naloxone and Bronchial-Spasm

Although respiratory heat loss with cooling of the tracheobronchial mucosa is responsible for the airway obstruction that develops after inhalation of subfreezing air in asthmatics, the mechanism by which airway cooling results in bronchoconstriction is not known. In order to test whether release of endogenous opiate peptides might play a role in mediating this response, asthmatic subjects were studied before and after isocapnic hyperventilation of subfreezing air after the administration of placebo or naloxone, given in a double-blind fashion. Five asthmatic subjects were tested with low-dose (0.8 mg) and 5 with high-dose (10 mg) naloxone given intravenously. Pretreatment with naloxone at either dose did not attenuate the decrease in FVC, FEV1, or FEF25--75 after cold air in comparison with placebo pretreatment. A slightly greater decrease in FEV1 and FEF25--75 after low-dose naloxone than placebo pretreatment can be partially explained by a difference in the temperature achieved during cold air inhalation. We conclude that endogenous opiate peptides are not involved in mediating the bronchoconstrictor response to cold air inhalation in asthmatics.

Topics: Adult; Asthma; Bronchi; Bronchial Spasm; Cold Temperature; Endorphins; Female; Humans; Hyperventilation; Lung Volume Measurements; Male; Naloxone; Premedication; Pulmonary Ventilation; Spirometry

Snorting or smoking heroin is a known trigger of acute asthma exacerbation. Heroin abuse may be a risk factor for more severe asthma exacerbations and intubation. Heroin and other opioids provoke pulmonary bronchoconstriction. Naloxone may play a role in decreasing opioid-induced bronchospasm. There are no known clinical cases describing the effect of naloxone on opioid-induced bronchospasm.. This is an observational study in which nebulized naloxone was administered to patients with suspected heroin-induced bronchospasm. Patients with spontaneous respirations were administered 2 mg of naloxone with 3 mL of normal saline by nebulization. We describe a case series of administrations for suspected heroin-induced bronchospasm.. We reviewed 21 administrations of nebulized naloxone to patients with suspected heroin-induced bronchospasm. Of these, 19 patients had a clinical response to treatment documented. Thirteen patients displayed clinical improvement (68%), 4 patients had no improvement (21%), and 2 patients worsened (10%). Of the 2 patients who had clinical decline, none required intubation. Of the patients who improved, 1 patient received only nebulized naloxone and 1 patient received naloxone and albuterol together. Seven patients showed clinical improvement after the administration of albuterol, atrovent, and naloxone together as a combination. Four patients showed additional improvement when the naloxone was administered after the albuterol and atrovent combination.. Naloxone may play a role in reducing acute opioid-induced bronchoconstriction, either alone or in combination with albuterol. Future controlled studies should be conducted to determine if the addition of naloxone to standard treatment improves bronchospasm without causing adverse effects.

Topics: Administration, Inhalation; Bronchial Spasm; Heroin; Humans; Naloxone; Narcotic Antagonists; Narcotics; Treatment Outcome

Topics: Adolescent; Aged; Bronchial Spasm; Furosemide; Humans; Hydrocortisone; Male; Midazolam; Naloxone; Phentolamine; Pulmonary Edema; Succinylcholine

Capsaicin given intravenously (i.v.) into the vena cava or intra-arterially (i.a.) into the aortic arch of anesthetized guinea-pigs induced dose-dependent increases in pulmonary-flow resistance (R) and dynamic thoracic elastance (E). Threshold doses were 0.5-1.0 micrograms/kg body weight; greater than 8.0 micrograms/kg induced tachyphylaxis. These responses to capsaicin, i.v. or i.a., were similar after decentralization, bilateral vagotomy, or glossopharyngealotomy, and after autonomic blockers (mecamylamine, atropine, mepyramine, and bethanidine). Morphine significantly reduced responses to capsaicin but had no effect on responses to substance P (SP). Naloxone did not reverse the inhibitory effect of morphine, and neither reduced nor enhanced capsaicin-induced increases. Of the two antagonists to SP examined (given i.v.), [D-Pro2,D-Trp7,9]SP had no effect on SP-induced increases but abolished capsaicin-induced increases in R, though without affecting increases in E, and [D-Arg1,D-Pro2,D-Trp7,9,Leu11]SP reduced increases in R induced by both SP and capsaicin but had no effect on increases in E. Capsaicin (2.0-32.0 micrograms/kg i.v. or i.a.) had no bronchospastic effect in guinea-pigs given this drug (50.0 mg/kg s.c.) 7 days earlier. We conclude that in guinea-pigs--unlike other species--capsaicin causes bronchospasm without stimulating any afferent receptors in a centrally mediated bronchospastic reflex arc.

Topics: Animals; Autonomic Agents; Bronchial Spasm; Capsaicin; Female; Guinea Pigs; Hemodynamics; Injections, Intra-Arterial; Injections, Intravenous; Male; Morphine; Naloxone; Neurons, Afferent; Pulmonary Circulation; Reflex; Respiration; Substance P