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Biomedical subjects

M Matsuda

Publications and source records attributed to M Matsuda.

At least 1,531 records · Page 85Linked to original sources

Hana kai ii: a 17-day dry saturation dive at 18.6 ATA. III. Body fluid balance.

Comprehensive studies on body fluid balance on 5 divers were conducted during the Hana Kai II dive (17 days at 18.6 ATA and 7 days of decompression). Daily urine flow increased from about 2000 ml at 1 ATA to 2600 ml at 18.6 ATA, at 31 degrees C. This diuresis was accompanied by a reduction in urine osmolality (from 650 to 500 mOsm) and a slight increase in osmolal clearance. Endogenous creatinine clearance remained at about 173 ml/min throughout the dive. Despite such a sustained diuresis, neither daily water intake nor total body water volume changed significantly. The plasma renin activity changed little, while both plasma aldosterone concentration and urinary aldosterone excretion increased significantly during the first week at 18.6 ATA. The plasma prolactin concentration showed a significant decrease during the first 3 days at 18.6 ATA. The daily excretion of antidiuretic hormone (ADH) decreased significantly (by 40%) 4 days after compression and remained low throughout the rest of the dive. Insensible waterloss at 18.6 ATA was 35% lower than that at 1 ATA. It is suggested that the observed hyperbaric diuresis is due primarily to suppression of ADH as a result of suppression of insensible water loss.

Aldosterone↗

Formation of lipoperoxide in isolated sciatic nerve by chinoform-ferric chelate.

Effects of chinoform and chinoform-ferric chelate on formation of lipoperoxide in isolated sciatic nerve were investigated. Free chinoform did not increase the lipoperoxide level, while chinoform-ferric chelate significantly increased it. Assuming that the lipoperoxide formed denatures the associated protein in the nerve, the effect of chinoform-ferric chelate could explain, at least partly, the demyelination of nerve tissues caused by massive doses of chinoform.

Animals↗

Fluorometric method for assay of kallikrein-like arginine esterases.

The fluorometric method of Nash for determination of methanol was applied in assay of kallikrein-like arginine esterases using N-a-tosyl-L-arginine methyl ester (TAME) as substrate. The results obtained using this method corresponded well with those obtained in the usual colorimetric methods using hydroxamate, chromotropic acid, and 3-methyl-2-benzothiazolone hydrazone and the present method was more sensitive than these colorimetric methods.

Arginine↗

A correlation between changes in gamma-aminobutyric acid metabolism and seizures induced by antivitamin B6.

The effects of DL-penicillamine (DL-PeA), hydrazine and toxopyrimidine (TXP, 2-methyl-6-amino-5-hydroxymethylpyrimidine) on gamma-aminobutyric acid (GABA) metabolism in mouse brain were studied. All these compounds inhibited the activity of glutamate decarboxylase [EC 4.1.1.15] (GAD) and slightly inhibited that of 4-aminobutyrate: 2-oxoglutarate aminotransferase [EC 2.6.1.19] (GABA-T). In contrast, very different effects were observed on GABA levels; hydrazine caused a marked increase, DL-PeA had no effect, and TXP caused a slight decrease in the content of the amino acid. These results could be described by an equation which related the excitable state to changes in the flux of the GABA bypass. Since the values obtained from the equation clearly reflect the seizure activity, it is suggested that the decreased GABA flux might be a cause of convulsions induced by these drugs.

4-Aminobutyrate Transaminase↗

Effect of acetylcholine on cerebral circulation.

Effects of intravertebral, intracarotid, and intravenous infusion of acetylcholine on cerebral blood flow (CBF) and metabolism was studied in 17 baboons anesthetized with pentobarbital. We measured CBF by the bilateral jugular venous outflow technique using two electromagnetic flowmeters. Effect of acetylcholine infusion on cerebral vascular response to hypercapnia was also assessed. Intravertebral infusion of acetylcholine (0.01 mg/kg/min) increased CBF by 27% and cerebral metabolic rate for oxygen by 19% and decreased cerebral vascular resistance by 25%. On intracarotid injection of acetylcholine, only an 8% increase in CBF was observed, and intravenous infusion produced no change in the parameters observed. Acetylcholine administered by any of the three routes did not enhance the CBF response to hypercapnia. Increase in CBF on intravertebral administration of acetylcholine is associated with an arousal effect and an increase in cerebral metabolism.

Acetylcholine↗

Effect of succinic semialdehyde on seizure caused by vitamin B6 antagonists.

Since gamma-hydroxybutyric acid (GHB) is known to be an effective anesthetic adjuvant in animal and a natural metabolite of succinic semialdehyde (SSA), the effect of SSA and GHB on the convulsive action of vitamin B6 antagonists was studied using the onset of seizure as a parameter. The administration of SSA and GHB to mice protected them against the convulsive action of B6 antagonist, such as castrix (2-chloro-4-dimethyl-6-methylpyrimidine), thiosemicarbazide, or penicillamine. The anticonvulsant effect of SSA seems to be due to an increase in brain levels of GHB converted in vivo from SSA.

Aldehydes↗

Effects of penicillamine on the contents of B6 vitamers of the mouse brain.

The contents of B6 vitamers were measured in the brains of mice treated with DL- and D-PeA. When a single convulsant dose of DL-PeA was injected, PLP content was decreased, being accompanied with production of PLP-thiazolidine. The effect of DL-PeA on PLP content was evident far before the occurrence of the convulsions. The administration of PN together with DL-PeA prevented the onset of seizures and lessened the effect of DL-PeA on PLP content. The same amount of D-PeA did not invoke seizures, but caused a small but significant decrease in PLP content.

Animals↗