Zhang X, Abdel-Rahman A R, Wooles W R
Department of Pharmacology, East Carolina University School of Medicine, Greenville, North Carolina 27858.
Proc Soc Exp Biol Med. 1988 Jan;187(1):14-21. doi: 10.3181/00379727-187-42630.
The acute effects of ethanol (0.33, 0.66, or 1 g/kg) on baroreflex control of heart rate (HR) and sympathetic efferent discharge (SED) were investigated in chloralose-anesthetized rats. The two higher doses of ethanol caused a progressive and significant increase in baseline SED and a slight increase in HR. That these effects were ethanol mediated is suggested by the absence of any change in blood pressure following ethanol injection in any amount used and the finding that equivolume saline had no effect on any of the tested parameters. On the other hand, the baroreflex slope of the MAP-SED relationship after ethanol was similar to the control (preethanol) value in contrast to a significant decrease in the baroreflex slope of MAP-HR under the same conditions. These findings suggest that the sensitivity of the reflex control of SED was preserved whereas that of HR was impaired after acute ethanol administration. Since these findings were obtained in the same animals, our data suggest that acute ethanol has a differential action on reflex control of SED and HR. Further, the significant increase in SED after moderate and high doses of ethanol suggests an increased central sympathetic tone as recordings were made from preganglionic nerve fibers (splanchnic nerve). The absence of an increase in baseline MAP, in spite of a significant increase in baseline SED following acute ethanol injection, could be explained, at least in part, by an ethanol-evoked reduction in pressor responsiveness to phenylephrine, an alpha-adrenergic agonist.
