Time course of histamine-induced bronchoconstriction and its adrenergic and H2 modulation

A. M. Lauzon; G. Dechman; J. G. Martin; J. H.T. Bates

doi:10.1016/0034-5687(94)00075-B

Time course of histamine-induced bronchoconstriction and its adrenergic and H₂ modulation

A. M. Lauzon, G. Dechman, J. G. Martin, J. H.T. Bates

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

We characterized the complete time course of histamine-induced bronchoconstriction and its modulation via the release of endogenous catecholamines and by its actions on H₂-receptors in anesthetized, tracheostomized, paralyzed, and artificially ventilated mongrel dogs. Respiratory resistance (R) and elastance (E) were estimated continuously with a recursive least squares estimator. Three protocols were followed in which multiple histamine bolus injections were given 1 h apart. We found that the time courses of E and R had consistent patterns (transient peak that returned to baseline within 1000 sec) even in cases of low mean arterial pressure (MAP). Indomethacin pre-treatments prevented tachyphylaxis to repeated i.v. challenges. β-blockade produced a mild increase in baseline and a potentiation of the histamine-induced response in E and these effects were not altered with further α-or H₂-blockade. Blockade of α-receptors increased the time to recovery in both E and MAP presumably by decreasing blood flow. Finally, we suggest that preventing the H₂-receptor induced increase in bronchial blood flow may have increased the time to maximal E without affecting the recovery time.

Original language	English
Pages (from-to)	127-138
Number of pages	12
Journal	Respiration Physiology
Volume	99
Issue number	1
DOIs	https://doi.org/10.1016/0034-5687(94)00075-B
Publication status	Published - Jan 1995
Externally published	Yes

Bibliographical note

Funding Information:
The authors are thankful to Mr. W. Lubenskyi from the Jewish General Hospital, Lady Davis Institute, 3755 St-Catherine, Montreal, Quebec, Canada, H3T 1E2, for performingt he HPLC cat-echolaminea ssays.T he authors are also indebtedt o Ciba-Geigy Canada Ltd., 6860 Century Avenue, MississaugaO, ntario,L5N 2W5, for kindly providing the phentolaminen eeded to accomplish this study. Finally, the authors want to thank Rosetta Pantano and Deanna Collin for their technicalh elp in getting blood samples in the awake dogs. This work was supportedb y the Medical ResearchC oun-cil of Canada, the J.T. Costello Memorial Research Fund, and the RespiratoryH ealthNetwork of Centers of ExcellenceA. .-M. Lauzon is supportedb y the ResearchI nstituteof the Montreal Chest Hospital, Montreal, G. Dechman is supportedb y the Physiotherapy Society of the Canadian Lung Association, J.G. Martin is a scientisto f the Medical Research Council of Canada, and J.H.T. Bates is a Chercheur-boursier of the Fonds de la Recherchee n Sant6 du Quebec.

ASJC Scopus Subject Areas

Physiology
Pulmonary and Respiratory Medicine

Access to Document

10.1016/0034-5687(94)00075-B

Cite this

@article{677e9e864f1e4fdfa3e7a9b99c2c017f,

title = "Time course of histamine-induced bronchoconstriction and its adrenergic and H2 modulation",

abstract = "We characterized the complete time course of histamine-induced bronchoconstriction and its modulation via the release of endogenous catecholamines and by its actions on H2-receptors in anesthetized, tracheostomized, paralyzed, and artificially ventilated mongrel dogs. Respiratory resistance (R) and elastance (E) were estimated continuously with a recursive least squares estimator. Three protocols were followed in which multiple histamine bolus injections were given 1 h apart. We found that the time courses of E and R had consistent patterns (transient peak that returned to baseline within 1000 sec) even in cases of low mean arterial pressure (MAP). Indomethacin pre-treatments prevented tachyphylaxis to repeated i.v. challenges. β-blockade produced a mild increase in baseline and a potentiation of the histamine-induced response in E and these effects were not altered with further α-or H2-blockade. Blockade of α-receptors increased the time to recovery in both E and MAP presumably by decreasing blood flow. Finally, we suggest that preventing the H2-receptor induced increase in bronchial blood flow may have increased the time to maximal E without affecting the recovery time.",

author = "Lauzon, {A. M.} and G. Dechman and Martin, {J. G.} and Bates, {J. H.T.}",

