Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle

Marion S. Gaide, Cynthia B. Altman, John S. Cameron, Charles J. Kaiser, Robert J Myerburg, Arthur L. Bassett

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

1. Histamine (10-3M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). 2. Histamine (10-3M) markedly enhanced the irregular rhythm of infarcted preparations. 3. The H1-receptor antagonist, chlorpheniramine (10-4M), and the H2-receptor antagonist, cimetidine (10-3M), antagonized the effects of histamine (10-3M) on the spontaneous rate of both control and infarcted preparations. 4. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10-4M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10-4M). The H2-receptor agonist, dimaprit, had no effect. 5. Similar to histamine (10-3M), PEA (10-4M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. 6. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.

Original languageEnglish
Pages (from-to)488-493
Number of pages6
JournalAgents and Actions
Volume15
Issue number5-6
DOIs
StatePublished - Dec 1 1984

Fingerprint

Histamine
Canidae
Histamine Agonists
Histamine H1 Receptors
Dimaprit
Chlorpheniramine
Histamine H2 Receptors
Tissue
Dogs
Cimetidine
Ligation
Cardiac Arrhythmias
Coronary Vessels

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology (medical)

Cite this

Gaide, M. S., Altman, C. B., Cameron, J. S., Kaiser, C. J., Myerburg, R. J., & Bassett, A. L. (1984). Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle. Agents and Actions, 15(5-6), 488-493. https://doi.org/10.1007/BF01966761

Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle. / Gaide, Marion S.; Altman, Cynthia B.; Cameron, John S.; Kaiser, Charles J.; Myerburg, Robert J; Bassett, Arthur L.

In: Agents and Actions, Vol. 15, No. 5-6, 01.12.1984, p. 488-493.

Research output: Contribution to journalArticle

Gaide, MS, Altman, CB, Cameron, JS, Kaiser, CJ, Myerburg, RJ & Bassett, AL 1984, 'Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle', Agents and Actions, vol. 15, no. 5-6, pp. 488-493. https://doi.org/10.1007/BF01966761
Gaide, Marion S. ; Altman, Cynthia B. ; Cameron, John S. ; Kaiser, Charles J. ; Myerburg, Robert J ; Bassett, Arthur L. / Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle. In: Agents and Actions. 1984 ; Vol. 15, No. 5-6. pp. 488-493.
@article{8c191635054f4aa88c18c79d22d66ed2,
title = "Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle",
abstract = "1. Histamine (10-3M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). 2. Histamine (10-3M) markedly enhanced the irregular rhythm of infarcted preparations. 3. The H1-receptor antagonist, chlorpheniramine (10-4M), and the H2-receptor antagonist, cimetidine (10-3M), antagonized the effects of histamine (10-3M) on the spontaneous rate of both control and infarcted preparations. 4. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10-4M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10-4M). The H2-receptor agonist, dimaprit, had no effect. 5. Similar to histamine (10-3M), PEA (10-4M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. 6. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.",
author = "Gaide, {Marion S.} and Altman, {Cynthia B.} and Cameron, {John S.} and Kaiser, {Charles J.} and Myerburg, {Robert J} and Bassett, {Arthur L.}",
year = "1984",
month = "12",
day = "1",
doi = "10.1007/BF01966761",
language = "English",
volume = "15",
pages = "488--493",
journal = "Inflammation Research",
issn = "1023-3830",
publisher = "Birkhauser Verlag Basel",
number = "5-6",

}

TY - JOUR

T1 - Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle

AU - Gaide, Marion S.

AU - Altman, Cynthia B.

AU - Cameron, John S.

AU - Kaiser, Charles J.

AU - Myerburg, Robert J

AU - Bassett, Arthur L.

PY - 1984/12/1

Y1 - 1984/12/1

N2 - 1. Histamine (10-3M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). 2. Histamine (10-3M) markedly enhanced the irregular rhythm of infarcted preparations. 3. The H1-receptor antagonist, chlorpheniramine (10-4M), and the H2-receptor antagonist, cimetidine (10-3M), antagonized the effects of histamine (10-3M) on the spontaneous rate of both control and infarcted preparations. 4. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10-4M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10-4M). The H2-receptor agonist, dimaprit, had no effect. 5. Similar to histamine (10-3M), PEA (10-4M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. 6. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.

AB - 1. Histamine (10-3M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). 2. Histamine (10-3M) markedly enhanced the irregular rhythm of infarcted preparations. 3. The H1-receptor antagonist, chlorpheniramine (10-4M), and the H2-receptor antagonist, cimetidine (10-3M), antagonized the effects of histamine (10-3M) on the spontaneous rate of both control and infarcted preparations. 4. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10-4M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10-4M). The H2-receptor agonist, dimaprit, had no effect. 5. Similar to histamine (10-3M), PEA (10-4M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. 6. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.

UR - http://www.scopus.com/inward/record.url?scp=0021743783&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021743783&partnerID=8YFLogxK

U2 - 10.1007/BF01966761

DO - 10.1007/BF01966761

M3 - Article

C2 - 6532174

AN - SCOPUS:0021743783

VL - 15

SP - 488

EP - 493

JO - Inflammation Research

JF - Inflammation Research

SN - 1023-3830

IS - 5-6

ER -