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Biomedical subjects

M Honma

Publications and source records attributed to M Honma.

At least 181 records · Page 10Linked to original sources
PubMed1981

Role of chemosensitivity during exercise in normal subjects and patients with pulmonary emphysema.

In 11 normal subjects (mean age = 22.8 years) and 8 patients with pulmonary emphysema (mean age = 70.4 years), the role of chemosensitivity in determining ventilation, cardiac output, lactic acid, and cyclic AMP and GMP was evaluated quantitatively during 150 or 30 W exercise and simulated exercise. Simulated exercise was done while the subjects took a rest by regulating arterial blood gases at exercise levels in patients and at PaO2 = 65 mm Hg and PaCO2 = 48 mm Hg in normal subjects. In normal subjects, the role of arterial blood gases in determining exercise ventilation, cardiac output, cyclic AMP and GMP are large, while those contributed much less to lactic acid. In patients, PaO2 contributed only half of the exercise ventilation. It accounted for a negligibly small portion of exercise cardiac output, lactic acid, and cyclic GMP. These results indicate, by deduction, that either augmentation of chemosensitivity, pH, or humoral factors is responsible for about half of the changes of exercise ventilation in patients with pulmonary emphysema. These factors seem to influence cardiac output, lactic acid, and cyclic AMP and GMP more strongly than PaO2 alone in exercising patients.

Adult↗
PubMed1981

Plasma cyclic AMP hyper-response to glucagon in manic patients on lithium treatment.

We have measured the rise in plasma cyclic AMP induced by glucagon and adrenaline in manic patients on lithium therapy. Glucagon-induced increases in the concentration of plasma cyclic AMP were larger, but the adrenaline-induced increases were smaller, in lithium-treated manic patients than in normal controls. In 3 manic patients, the enhanced response to glucagon was normalized 3 weeks after the cessation of lithium treatment. Though the underlying mechanism is unknown, the unusual plasma cyclic AMP responses may reflect altered receptor sensitivity which would be closely related to the curative effect of lithium on symptoms of mania.

Adult↗
PubMed1980

Anomalous plasma cyclic AMP responses to glucagon in patients with liver disease.

The purpose of the present study is to show anomalies of the plasma cAMP response of patients with hepatic disorders to a single injection of a low dose of glucagon (1 microgram/kg body wt). The response was markedly blunted in patients with liver cirrhosis and potentiated in patients with acute or chronic hepatitis. This glucagon test is, therefore, promising for development as a simple diagnostic means without undertaking liver biopsy to distinguish cirrhosis from chronic hepatitis.

Adult↗
PubMed1980

Changes in plasma cyclic nucleotides levels during various acute physical stresses.

Studies were performed with healthy volunteers to determine the effects of various stresses known to increase sympathetic nerve activity on the plasma concentration of cyclic AMP and cyclic GMP. Plasma cyclic AMP rose promptly in response to exercise; the elevation was completely abolished by a simultaneous injection of propranolol. Plasma cyclic GMP rose slightly after exercise; the elevation was completely abolished by a simultaneous injection of atropine. No significant changes occurred during tilting and cold pressor stress. The increase in plasma concentrations of cyclic AMP and cyclic GMP may serve as putative indices for beta-adrenergic, and cholinergic functions respectively during exercise of humans.

Adolescent↗
PubMed1980

Plasma cyclic nucleotide responses to insulin-induced hypoglycaemia and methacholine in patients with hyperthyroidism.

The effect of insulin-induced hypoglycaemia and methacholine on plasma cAMP and cGMP levels was studied in normal volunteers, hyperthyroid and hypothyroid patients. A significant positive correlation existed between the maximal increase in plasma cAMP and the maximal decrease in plasma glucose in normals during insulin-induced hypoglycaemia. Therefore, the plasma cAMP response is considered to be dependent on the degree of hypoglycaemia, rather than the dose of insulin. The cAMP response to hypoglycaemia was significantly higher in hyperthyroid patient, and was lower in patients with hypothyroidism than in normals. The cAMP response of the hyperthyroid patients was normalized when their hyperthyroidism was controlled after 3 months of treatment. The plasma level of cGMP was slightly elevated during hypoglycaemia, but there was no significant difference between controls and hyperthyroid patients. The cGMP response to methacholine, which is probably mediated by cholinergic receptors, was significantly potentiated in hyperthyroid patients. The cAMP response, which is presumably dependent on endogenous catecholamines secreted during methacholine-induced hypotension, was also enhanced in hyperthyroid patients. It is likely that beta-adrenergic receptor responses and cholinergic receptor responses are both enhanced in hyperthyroidism.

Adolescent↗
PubMed1979

Metabolic acidosis in patients receiving anticonvulsants.

Blood pH, bicarbonate, PCO2, serum calcium, alkaline phosphatase and red cell carbonic anhydrase were measured in 37 selected patients receiving anticonvulsants. Patients with metabolic acidosis showed a high incidence of hypocalcemia with increased alkaline phosphatase and a significant reduction of carbonic anhydrase-B activity. High iPTH levels were found in 13 patients, but this was not correlated with acid-base balance status. Anticonvulsant drugs seemed to inactive carbonic anhydrase-B activity. Metabolic acidosis might be one of the factors causing a disturbance of calcium metabolism in these patients.

Acidosis↗
PubMed1978

Increases in plasma cyclic AMP dependent on endogenous catecholamines.

Administration of tyramine (with or without phentolamine) as well as induction of ether anesthesia or insulin hypoglycemia caused a sharp increase in plasma cyclic AMP in rats. Based on the findings that the treatment of rats with reserpine, 6-hydroxydopamine, cocaine or propranolol totally abolished tyramine-induced increases in plasma cyclic AMP, it was concluded that catecholamines released from sympathetic neuronal terminals by tyramine could activate adenylate cyclase via the stimulation of postsynaptic beta-adrenoceptors. In contrast, catecholamines secreted from adrenal medulla were largely responsible for the increase in plasma cyclic AMP induced by ether anesthesia; whereas glucagon, in addition to adrenal catecholamines, played a significant role in hypoglycemia-induced increases in plasma cyclic AMP. Assay of plasma cyclic AMP following these stimuli is very promising as a test for adrenergic activities in experimental and clinical studies.

Animals↗