Postradiation cardiovascular dysfunction.
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Animals↗
Biomedical subjects
R N Hawkins
Publications and source records attributed to R N Hawkins.
Effect of ionizing radiation on physiological function in the anesthetized rat.
Exposure of pentobarbital-anesthetized rats to 14.5-MeV electrons results in radiation-induced physiological dysfunction. Responses include transient hypotension, a transient decrease in heart rate, respiratory dysrhythmias, and a prolonged increase in pulse pressure. Magnitudes of these responses are dose related, and maximal responses can be elicited by either whole- or partial-body (head or abdominal) exposure to 10,000 rad. These responses were associated with a fivefold increase in arterial plasma concentration of epinephrine, whereas histamine, norepinephrine, and beta-endorphin did not change during the first minute after the onset of exposure. Administration of diphenhydramine, a histamine receptor antagonist, resulted in a significant decline of baseline cardiovascular function and inhibited radiation-induced cardiovascular dysfunction. The diphenhydramine-induced decrease in preexposure blood pressure was reversed by angiotensin infusion, but this procedure failed to restore the mechanism(s) responsible for the cardiovascular responses to radiation. Results of these experiments and information available in the literature support the hypothesis that these responses are due to an interference in the autonomic pathways that modulate cardiovascular function.
Anesthesia↗
Barbiturate depression of neurally mediated reflexes to coronary artery occlusion.
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Animals↗
Etiology of the negative chronotropic responses to transient coronary artery occlusion in the anesthetized rhesus monkey.
Etiology of the negative chronotropic response to coronary artery occlusion was studied in chloralose-anesthetized monkeys. One-minute occlusion of the circumflex (CIRC) coronary artery resulted in marked negative chronotropic responses and consistent alterations in atrial electrograms. These responses were dependent on interruption of flow to a small proximal CIRC branch, and postmortem examination revealed that it perfused the sinus node region. The negative chronotropic response was not dependent on any apparent neural reflexes because it was not affected by autonomic blockade. Coronary artery occlusion in anesthetized monkeys can result in significant decreases in heart rate and changes in atrial electrical activity when flow to the pacemaker region is interrupted. We suggest that (1) rhesus monkeys may be suitable for study of the sick sinus syndrome, and (2) atropine-resistant bradycardia and atrial arrhythmias observed in postinfarction patients may be due to sinus node artery blockade.
Anesthesia, General↗