✓ The cardiovascular events resulting from experimental head injury were studied to determine the incidence of cardiac arrhythmias and to define the autonomic mechanisms responsible for these changes. Electrocardiograms and arterial blood pressure were recorded in anesthetized monkeys before and after the animals were subjected to temporoparietal head impact. Cardiac arrhythmias and hypotension occurred immediately following impact in every animal studied. Various atrioventricular nodal and ventricular arrhythmias were seen. Cholinergic blockade was found to prevent arrhythmias induced by head injury whereas adrenergic blockade was found to be ineffective.
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.
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