The mechanism of the chloroform-epinephrine and cyclopropane-epinephrine cardiac arrhythmias, with observations on the protective effects of Glycolic acid and glycine
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Abstract
The literature pertinent to the mechanism of the cyclopropane-epinephrine and chloroform-epinephrine arrhythmias has been reviewed. The development of the cyclopropane arrhythmias has been shown to be the result of a reflex sensitization of the heart. This reflex increase in ventricular irritability involves afferent fibers in the splanchnic nerves which originate (possibly in Pacinian corpuscles) in the peripheral part of the mesentery, the long sympathetic tracts of the spinal cord, certain nuclei located in the hypothalamus, and the sympathetic efferent pathways to the heart. The probability that the chloroform-conditioned arrhythmias are mediated by a similar means is discussed, and the implementation of this mechanism as an explanation for the chloroform arrhythmias is shown not to disagree with the data which have been published concerning this matter.
The observations which have been made regarding the importance of arterial pressure in the causation of these anesthetic cardiac arrhythmias is reviewed. No opposing points of view are presented: one holds that the blood pressure level, or an abrupt change in blood pressure, which produces cardiac strain or dilatation, is the essential exciting cause of the irregularities; the other maintains that the blood pressure change is an associated variable and not the primary exciting cause in their development. The first school points out that agents which abolish the pressor response to injected epinephrine prevent the arrhythmias, while the second emphasizes the experiments which indicate protection from the cardiac disturbance by the same agents in doses which do not nullify this response.
One group has presented observations indicating that the ventricular irregularities do not occur in the absence of a pressor effect, while the other group has published results to show that the irregularities may fail to appear in the presence of such an effect. Since these conditions are not mutually exclusive, no definite conclusions can yet be drawn in this controversy. The occurrence of cardiac arrhythmias in cats and humans independently of the injection of exogenous epinephrine or of any marked pressor effects, however, seems to negate the importance of abrupt blood pressure changes as exciting causes in their developnent, to some extent at least. The writer is inclined to agree with the better versed authorities in this field, who hold that the blood pressure is an influencing but not a determining factor and that the primary exciting cause of the chloroform-epinephrine and cyclopropane-epinephrine arrhythmias is the direct action of epinephrine on the sensitized heart.
Original research is presented which indicates that the cyclopropane-epinephrine arrhythmias may be prevented in dogs by glycolic acid, and by glycine and its salts. The protection offered by glycolic acid is slow in onset and of long duration; and since the salts of this acid have no prophylactic effect, it is at least possible that pH may be a factor in the prevention of ventricular irregularities by this agent. The effects of glycine are early in onset and of brief duration, and the sodium salt is as active as the amino acid itself in protection against the arrhythmias so that a purely pH effect is probably excluded in this case. The conclusions drawn are limited and further experiments are proposed in order to clarify them.
The observation of the protective effects of glycolic acid and glycine are not in disagreement with the idea that the pharmacological activity of a compound may be in some way related to its electrical asymmetry.
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Thesis (M.A.)--Boston University
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