Biomedical subjects
Publications and source records attributed to H Satoh.
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Effects of L-dopa, L-5HTP, a few amines, and related compounds on the pancreatic rate of flow, protein secretion, and bicarbonate secretion were studied in conscious rats. Single injections of L-dopa, DA and apomorphine did not modify the rate of flow, while an increase was seen with infusion of DA. L-dopa stimulated the protein secretion. L-5HTP and 5-HT decreased the rate of flow and protein secretion. Effects of L-dopa and L-5HTP on the protein secretion were prevented by DA- and 5-HT blockers, respectively. Neither L-dopa nor L-5HTP had any effect on the bicarbonate secretion. Secretin and cholinergic agents (acetylcholine and carbamylcholine) strongly stimulated the rate of flow of pancreatic juice. alpha-Agonists (phenylephrine and clonidine) decreased the rate of flow, and the effects were inhibited by an alpha-blocker. The alpha-agonists had no effect on protein secretion. Although, alpha-blockers (phenoxybenzamine and phentolamine) had no effects on the rate of flow, they did decrease the protein secretion. Isoproterenol was a potent secretagogue, and the effect was suppressed by a beta-blocker. Histamine had no effect on the rate of flow. The results were discussed in relation to our previous histochemical and chemical findings, and the species difference between rats and dogs in response to the amines.
Mercury concentrations in the brain of man exposed to mercury vapor at or around the maximum permissible concentration were estimated by two mathematical models using informatins obtained from human and animal experiments. (formula: see text) Ac=concentration in the brain, C=concentration in air, V=ventilation volume, T=daily exposure time, R=proportion of mercury vapor retained after a single inhalation, D=proportion distributed to the brain, W=weight of the brain, b=elimination constant of mercury vapor in the brain, d=elimination constant of mercuric mercury in the brain, c=proportion of oxidization of elemental mercury in the brain. Model 1 is composed from a simple hypothesis that mercury vapor retained in the brain takes a single elimination coefficient, and in Model 2, a modification of Model 1, the part of elemental mercury retained in the brain is oxidized and thus has a different biological half-time from elemental mercury. During exposure to mercury vapor at the concentration of 0.05 mgHg/m3, estimated concentrations in the brain by Model 1 do not exceed a hypothetical critical concentration in the brain of 1.0 micrometerHg/g tissue but the estimated concentration by Model 2 exceeds this level.
The supernatant solutions of homogenates of organs of pregnant mice and fetuses on day 14 and 17 of gestation were measured for hemoglobin (Hb) content after a maximal blood extraction at sacrifice. Residual blood volumes of the organs and fetuses were calculated from the Hb contents and blood Hb concentrations. The greatest value was found for the spleen and the lowest for the brain. The residual blood volumes of the uterus, placenta and fetuses on day 17 were greater than on day 14 of gestation.
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Cefamandole sodium (CMD) was intravenously administered and following laboratoric and clinical results were obtained. (1) The peak blood concentration was 32 approximately 44 micrograms/ml when the drip infusion was finished. At 1 hour after the end of the drip infusion the blood concentration was 7.6 approximately 8.1 micrograms/ml. Half life was approximately 0.64 hours. (2) Urinary recovery rate was 84.5 approximately 95% in active state within 6 hours. (3) Penetration of cerebrospinal fluid was found in 2 cases. (4) In most of 170 strains of Streptococcus haemolyticus MICs of cefamandole were 0.05 microgram/ml. They were less susceptible to cefazoline, cefmetazole and ceftezole. (5) CMD was administered to 35 pediatric patients (upper or lower RTI, lymphadenitis, enteritis or UTI) at 100 mg/kg/day for 3 approximately 9 days, the efficacy rate was 97.1%. (6) Side effect: Rash occurred in one case, and eosinophilia was observed in 4 cases. No abnormal finding of renal and liver function was observed.
A series of studies on cefuroxime (CXM) were carried out and the following results were obtained. 1) Most of MICs to recent clinical isolates of Group A hemolytic Streptococcus were less than 0.0125 micrograms/ml. 2) A single intravenous bolus dose of 36.5 mg/kg of CXM was given to two children, and the peak blood levels of 30 and 40 micrograms/ml were obtained at 30 minutres after injection; mean half-life in blood was 1.02 hours. The doses of 25 approximately 50 mg/kg were given over 1 hour by intravenous instillation to six children. The peak blood level appeared at the end of instillation, and half-life in blood was distributed between 0.56 and 0.81 hour. With both of these administrations, measurable blood levels were maintained up to 6 hours, and urinary excretion rate in active form up to 6 hours was distributed between 40.5 and 96%. 3) Serious upper respiratory tract inflammations, low respiratory tract inflammations (acute bronchitis and bronchopneumonia), staphylococcal exanthema and acute urinary tract infections mostly responded well to CXM intravenous administration (one shot injection, or instillation at dose of 50 approximately mg/kg/day in 2 approximately 3 daily divided doses. 4) Staphylococcal pyothorax was completely cured by 17 day-long CXM intravenous instillation at dose of about 150 mg/kg/day. 5) No difference in CXM therapy result was seen between the two administration forms used, i.e., one shot injection and instillation. 6) Clinical efficacy rate in 48 patients was 100% (excluding 1 unassessable case). As for side effect, transitory elevation of GPT and Al-P were seen in only 1 case each. The summary of this paper was reported on June 9, 1979 at 27th General Meeting of Japan Society of Chemotherapy (Fukuoka).
