Biomedical subjects

M Shimojo

Publications and source records attributed to M Shimojo.

75 records · Page 5Linked to original sources

PubMed1989

Mechanisms involved in the effect of M6434 on experimental hemorrhagic shock: II. Effects on energy metabolism and organ blood flow.

Effects of M6434 on survival time and hepatic energy metabolism of hemorrhagic-shocked rats were examined. Effects of the compound on rat mitochondrial respiration and regional blood flow in hemorrhagic-shocked rats were also studied to clarify the mechanisms of the antishock effects. Intravenous infusion of M6434 (3 or 10 micrograms/kg/min) prolonged the survival time of hemorrhagic-shocked rats. M6434 at 10 micrograms/kg/min significantly suppressed the decline of adenosine triphosphate contents and energy charge of the liver, shifted the blood flow distribution from skin and skeletal muscles to vital organs such as the liver and the heart, and also increased cardiac output in hemorrhagic-shocked rats. The mitochondrial respiration was unaffected by M6434 in vitro (10(-6)-10(-5) M). These data suggest that mechanisms of the beneficial effect of M6434 in hemorrhagic-shocked rats may not be based on the direct activation of energy metabolism, but rather on the redistribution of organ blood flow as well as an increase in cardiac output.

Animals↗

PubMedDate not supplied

Determination of enalapril and its active metabolite enalaprilat in plasma and urine by gas chromatography/mass spectrometry.

The method for the simultaneous determination of angiotensin-converting enzyme (ACE) inhibitor enalapril and its active metabolite enalaprilat in plasma and urine was developed by gas chromatography/mass spectrometry. Enalapril and enalaprilat in plasma and urine were extracted and cleaned up by using Sep-Pak C18 and silica cartridges. Derivatization was carried out using diazomethane and trifluoroacetic anhydride. Detection by selected ion monitoring was selected to m/z 288 (enalaprilat) and 302 (enalapril). The detection limit of enalapril and enalaprilat was 200 pg/mL in plasma and 2 ng/mL in urine. This method was applied to the pharmacokinetic analysis of enalapril and enalaprilat in body fluids.

Enalapril↗

PubMedDate not supplied

Apparent mineralocorticoid excess syndromes.

Apparent mineralocorticoid excess (AME) is a syndrome attributable to congenital deficiency of the enzyme 11 beta-dehydrogenase (11 beta-OHSD) which converts active glucocorticoid cortisol to inactive cortisone. When 11 beta-OHSD activity is impaired, cortisol acts as a potent mineralocorticoid and causes hypertension and hypokalemia with a suppression of the renin-angiotensin-aldosterone system. The increased ratio of urinary cortisol/cortisone metabolites and a prolonged half-life of cortisol are useful for the diagnosis. Dexamethasone and/or potassium sparing diuretics have been used for medication of AME. Licorice ingestion induces a mineralocorticoid excess state, and it seems that this is the result of acquired inhibition of 11 beta-DH by glycyrrhetinic acid. The existence of a second 11 beta-OHSD isoform has been suggested strongly for a long time, and recently, a human 11 beta-OHSD 2 cDNA has been isolated. It appears that 11 beta-OHSD 2 conveys specificity upon the renal MR, and a defect in its activity seems likely to account for the phenotype of AME.

11-beta-Hydroxysteroid Dehydrogenases↗