Using selective agonists and antagonists of alpha2 adrenoceptors, attempts were made to identify the subtype alpha2 adrenoceptors in the blood vessels of the canine dental pulp. In chloralose-anaesthetized dogs, intra-arterial administration of noradrenaline and guanabenz in different doses produced a dose-related pulpal vasoconstriction which was measured using hydrogen-gas clearance. The vasoconstrictor response to noradrenaline was inhibited by phentolamine, a non-selective alpha adrenoceptor antagonist. The response to guanabenz was inhibited by rauwolscine, a highly selective alpha2 adrenoceptor antagonist. The results demonstrated that alpha2 adrenoceptors are present in the blood vessels of dog dental pulp.

Experiments were carried out on 25 grown-up dogs of both sex in general anesthesia. The supraduodenal part of the choledochus was excised and the reconstruction of the defect with a free venous autograft was made by an end to end anastomosis without use of a transitory or permanent prosthesis. The experimental animals were observed for 60 days, during which period they were checked clinically, biochemically and radiologically. After this period the animals were sacrificed and surgical peroperative control and sampling of material for histological study were made. Out of 25 experimental animals 18 (72%) survived a period of 60 days and 7 dogs died. On autopsy it was found that the cause of death in all animals was biliary peritonitis, but in only one case due necrosis of the graft. The values of bilirubin concentration at the end of the experiment showed almost normal level, but the values of the alkaline phosphate activity and transminase showed significant increased values. Intravenous biligraphy showed significant excretion of the contrast material, freely passing the graft, which was dilated due to stenotic changes of the distal anastomosis. After sacrificing the animals we found: the graft increased length, diameter, thickness wall and stenosis of the distal anastomosis. By histological exploration we found in the liver the signs of the biliary stasis and in the grafts substitution of its endothelium by biliary epithelium. Free venous autograft used as a substitute in the reconstruction of the bile duct which survived 60 days postoperatively, remained transient but with changes in the sense of elongation and dilatation caused by the stenosis od distal anastomosis. Histologically the grafts were entirely bridged by biliary epithelium.

The liver blood flow has been extensively studied in hemorrhagic shock, but considerable disagreement exists as to the nature of hemodynamic changes and their controlling mechanism. The present investigation was undertaken in order to determine the effects of hemorrhage and phenoxybenzamine (PBZ) on the participation of hepatic artery (HAF) and portal vein flow (PVF) in total liver blood flow (LBF) changes. The dynamics of LBF (H2 washout method), HAF and PVF (electromagnetic flowmeter) during 3-hours posthemorrhagic hypotension (90 min. = 50-60 mmHg; 90 min. = 25-30 mmHg) and one-hour postretransfusion period were investigated on 20 mongrel dogs under chloralose anesthesia. All animals were divided into 2 groups (control and PBZ-treated--5 mg/kg b.w. 30 minutes following first bleeding). Half an hour following bleeding there occurred a significant decrease of LBF (P less than 0.001) in dogs of both experimental groups. This degree of decrease was due to equal decrease in the PVF and HAF. The infusion of PBZ caused a slight tendency towards increase of LBF, while the subsequent decrease in blood flow values during second hypotensive period in the treated dogs was not so pronounced as in the untreated dogs. Although retransfusion led to an increase of LBF, HAF and PVF in both groups, the restauration was significantly better in PBZ-treated animals. The degree of metabolic acidosis was more pronounced in the untreated dogs than in PBZ-treated.

In previous reports it was found that in mesenteric blood vessels exist profound alpha-adrenergic, and less profound beta-adrenergic receptors. Our experiments were done on 20 mongrel dogs, both sexes, weighing 6.5-22.5 kg, age from 1-2 years, which were divided into 2 groups: experimental (14 dogs) and control (6 dogs). Experimental group of animals passed through the posthemorrhagic hypotension (180 min. at 5.3 kPa). Aim of investigation was to clarify mesenteric vascular reactivity changes during posthemorrhagic hypotension. In order to reach this goal, phenylephrine and isoproterenol were injected alternatively in one hour intervals through cannulated superior mesenteric artery first proximal branch. Our results indicate that mesenteric blood flow responses to those drugs changed quantitatively, but never ceased. It is apparent from our experiments that those quantitative changes are due to beta 2 adrenoceptors changes during the posthemorrhagic hypotension.

Somatomedin activity in rat serum was measured by sulfate incorporation into embryonic chick cartilage. Hypophysectomized male rats were treated daily for 21 days with 20 microgram/kg L-thyroxine (T4) and/or 25 microgram bovine (b) GH. Serum from rats given T4 alone or with bGH had somatomedin potencies of 0.88 and 0.83, respectively, comparable to normal serum (1.00) and significantly greater than serum from bGH-treated hypophysectomized rats (0.62). Hypophysectomized rats had no measurable somatomedin activity. T4 treatment resulted in a return to normal of the basal metabolic rate and serum T4 and T3 concentrations. Addition of T4 or T3 to serum from normal rats to produce concentrations comparable to those found in serum of hypophysectomized rats after T4 and/or bGH treatment did not alter the somatomedin activity. Higher concentrations of T4 (10(-7) M) or T3 (10(-8) or 10(-7) M) did, however, enhance the sulfation potency of normal serum. T4 (10(-9) M to 10(-6) M) or T3 (10(-10) M to 10(-7) M) added to serum-free medium provided minimal sulfation activity that represented only a fraction of the activity of serum. T4 may stimulate production of somatomedin in the absence of adequate bGH or may be metabolized to an active sulfation factor.

In the isolated, perfused rat pancreas, prostaglandins (PGs) E1 and E2 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2alpha had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicylic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter three agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2alpha inhibited the vasoconstrictor responses to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.