Effect of procaine on the SA node of the dog heart was studied in situ using a selective perfusion technique of the SA node artery. Procaine in doses from 100 mug to 1 mg produced a sinus depression followed by a prolonged phase of the increased heart rate. The depression became more prominent with increasing the dose. The threshold dose for inducing the tachycardiac response was lower, but the sinus acceleration was not proportional to the dose. The initial depression was not affected by atropine, whereas the occurrence of the stimulatory phase was inhibited by prior administration of propranolol or tetrodotoxin into the SA node artery or in the reserpine-treated dogs. The results indicate that the biphasic response is induced by a direct negative chronotropic action of procaine on the SA node and by an indirect effect mediated by an interaction with the postganglionic adrenergic nerves.
The spasmolytic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) on the biliary tract was investigated in anesthetized dogs. Intravenous administration of AA-149 at 2 mg/kg and higher doses produced a dose-dependent reduction in passage resistance through the choledochoduodenal junction and in gallbladder pressure, and a dose-dependent increase in bile flow. AA-149, like cholecystokinin, decreased biliary ductal pressure in spite of increasing the bile flow in dogs with ligation of the cystic duct of the gallbladder, whereas taurocholate increased the pressure as well as the bile flow. Moreover, the spasmic response of the choledochoduodenal junction to morphine was depressed strongly by AA-149, BUT NOT CONSISTENTLY BY ATROPINE. The effects of AA-149 were not influenced by pretreatment with atropine, phentolamine or propranolol. These findings strongly suggest that AA-149 relaxed the biliary tract and depressed the morphine-induced spasm by a mechanism different from those of anticholinergic and sympathomimetic agents.
The choleretic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) was studied in anesthetized dogs. AA-149 produced a dose-dependent increase of the bile flow with both i.v. and intrajejunal administration of doses 1 mg/kg and higher. Biliary clearance of 14C-erythritol showed that AA-149 stimulated canalicular bile formation without enhancement of water secretion and/or inhibition of bile reabsorption in the biliary ductules and ducts. AA-149 did not increase the excretion of bile acids into the bile, but enhanced the excretion of the biliary electrolytes, in particular sodium ion, in proportion to an increase of the bile flow. About 3--4% of AA-149 administered i.v. was excreted into the bile during the first 1 h period, so that biliary AA-149 was insufficient to increase the bile flow via its osmotic effect. These results strongly suggest that the choleretic action of AA-149 is attributable to stimulation of a bile acid-independent bile formation in the canaliculi coupled with an active sodium transport system.
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The toxicity of the bis-succinyl derivative of the protein antibiotic, neocarzinostatin, was compared with the parent compound, neocarzinostatin (NCS), in rats. The derivative was found to be about two to five fold more active than NCS in vivo. The antitumor activity in rats bearing eleven distinct Yoshida hepatoma ascitic cell lines was tested under four possible combinations with regard to sites of drug and tumor cell administration. The results indicate that the antitumor spectrum of the derivative had changed slightly. Antitumor activity in mice was also tested with L1210 and P388 lymphatic leukemia, and with B16 melanocarcinoma. When the effect of the derivative was compared with parental NCS at the molecular level with respect to the inhibition of DNA synthesis in vitro, the specific activities of the two were found to be almost identical. These results were interpreted to indicate that the succinyl derivative of NCS was more stable to inactivation and proteolytic break-down in vivo than NCS as observed previously in in vitro studies.
Approximately 800 amino acid derivatives have been synthesized and screened in order to evaluate their antitumor activity against various transplantable rat ascites hepatomas. Among them, N6,N9-bis(butyloxycarbonylaminomethyl)-L-citrulline (A-924) was found to be highly effective against various rat ascites hepatomas. A-924, when given orally, exhibited prolongation of survival of rats implanted intravenously with ascites hepatoma cells such as AH-44, AH-66, AH-130, AH-66F, or AH-41C.
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Effect of several cross-linking agents added to MMA on the mechanical properties of self-cured fluid resins was studied. The cross-linking agents were 2,2-bis (4-methacryloxyethoxyphenyl) propane, trimethylolpropane trimethacrylate, neopentylglycol dimethacrylate, hexamethyleneglycol dimethacrylate and 1,2-polybutadiene. Their concentrations in MMA were 1,3,5 and 10 wt%. Measured mechanical properties were Brinell hardness, tensile strength, impact strength and transverse strength. The best composition was 5% neopentylglycol dimethacrylate in MMA among studied samples. Microscopic observation of the surface after tensile test suggested that diffusibility of cross-linking agents into PMMA powder affected the mechanical properties. Mechanical properties of both matrix and powder, and their adhesion at the interface had influence upon the mechanical properties of resins processed by powder-liquid method.
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Effects of sulpiride on the central nervous system were studied in catalepsy induction (I) and antagonism to gnawing behaviour (II) induced by apomorphine and methamphetamine in normal rats, and in antagonism to rotational behaviour (III) induced by apomorphine and methamphetamine in rats with substantia nigra unilaterally lesioned chronically by microinjection of 6-hydroxydopamine. Sulpiride was administered orally and intraventricularly, and the effects of sulpiride were compared to those of haloperidol and chlorpromazine administered through the same routes. In oral administration, sulpiride was almost inactive in (I), and was several hundreds to a thousand times less potent than haloperidol in (II) and (III), while chlorpromazine was 20 to 150 times stronger than sulpiride. In intraventricular administration, sulpiride was almost equipotent to haloperidol in (I), and was equally effective to or 2 to 3 times more effective than halopridol in (III), although several times less in all respects. These findings suggest that sulpiride is essentially a potent inhibitory substance on dopamine receptors in the central nervous system and the rather weak central effects of peripherally given sulpiride are due to poor penetration through the blood brain barrier.
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