Search PubMed⌕ Search

Biomedical subjects

Y Kurogochi

Publications and source records attributed to Y Kurogochi.

28 records · Page 2Linked to original sources
PubMed1982

Heterogeneity of hepatic nicotine oxidase.

When rats were pretreated with 3-methylcholanthrene of beta-naphthoflavone, hepatic nicotine oxidase activity per cytochrome P-448 molecule decreased, but the specific activity of the enzyme remained unchanged. After phenobarbital pretreatment, the specific activity of nicotine oxidase increased while the activity of the enzyme per cytochrome P-450 molecule decreased. alpha-Naphthoflavone selectively inhibited the activities of phenobarbital-induced nicotine oxidase and constitutive form(s) of the enzyme. These results show that phenobarbital-induced cytochrome P-450 and constitutive form(s) of the enzyme may be active in hepatic nicotine oxidation.

Animals↗
PubMed1982

Hyperkalemia, hyperglycemia, and plasma levels of cyclic AMP and cyclic GMP induced by portal vein injection of cyclic nucleotides and their butyryl derivatives into dogs.

The levels of serum potassium, blood glucose, and plasma adenosine cyclic 3':5'-monophosphate (cAMP) and guanosine cyclic 3':5'-monophosphate (cGMP) were studied after the portal vein injection of cyclic nucleotides and their derivatives, (cAMP, cGMP, N6, O2'-dibutyryl adenosine 3':5'-monophosphate (DBcAMP), N6-monobutyryl adenosine cyclic 3':5'-monophosphate (NMBcAMP), and O2'-monobutyryl adenosine cyclic 3':5'-monophosphate (OMBcAMP), into dogs. Dose-related hyperglycemic responses were observed after the injection of DBcAMP (1-8 mg/kg). Transient and prominent hyperkalemia and hyperglycemia were caused by the injection of DBcAMP, NMBcAMP, and OMBcAMP (4 mg/kg). The hyperkalemic response was highest with NMBcAMP (1.22 mequiv./L), followed by OMBcAMP (0.64), DBcAMP (0.54), cGMP (0.47), and cAMP (0.41), whereas the hyperglycemic response was highest with NMBcAMP (146 mg/100 mL), followed by DBcAMP (93.6), OMBcAMP (77.1), and cAMP (56.0), and there was only a slight change with cGMP (28.4) compared with the control. The plasma level of cAMP was maximal with DBcAMP (1.92 nmol/mL), followed by NMBcAMP (1.28) and OMBcAMP (0.76), whereas the plasma levels of cGMP showed no evident change, except that caused by DBcAMP (0.27). Of the cyclic nucleotides tested, NMBcAMP was found to be most potent in causing both hyperkalemia and hyperglycemia. Based on these results, possible correlations between hyperkalemia, hyperglycemia, and plasma levels of cAMP and cGMP are discussed.

Animals↗
PubMed1980

Effects of hexose infusion with insulin and of additional epinephrtine injection on the levels of serum potassium and blood glucose in dogs.

The hypokalemic response was roughly proportional to the dose of insulin. The hypokalemia due to adding insulin to galactose or fructose loading was slightly greater than that with insulin and glucose or mannose loading, suggesting a hexose stereospecificity of the response. When epinephrine (13.6 nmol/kg, i.v.) was given after one of the hexoses plus insulin, the hyperkalemia with glucose and galactose was 2.5-3 mEq/l, about twice that due to fructose or mannose. The hyperglycemia was about 2 mmol/l for glucose, 1 mmol/l for galactose, mannose, fructose, and ouabain with glucose, and 0.25 mmol/l for phloridzin with glucose. Addition of epinephrine, isoproterenol, and cAMP caused a significant depression of Na+,K+-ATPase activity in rat liver (P < 0.01) but the addition of insulin did not. These results show that there was a relation between the levels of blood glucose and serum potassium after an insulin-containing hexose infusion and that membrane permeability was stereospecific.

Animals↗