note = "Funding Information: The authors are thankful to Mr. W. Lubenskyi from the Jewish General Hospital, Lady Davis Institute, 3755 St-Catherine, Montreal, Quebec, Canada, H3T 1E2, for performingt he HPLC cat-echolaminea ssays.T he authors are also indebtedt o Ciba-Geigy Canada Ltd., 6860 Century Avenue, MississaugaO, ntario,L5N 2W5, for kindly providing the phentolaminen eeded to accomplish this study. Finally, the authors want to thank Rosetta Pantano and Deanna Collin for their technicalh elp in getting blood samples in the awake dogs. This work was supportedb y the Medical ResearchC oun-cil of Canada, the J.T. Costello Memorial Research Fund, and the RespiratoryH ealthNetwork of Centers of ExcellenceA. .-M. Lauzon is supportedb y the ResearchI nstituteof the Montreal Chest Hospital, Montreal, G. Dechman is supportedb y the Physiotherapy Society of the Canadian Lung Association, J.G. Martin is a scientisto f the Medical Research Council of Canada, and J.H.T. Bates is a Chercheur-boursier of the Fonds de la Recherchee n Sant6 du Quebec.",

year = "1995",

month = jan,

doi = "10.1016/0034-5687(94)00075-B",

language = "English",

volume = "99",

pages = "127--138",

journal = "Respiration Physiology",

issn = "0034-5687",

publisher = "Elsevier",

number = "1",

}

TY - JOUR

T1 - Time course of histamine-induced bronchoconstriction and its adrenergic and H2 modulation

AU - Lauzon, A. M.

AU - Dechman, G.

AU - Martin, J. G.

AU - Bates, J. H.T.

N1 - Funding Information: The authors are thankful to Mr. W. Lubenskyi from the Jewish General Hospital, Lady Davis Institute, 3755 St-Catherine, Montreal, Quebec, Canada, H3T 1E2, for performingt he HPLC cat-echolaminea ssays.T he authors are also indebtedt o Ciba-Geigy Canada Ltd., 6860 Century Avenue, MississaugaO, ntario,L5N 2W5, for kindly providing the phentolaminen eeded to accomplish this study. Finally, the authors want to thank Rosetta Pantano and Deanna Collin for their technicalh elp in getting blood samples in the awake dogs. This work was supportedb y the Medical ResearchC oun-cil of Canada, the J.T. Costello Memorial Research Fund, and the RespiratoryH ealthNetwork of Centers of ExcellenceA. .-M. Lauzon is supportedb y the ResearchI nstituteof the Montreal Chest Hospital, Montreal, G. Dechman is supportedb y the Physiotherapy Society of the Canadian Lung Association, J.G. Martin is a scientisto f the Medical Research Council of Canada, and J.H.T. Bates is a Chercheur-boursier of the Fonds de la Recherchee n Sant6 du Quebec.

PY - 1995/1

Y1 - 1995/1

N2 - We characterized the complete time course of histamine-induced bronchoconstriction and its modulation via the release of endogenous catecholamines and by its actions on H2-receptors in anesthetized, tracheostomized, paralyzed, and artificially ventilated mongrel dogs. Respiratory resistance (R) and elastance (E) were estimated continuously with a recursive least squares estimator. Three protocols were followed in which multiple histamine bolus injections were given 1 h apart. We found that the time courses of E and R had consistent patterns (transient peak that returned to baseline within 1000 sec) even in cases of low mean arterial pressure (MAP). Indomethacin pre-treatments prevented tachyphylaxis to repeated i.v. challenges. β-blockade produced a mild increase in baseline and a potentiation of the histamine-induced response in E and these effects were not altered with further α-or H2-blockade. Blockade of α-receptors increased the time to recovery in both E and MAP presumably by decreasing blood flow. Finally, we suggest that preventing the H2-receptor induced increase in bronchial blood flow may have increased the time to maximal E without affecting the recovery time.

AB - We characterized the complete time course of histamine-induced bronchoconstriction and its modulation via the release of endogenous catecholamines and by its actions on H2-receptors in anesthetized, tracheostomized, paralyzed, and artificially ventilated mongrel dogs. Respiratory resistance (R) and elastance (E) were estimated continuously with a recursive least squares estimator. Three protocols were followed in which multiple histamine bolus injections were given 1 h apart. We found that the time courses of E and R had consistent patterns (transient peak that returned to baseline within 1000 sec) even in cases of low mean arterial pressure (MAP). Indomethacin pre-treatments prevented tachyphylaxis to repeated i.v. challenges. β-blockade produced a mild increase in baseline and a potentiation of the histamine-induced response in E and these effects were not altered with further α-or H2-blockade. Blockade of α-receptors increased the time to recovery in both E and MAP presumably by decreasing blood flow. Finally, we suggest that preventing the H2-receptor induced increase in bronchial blood flow may have increased the time to maximal E without affecting the recovery time.

UR - http://www.scopus.com/inward/record.url?scp=0028873558&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028873558&partnerID=8YFLogxK

U2 - 10.1016/0034-5687(94)00075-B

DO - 10.1016/0034-5687(94)00075-B

M3 - Article

C2 - 7740200

AN - SCOPUS:0028873558

SN - 0034-5687

VL - 99

SP - 127

EP - 138

JO - Respiration Physiology

JF - Respiration Physiology

IS - 1

ER -