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Title: Carbon monoxide and lethal arrhythmias

Abstract

The effect of acute exposure to carbon monoxide on ventricular arrhythmias was studied in a previously described chronically maintained animal model of sudden cardiac death. In 60 percent of dogs with a healed anterior myocardial infarction, the combination of mild exercise and acute myocardial ischemia induces ventricular fibrillation. The events in this model are highly reproducible, thus allowing study by internal control analysis. Dogs that develop ventricular fibrillation during the test of exercise and acute myocardial ischemia are considered at high risk for sudden death and are defined as 'susceptible'; dogs that survive the test without a fatal arrhythmia are considered at low risk for sudden death and are defined as 'resistant.' In the current study, the effects of carboxyhemoglobin levels ranging from 5 to 15 percent were tested in resistant and susceptible dogs. A trend toward higher heart rates was observed at all levels of carboxyhemoglobin, although significant differences were observed only with 15 percent carboxyhemoglobin. This trend was observed at rest and during exercise in both resistant and susceptible dogs. In resistant animals, in which acute myocardial ischemia is typically associated with bradycardia even under the control condition, this reflex response occurred earlier and was augmented after exposuremore » to carbon monoxide. This effect may depend on the increased hypoxic challenge caused by carbon monoxide, and thus on an augmentation of the neural reflex activation or a sensitization of the sinus node to acetylcholine induced by hypoxia. In both resistant and susceptible dogs, carbon monoxide exposure induced a worsening of ventricular arrhythmias in a minority of cases. This worsening was not reproducible in subsequent trials. These data indicate that acute exposure to carbon monoxide is seldom arrhythmogenic in dogs that have survived myocardial infarction. (Abstract Truncated)« less

Authors:
; ; ; ;  [1]
  1. (Univ. of Oklahoma Health Sciences Center, Oklahoma City (USA))
Publication Date:
OSTI Identifier:
5472535
Alternate Identifier(s):
OSTI ID: 5472535
Resource Type:
Journal Article
Journal Name:
Research Report Health Effects Institue; (USA)
Additional Journal Information:
Journal Volume: 36; Journal ID: ISSN 1041-5505
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; CARBON MONOXIDE; TOXICITY; HEART; SENSITIVITY; ACUTE EXPOSURE; BLOOD PRESSURE; CARBOXYHEMOGLOBIN; DOGS; EXERCISE; MAXIMUM PERMISSIBLE EXPOSURE; MYOCARDIAL INFARCTION; ANIMALS; BODY; CARBON COMPOUNDS; CARBON OXIDES; CARDIOVASCULAR DISEASES; CARDIOVASCULAR SYSTEM; CHALCOGENIDES; DISEASES; MAMMALS; ORGANS; OXIDES; OXYGEN COMPOUNDS; SAFETY STANDARDS; STANDARDS; VERTEBRATES 560300* -- Chemicals Metabolism & Toxicology

Citation Formats

Farber, J.P., Schwartz, P.J., Vanoli, E., Stramba-Badiale, M., and De Ferrari, G.M. Carbon monoxide and lethal arrhythmias. United States: N. p., 1990. Web.
Farber, J.P., Schwartz, P.J., Vanoli, E., Stramba-Badiale, M., & De Ferrari, G.M. Carbon monoxide and lethal arrhythmias. United States.
Farber, J.P., Schwartz, P.J., Vanoli, E., Stramba-Badiale, M., and De Ferrari, G.M. Sat . "Carbon monoxide and lethal arrhythmias". United States.
@article{osti_5472535,
title = {Carbon monoxide and lethal arrhythmias},
author = {Farber, J.P. and Schwartz, P.J. and Vanoli, E. and Stramba-Badiale, M. and De Ferrari, G.M.},
abstractNote = {The effect of acute exposure to carbon monoxide on ventricular arrhythmias was studied in a previously described chronically maintained animal model of sudden cardiac death. In 60 percent of dogs with a healed anterior myocardial infarction, the combination of mild exercise and acute myocardial ischemia induces ventricular fibrillation. The events in this model are highly reproducible, thus allowing study by internal control analysis. Dogs that develop ventricular fibrillation during the test of exercise and acute myocardial ischemia are considered at high risk for sudden death and are defined as 'susceptible'; dogs that survive the test without a fatal arrhythmia are considered at low risk for sudden death and are defined as 'resistant.' In the current study, the effects of carboxyhemoglobin levels ranging from 5 to 15 percent were tested in resistant and susceptible dogs. A trend toward higher heart rates was observed at all levels of carboxyhemoglobin, although significant differences were observed only with 15 percent carboxyhemoglobin. This trend was observed at rest and during exercise in both resistant and susceptible dogs. In resistant animals, in which acute myocardial ischemia is typically associated with bradycardia even under the control condition, this reflex response occurred earlier and was augmented after exposure to carbon monoxide. This effect may depend on the increased hypoxic challenge caused by carbon monoxide, and thus on an augmentation of the neural reflex activation or a sensitization of the sinus node to acetylcholine induced by hypoxia. In both resistant and susceptible dogs, carbon monoxide exposure induced a worsening of ventricular arrhythmias in a minority of cases. This worsening was not reproducible in subsequent trials. These data indicate that acute exposure to carbon monoxide is seldom arrhythmogenic in dogs that have survived myocardial infarction. (Abstract Truncated)},
doi = {},
journal = {Research Report Health Effects Institue; (USA)},
issn = {1041-5505},
number = ,
volume = 36,
place = {United States},
year = {1990},
month = {12}
}