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Biomedical subjects

M Sano

Publications and source records attributed to M Sano.

At least 577 records · Page 32Linked to original sources
PubMed1985

The correlation between cholecystectomy and fecal bile acids, and large-bowel cancer induced with 1,2-dimethylhydrazine in mice.

The relationship between cholecystectomy and large-bowel cancer development was investigated in animal models. Female ICR mice underwent cholecystectomy, and received 15 weekly intragastric administrations (Experiment 1) or 10 weekly subcutaneous injections (Experiment 2) of 15 mg/kg body weight of large-bowel carcinogen 1,2-dimethylhydrazine (DMH). Autopsy at 28 weeks after surgery showed that cholecystectomized mice had a nonsignificantly increased incidence of large-bowel carcinomas, compared to sham-operated and/or unoperated control mice (85 vs. 64 percent in Experiment 1; 31 vs. 16 and 20 percent in Experiment 2). Cholecystectomy alone without DMH treatment did not produce any cancer. Cholecystectomized mice excreted a significantly increased level of primary bile acids but an unchanged level of secondary bile acids in the feces, compared with unoperated control mice. It is obvious that cholecystectomy enhanced the development of DMH-induced, large-bowel carcinomas along with the change of fecal bile acid composition, suggesting that changes of bile acid metabolism after cholecystectomy may enhance or promote large-bowel carcinogenesis in man as well. This association of cholecystectomy and large-bowel cancer is not a strong one, however, as presented in epidemiologic as well as experimental studies.

Animals↗
PubMed1985

A pituitary-salivary mixed gland induced by tissue recombination of embryonic pituitary epithelium and embryonic submandibular gland mesenchyme in mice.

Renal subcapsular syngrafts of Day 9 to 11 mouse embryonic pituitary epithelium with Day 14 mouse embryonic submandibular gland mesenchyme produced mixed organs that include residual cleft structure surrounded by anterior pituitary cells some which are stained by anti-ACTH antiserum and submandibular gland-like structure with differentiated acinar cells which are stained by anti-alpha-amylase antiserum. However, when Day 8.5 or 12 embryonic pituitary epithelium was recombined with submandibular gland mesenchyme and syngrafted, development of submandibular gland-like or anterior pituitary tissues resulted, respectively. Thus, during organogenesis of the mouse anterior pituitary, there exists a developmental stage (Day 8.5-11 in utero), when prospective pituitary epithelium can respond to heterotypic submandibular gland mesenchyme with the development of a submandibular gland-like tissue.

Animals↗
PubMed1985

[Effect of ketanserin on blood pressure in rats].

Ketanserin, a selective serotonergic (5-HT2) antagonist, also has affinity for alpha 1-adrenoceptors. It is not clear whether the hypotensive mechanism of ketanserin is due to its antagonistic action to 5-HT2 receptor or to its affinity for alpha 1 adrenoceptors. The hypotensive mechanism of ketanserin was studied in both stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY). Anesthetized rats were used (alpha-chloralose + urethane, i.p.). Up to 3 ml of blood was drawn from each rat for analysis. Plasma norepinephrine (NE) was determined by radioenzymatic assay. Plasma serotonin (5-HT) was determined by HPLC-ECD. Adrenal nerve discharges were counted by a digital pulse counter. Ketanserin (0.5 mg/kg, 5.0 mg/kg, i.v.) produced a dose-dependent reduction of mean arterial pressure (MAP) in both SHRSP and WKY. MAP of SHRSP decreased significantly as compared with WKY. Both plasma NE and 5-HT showed a tendency to increase during ketanserin administration (5.0 mg/kg, i.v.). Ketanserin significantly antagonized the BP response induced by exogenously injected 5-HT (30 micrograms/kg) and NE (10 micrograms/kg). Adrenal nerve activity was reduced in parallel with the decrease in BP and HR. These findings suggest that ketanserin produced a decrease in BP via both peripheral and central action in rats.

Adrenal Glands↗
PubMed1985

An improved technique for dissociating hepatocytes from fixed mouse liver for cytochemistry.

A refined version of a method described previously for dissociating hepatocytes from fixed liver is described. The objective was to develop a procedure that would dispense with the postosmication of previously fixed tissue. In the new procedure fixed liver blocks are wrapped with a quadruple layer of nylon cloth, and, by squeezing them in a buffer solution, individually dissociated cells pass through the cloth without significant damage. The procedure makes it possible to dissociate liver tissue fixed with modified Karnovsky's fixative, Zamboni's fixative or cacodylate buffered glutaraldehyde. The subsequent compatibility of the single cells obtained with many cytochemical procedures has been confirmed.

