory minute volume of 37%. Changes in pulmonary resistance could still be elicited after the following procedures: bilateral acute or chronic upper thoracic sympathectomy, bilateral adrenalectomy, intravenous administration of hexamethonium, reserpine, guanethidine or bretylium. The only drug which eliminated the response was compound MJ 1999 (dl-4-(2-isopropylamino-1-hydroxethyl)-methanesulfonanilide HCl), a beta adrenergic blocking agent. We conclude that halothane stimulates the beta receptors in the airway.
Footnotes
- Received March 20, 1967.
- Accepted May 23, 1967.
- © 1967 by The Williams & Wilkins Company
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