STUDIES ON SYMPATHOMIMETIC ACTION OF ACETALDEHYDE:I. EXPERIMENTS WITH BLOOD PRESSURE AND NICTITATING MEMBRANE RESPONSES

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Since Handovsky (1) observed that intravenous administration of small amounts of acetaldehyde in anesthetized dogs produced a sharp rise in blood pressure and cardiac acceleration, many investigations have been done on the cardiovascular effects of acetaldehyde. Nelson (2) showed that acetaldehyde, given intravenously, had a pressor activity resembling epinephrine, and that this pressor response was markedly potentiated by cocaine and it was not due to the liberation of epinephrine from the adrenal glands. Christensen (3) reported that the action of epinephrine upon the blood pressure was duplicated by acetaldehyde in an amount "100 times larger" and the pressor response to acetaldehyde was reversed by an adrenolytic drug, C-7337, in dogs under pentobarbital anesthesia. Feingold (4) reported that the pressor response to acetaldehyde in dogs was not wholly due to the release of epinephrine from the adrenals and was reversed by an adrenergic blocking drug SY-28, when the bilateral adrenal vessels were ligated. Seibert et al. (5) found that the pressor response to acetaldehyde in dogs was blocked by dibenamine and by Priscoline. Wingard et al. (6) carried out a long-range study on the actions of aldehydes and found that the blood pressure responses of acetaldehyde were qualitatively quite similar to epinephrine. Recently Eade (7) has reported that in spinal cats treated with reserpine acetaldehyde caused a fall in blood pressure, and in the normal animals the sympathomimetic aldehydes appeared to exert a part of their action upon cardiovascular system by the release of catecholamines from tissue stores other than the adrenal medulla. Further, he has found that the releasing action of the aldehydes appeared to differ from that of tyramine. However, he did not definitely describe the mechanism or mode of action of acetaldehyde. Romano et al. (8) and Eade (7) suggested that the nature of the catecholamine released by the aldehydes in normal animals was more like that of norepinephrine than epinephrine. However, the findings that the pressor response to acetaldehyde is reversed by pretreatment with dibenamine in normal spinal cats, and the depressor response to this drug is observed in chronically reserpinized spinal cats are not fully explained only by the action of acetaldehyde releasing norepinephrine. We have performed pharmacological studies on acetaldehyde for several years. Some years ago, Yokokawa (9) in this department investigated the cardiovascular actions of acetaldehyde. The effect of acetaldehyde on cardiovascular system may explain some pharmacological actions of alcohol, especially acute after-effects of alcoholic beverages (10). The present investigation was carried out in order to correlate the pressor response and the nictitating membrane response of the spinal cat to acetaldehyde and to elucidate the mechanism of action of acetaldehyde on the cardiovascular system. In this study the pressor and the nictitating membrane responses to acetaldehyde were compared with those caused by tyramine, epinephrine and norepinephrine.
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STUDIES ON SYMPATHOMIMETIC ACTION OF ACETALDEHYDE:I. EXPERIMENTS WITH BLOOD PRESSURE AND NICTITATING MEMBRANE RESPONSES

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