Regional hemodynamic responses to nicotine in conscious and anesthetized dogs: comparative effects of pentobarbital and chloralose

This study was conducted in 12 dogs to evaluate regional hemodynamic responses during intravenous infusion of nicotine (36 micrograms/kg/min) in the conscious state and compare them with those in the same dogs following either pentobarbital (n = 6) or chloralose anesthesia (n = 6). Values for regional blood flow were obtained with 15-microns radioactive microspheres and used to calculate regional vascular conductance. In the conscious state, nicotine increased aortic pressure (+70%) and caused hyperventilation that reduced arterial PCO2 (-44%). These systemic effects were associated with decreases in vascular conductance in the renal cortex (-48%), pancreas (-81%), duodenum (-58%), and cerebral cortex (-55%), whereas no significant change in vascular conductance was evident in spleen, liver, or myocardium. Pentobarbital anesthesia blunted the increases in aortic pressure and respiratory activity and the reductions in vascular conductance in the renal cortex, pancreas, duodenum, and cerebral cortex during nicotine infusion. In contrast, chloralose anesthesia accentuated the increase in aortic pressure and the decrease in vascular conductance in the renal cortex during nicotine infusion, while it converted no change in vascular conductance in the spleen into a decrease and no change in vascular conductance in the myocardium into an increase. Chloralose anesthesia blunted nicotine-induced hyperventilation. These findings demonstrate that general anesthetic agents may have markedly different effects on cardiovascular reflex pathways. They emphasize the importance of considering the particular characteristics of the anesthetic agent used in interpreting results from studies of cardiovascular pharmacology and physiology in anesthetized animals.     

Thermoregulatory physiology of menopausal hot flashes: a review

Hot flashes during the climacteric years have long been a frequent clinical complaint, generally considered within the realm of the internist, gynecologist, or endocrinologist. Yet the underlying mechanism of hot flashes remains unknown. Only within the past 10 years has there been significant research on hot flashes as a disturbance of thermoregulation. This paper focuses on thermoregulatory aspects of hot flashes, reviewing current knowledge of the thermoregulatory physiology and endocrinology of hot flashes and discussing future avenues for research. Hot flashes are compared with fever in terms of thermoregulatory changes and speculated mechanisms. Although several substances in the peripheral circulation are found in increased concentrations during hot flashes, none is a trigger for a hot flash. The pattern of hot flash occurrence is striking in its regularity, and the possibility of endogenous rhythmicity is discussed. Recently, investigators have begun to explore a primate model of menopausal hot flashes. These studies are summarized. Finally, the multiple effects of estrogen on various systems of the body and their interrelationships are discussed. An understanding of the mechanism of hot flashes would not only be of importance to women suffering with hot flashes but would further our knowledge of thermoregulatory function and the interactions between thermoregulatory and reproductive systems.     

The effects of agents modifying sympathetic nerve function on the response of the isolated rat tail artery to etilefrine and tyramine.

The effects of etilefrine on the ventral caudal artery of the rat have been examined in the presence of agents modifying sympathetic nerve function. Catecholamine levels were also measured in adjacent segments of artery to those studied pharmacologically and an attempt made to relate vascular response to etilefrine (and tyramine) with catecholamine content. Both guanethidine and reserpine produced significant attenuation of the vascular effects of etilefrine and tyramine. Pre-treatment with a monoamine oxidase inhibitor caused an increase in tissue catecholamine levels but, paradoxically, depressed the vascular response to etilefrine. The significance of some of the findings in terms of an indirect component to etilefrine's action are discussed.     

Vascular effects of etilefrine. Further studies to substantiate the predominant indirect sympathomimetic action of this agent.

The suggested use of etilefrine in the treatment of patients with orthostatic hypotension is based on the premise that it has an action similar to that of noradrenaline (Miller, Wiener and Bloomfield, 1973). However, earlier work from this laboratory (Frost, Frewin and Gerke, 1977; Frost, Frewin, Gerke and Downey, 1978; Frost, Halloran, Frewin, Gerke and Downey, 1978) on blood vessels in the rat tail has suggested that the drug acts predominantly as an indirect sympathomimetic agent. The present study examined the action of etilefrine on the central artery of the rabbit ear. This vessel is known to have a rich sympathetic innervation (de la Lande, Frewin and Waterson, 1967) and has the added advantage that it can be surgically denervated. It therefore became possible to examine the effects of etilefrine on both normal and denervated arteries and to quantitate the extent to which the drug relied on the symphathetic nerves for its vasoconstrictor effects.     

Opsonization of Staphylococcus aureus by Guinea Pig 7S Gamma-Globulin

Opsonization of Staphylococcus aureus to phagocytosis by guinea pig peritoneal exudate cells (PEC) was examined with various isolated serum globulins. Significant enhancement of in vitro phagocytosis was afforded by partially purified 7S_γ1-immunoglobulin. The rate of killing or the rate of ingestion of ³H-thymidine labeled bacteria by PEC was used as an index of phagocytosis. The results indicate that the immunoglobulin can mediate the adsorption of an allogeneic surface independent of a specific antigenic component.