Animals↗
PubMed1985

Chemical modification of spiramycins. VI. Synthesis and antibacterial activities of 3,3''-di-O-acyl-4''-O-sulfonyl and 3,3''-di-O-acyl-4''-O-alkyl derivatives of spiramycin I.

3,3''-Di-O-acyl-4''-O-sulfonyl and 3,3''-di-O-acyl-4''-O-alkyl derivatives of spiramycin I were synthesized and evaluated by four parameters, antibacterial activity, affinity to ribosomes, lypophilicity and therapeutic effects. Among them, 3,3''-di-O-acetyl-4''-O-mesyl and 3,3''-di-O-acetyl-4''-O-methylspiramycin I having relatively small substituents at 4''-position were the most effective in mouse protection tests, and the results were comparable to acetylspiramycin.

Animals↗
PubMed1985

Effects of atropine and pirenzepine on healing of gastric ulcer induced by mucosal excision in rats.

We studied the effects of atropine and pirenzepine on acid secretion induced by electrical vagal stimulation (EVS) and on healing of gastric ulcers after mucosal excision in rats. Both atropine (50, 125, and 250 micrograms/kg/hr) and pirenzepine (2.5, 5.0, and 12.5 mg/kg/hr), administered intraperitoneally, inhibited vagally stimulated acid secretion in a dose-dependent manner. Pirenzepine given at a rate of 0.25 mg/kg/hr had no effect on the acid secretory response to EVS. Either atropine (125 micrograms/kg/hr) or pirenzepine (2.5 mg/kg/hr) given for one week caused an inhibition of approximately 80% in acid secretory response to EVS. The antisecretory dosage of pirenzepine caused a significant reduction in the surface area of the ulcer by the seventh postoperative day, whereas neither the antisecretory dosage of atropine nor the nonantisecretory dosage of pirenzepine significantly affected the size of the ulcer. We conclude that an antisecretory dosage of pirenzepine accelerates the healing of gastric ulcers produced in rats.

Animals↗
PubMed1985

Platelet involvement in the nephritis of acute serum sickness in rabbits: protection by dipyridamole and FUT-175.

In the acute serum sickness model in rabbits, we investigated platelet release of 5-HT, platelet surface immunoglobulins, and platelet aggregation in response to ADP, together with the effect of dipyridamole and the Clr antagonist FUT-175. The immune release of 5-HT from platelets occurred between 4 and 6 days after injection of bovine serum albumin (BSA), before immune elimination and proteinuria, but coincident with the appearance of immune complexed BSA in the circulation. Nevertheless, platelet turnovers were not detectably accelerated. Treatment with dipyridamole 50 mg/kg/24 h prevented the release of 5-HT and inhibited proteinuria, glomerular hypercellularity and immune complexes in the glomeruli. Using the Clr antagonist FUT-175, similar abrogation of the disease was obtained. We conclude that in the nephritis of acute serum sickness in rabbits, some of the immune release from platelets may be the result of immune complex binding to the platelet, perhaps through the receptor for C3b.

Adenosine Diphosphate↗
PubMed1985

[Effects of new antihypertensive agent, 2-[4-(n-butyryl)-homopiperazine-1-ul]-4-amino-6, 7-dimethoxy-quinazoline (E-643), on blood pressure, urinary sodium excretion and urinary norepinephrine excretion rate in stroke-prone, spontaneously hypertensive rats].

Present study was undertaken to elucidate the effects of E-643, on blood pressure, urinary electrolyte (U-Na, U-K) and catecholamines excretion rates in stroke-prone spontaneously hypertensive rats (SHRSP). An attempt was also made to clarify the effects of E-643 on plasma catecholamine concentration and sympathetic efferent nerve discharges including renal and adrenal nerve activity. E-643 (10 mg/kg/day X 4 weeks, p.o.) administered SHRSP (E-643 SHRSP) produced a significant hypotensive effect as compared with sex-age matched nondrug control SHRSP (control SHRSP). Both U-Na and U-K in E-643 SHRSP increased significantly as compared with those of control SHRSP. Urinary norepinephrine content (U-NE) also increased significantly in E-643 SHRSP. Plasma NE concentration tended to increase in E-643 SHRSP. While, plasma epinephrine (E) concentration decreased significantly in E-643 SHRSP. E-643 did not produce any significant effects on both sympathetic renal nerve activity and adrenal nerve activity in SHR. The changes induced by exogenous administered NE (blood pressure rise, tachycardia and the change in sympathetic nerve activity) were antagonized by pretreatment of E-643 in SHR. It was demonstrated that therapeutic doses of E-643 did not seem to produce any significant effect on central nervous system. These findings suggest that E-643 is a peripherally acting alpha 1 antagonist with natriuretic effect.

Animals↗