Service, I treated scorpion bites on three occasions. I learned from my colleagues that there was little to do for these patients but sedate them with barbiturates and observe them for a day or two if they seemed to have very toxic effects. This required in some cases huge or repeated doses of barbiturates and could take hours of observation.During the treatment of my first case in a 4-year-old girl, she appeared to be psychotic and I administered a small amount of chlorpromazine, intravenously. This was after approximately three hours of unsuccessful atempts at sedation with barbiturate, a total amount of a fantastic 160 mg of phenobarbital. The chlorpromazine yielded dramatic results within minutes. Subsequently I treated two similar reactions in 8-and 10-year-old boys with chlorpromazine intramuscularly with the same dramatic results, much to the dismay of emergency room personnel accustomed to the barbiturate therapy. I reported this to my colleagues at the time but have since had pangs of conscience for not trying to communicate to a larger audi¬ ence. For anyone who must treat this type of reaction, perhaps this much information can be of some benefit. The intramuscular route of administration is obviously pre¬ ferred for safety's sake. of angina pectoris reveals that all cardiovascular signs are signs of sympathetic overactivity, such as tachycardia, increase of blood pressure, arterial hypertonia, or increase of myocardial demands. The sympathetic system also exerts a coronary vasodilation action. The overactivity of the sympathetic system in angina pectoris explains why the drugs useful here are sympatholytics or antiadrenergics and the new treatments of this disease (propranolol hydrochloride and the electric stimulation of the carotid sinus) provide the same action. The good results published by Wasserman in 1928 through mechanical stimulation of the carotid sinus have been amply confirmed.1The carotid sinus stimulation may have resulted in a decrease of the sympathetic activity or in an increase of vagal activity.2 Wasserman wondered how it is possible to reduce the anginal pain when the resultant vagal stimulation produces a coronary vasoconstriction.The explanation is that the vagal stimulation and the resultant coronary vasoconstriction are associated with a decrease of myocardial needs (the anabolic action of the parasympathetic) and, therefore, this stimulation cannot produce a coro¬ nary insufficiency, which is the cause of angina pectoris. On the other hand we do not find signs of parasympathetic overactivity during the attack of angina pectoris. In contrast, the sympathetic stim¬ ulation thanks to its neurohormones (noradrenaline and adrenaline) pro¬ duces coronary vasodilation, but provokes at the same time an in¬ crease in myocardial demands, to a degree greater than is met by this increase of blood supply. The same insufficient increase of blood supply is also the cause of angina pectoris in pheocromocytoma during the re¬ lease of noradrenaline or adrenaline, which are ordinary dilators.3 ...
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