Document Detail

Effect of chronic resistive loading on ventilatory control in a rat model.
MedLine Citation:
PMID:  7633724     Owner:  NLM     Status:  MEDLINE    
Acute resistive loading of the airway has been shown to activate the endogenous opioid system, with subsequent depression of ventilation. The present investigation was designed to assess the effect of chronic airway loading on ventilation and CO2 sensitivity, and to determine whether the endogenous opioid system contributes to long-term modulation of ventilatory control in this setting. A flow-resistive ventilatory load was imposed in 2-mo-old rats by surgical implantation of a circumferential tracheal band that approximately tripled tracheal resistance. Respiration and CO2 sensitivity were serially and noninvasively assessed by barometric plethysmography over a period of 21 wk. Ventilatory output was assessed as minute inspiratory effort, which was defined as the product of plethysmograph signal amplitude, inspiratory time, and respiratory rate (RR). CO2 sensitivity was calculated as the percent change in minute inspiratory effort from room air to CO2 exposure. The effect of naloxone administration on these parameters was also determine. Arterial blood gases demonstrated hypercapnia with maintenance of normoxia in loaded rats; these findings persisted for the duration of the study. Two days after surgery, rats with tracheal obstruction demonstrated a lower RR than controls during room air breathing and during CO2 stimulation. CO2 sensitivity was significantly depressed in obstructed animals at this time. Escape from suppression of RR and CO2 sensitivity was evident by 14 to 21 d after obstruction; however, suppression of these parameters reappeared and was maintained from 56 to 147 d after obstruction. Naloxone augmented minute inspiratory effort during CO2 stimulation at 2 d after obstruction but not thereafter; naloxone had no effect in control rats. These data indicate that chronic airway loading suppresses RR and CO2 sensitivity in a triphasic manner. The early suppression is partially reversible by naloxone; late-appearing suppression is unaffected by naloxone and is presumably mediated by mechanisms that do not involve endogenous opioids.
H E Greenberg; A Tarasiuk; R S Rao; M Kupferman; N Kane; S M Scharf; M ] Kuperferman M [corrected to Kupferman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  152     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  1995 Aug 
Date Detail:
Created Date:  1995-09-14     Completed Date:  1995-09-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  666-76     Citation Subset:  AIM; IM    
Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, New Hyde Park, NY 10042, USA.
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MeSH Terms
Airway Obstruction / physiopathology*
Airway Resistance / physiology*
Carbon Dioxide / administration & dosage,  blood,  pharmacology
Chronic Disease
Disease Models, Animal
Hypercapnia / physiopathology
Inhalation / physiology
Naloxone / pharmacology
Opioid Peptides / antagonists & inhibitors,  physiology
Oxygen / blood
Oxygen Consumption / physiology
Pulmonary Ventilation / physiology
Rats, Sprague-Dawley
Respiration / drug effects,  physiology*
Tracheal Diseases / physiopathology
Reg. No./Substance:
0/Opioid Peptides; 124-38-9/Carbon Dioxide; 465-65-6/Naloxone; 7782-44-7/Oxygen
Erratum In:
Am J Respir Crit Care Med 1996 Jun;153(6 Pt 1):2028

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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