The studies were carried out to investigate the effect of recovery in rewarming using the esophageal thermal tube in the deep hypothermia(25+_1 degrees centigrade ; rectal temp) in rabbits. Fifteen rabbits were divided into control group(n=6), peritoneal dialysis group(n=5) irrigated with dialysate at 42+_1 degrees centigrade, and esophageal rewarming group(n=6), peritioneal dialysis group(n=5) irrigated with dialysate at 42+_1 degrees centigrade, and esophageal rewarming group(n=4) perfused with circulating water at 38+_1 degrees centigrade. Rewarming of the rabbits was performed for 5 hours. MAP, HR, RR, esophageal temp, rectal temp, pH, pCO2, pO2, Na+, and K+ were observed. The results obtained in these experiments were summarized as follows:Esophageal rewarming group(38+_1 degrees centigrade) had more effect on esophageal temperature than other groups. Peritoneal dialysis group(42+_1 degrees centigrade) had more effect on rectal temperature and pO2 than other groups. The both groups also had more effects on MAP, HR, RR, and pCO2 than control group. Three groups had no significant effect on pH, Na+, and K+. In conclusion, we found that the simple, safe, and non-invasive esophageal rewarming method had an effect on the treatment of profound hypothermia as well as the peritoneal dialysis method in spite of the temperature difference between the dialysate and the circulating water, and the circulating water at 38+_1 degrees centigrade for esophageal rewarming also had an effect on the recovery of deep hypothermia.

We studied the effects of trazodone on arterial blood pressure in anesthesized guinea pigs, and on vascular responses in isolated thoracic aorta. Trazodone produced a concentration-dependent relaxation in phenylephrine-precontracted endothelium intact (+E) rings, but not in a KCl-precontracted aortic rings. These relaxant effects of trazodone on +E rings were siginificantly greater than those on denuded (-E) rings. The trazodone-induced relaxation was suppressed by gilbenclamide and tetrabutylammonium, but not by N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), methylene blue (MB), nifedipine, indomethacin, 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC) and clotrimazole. In vivo, infusion of trazodone elicited a significant decrease in arterial blood pressure.

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor responses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into an ear vein, and the same procedures were performed 1-2 min after treatment with intravenous verapamil. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. Pressor responses to intravenous norepinephrine (10 micro g/kg) and phenylphrine (30 micro g/kg) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. Pressor responses to intravenous norepinephrine (3 micro g/kg), phenylephrine (20 micro/kg) and clonidine (300 micro g/kg) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. Pressor responses to intravenous norepinephrine (3 micro g/kg) and phenylephrine (10 micro g/kg) were inhibited by pretreatment with intravenous verapamil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil

To examine the selectivity of diltiazem, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor responses, effect of diltiazem on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits and spinal rabbits. Intravenous diltiazem(10,30,100,300,1000 micro g/kg) produced dose-dependent depressor response in rabbits. Pressor responses to intravenous norepinephrine(10 micro g/kg) and phenylephrine (30 micro g/kg) were inhibited by pretreatment with intravenous diltiazem in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by diltiazem. Pressor responses to intravenous norepinephrine (3 micro g/kg), phenylephrine (20 micro g/kg) and clonidine (300 micro g/kg) were inhibited by pretreatment with intravenous diltiazem in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by diltiazem. The inhibition of clonidine-induced pressor response by diltiazem was slightly more prominent than that of norepinephrine-or phenylephrine-induced pressor response. These results suggest that diltiazem significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors