Eugenol introduced directly into the circulatory system of the dog caused a strong but transient reduction in arterial blood pressure and myocardial contractile force, without appreciably changing heart rate or electric activity. Intra-arterial injection of the drug resulted in increased blood flow to the region.

Incubation of [14C]-arachidonic acid with slices of inflamed human gingivae in the absence of glutathione resulted in formation of 6-keto-PGF1 alpha, the stable hydrolytic product of prostacyclin. Significantly smaller amounts of this product were obtained when normal gingivae were treated in a similar manner. The formation of prostacyclin in inflamed gingivae may play an important role in alveolar bone resorption and as a mediator of inflammation in periodontal disease.

A dose-response curve was established based on increases in venous infusion pressure evoked by injection of a series of small doses of norepinephrine, before and after slow infusion of a prazosin solution into the accessory cephalic vein of anesthetized dogs. During the prazosin infusion, there was an increase in venous infusion pressure, which returned to control levels by the end of the infusion period. The reduction in arterial pressure that occurred during the infusion persisted throughout the experiment. Immediately following the prazosin infusion, venous constrictor responses to norepinephrine were greatly inhibited, an effect that was still present 1 hr later. Prazosin has a marked in vivo a-adrenergic receptor inhibiting action in the accessory cephalic vein of the dog. This effect may be preceded by an agonistic action on these receptors at this site, as suggested by the increase in venous infusion pressure during the period of prazosin administration.

Wood, W.B., F.D. Sticht, S.S. Cardoso, and E.E. Elko: Effect of clonidine on responsiveness of venous smooth muscle to sympathetic neurotransmitter. Drug Dev. Res. 3~453-460, 1983.The presence of both longitudinal and circular smooth muscle makes the canine accessory cephalic vein a sensitive preparation for the evaluation of venomotor activity. Infusion of clonidine (10 pglkg) into this intact, peripheral vein results in transient, localized venoconstriction and prolonged arterial hypotension. Bradycardia, paralleling the hypotension in onset and duration, is a consistent concomitant. Exposure of the test vein smooth muscle to clonidine diminishes responsiveness of this vein to subsequent close injections of norepinephrine. This inhibition, though pronounced, is short-lived and usually abates within an hour.

Diazoxide-induced modification of renal vascular responses to norepinephrine and angiotensin II was studied in dogs. Diazoxide was infused directly into the renal artery in order to minimize the effect of high plasma protein binding and to obtain maximum exposure of the test vessel to the administered drug. During the 30-min infusion period, renal blood flow showed an initial, transitory increase followed by a progressive decline which paralleled the induced fall in systemic blood pressure. In the presence of diazoxide, renal vasoconstrictor responses to intravenous and intraarterial norepinephrine and intravenous angiotensin II were significantly attenuated. In contrast, the renal vasoconstrictor response to intraarterial angiotensin II was not significantly modified by diazoxide. This differential inhibition by diazoxide of renal vasoconstriction to norepinephrine or angiotensin I 1 may warrant consideration when these pressor agents are being used to overcome the excessive hypotension resulting from inadvertent diazoxide overdosage.