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Biomedical subjects

A A Mathé

Publications and source records attributed to A A Mathé.

At least 91 records · Page 5Linked to original sources
PubMed1983

Effects of propantheline bromide on basal growth hormone, cortisol and prolactin levels.

Propantheline bromide, a peripheral anticholinergic drug with muscarinic and nicotinic blocking properties, was given by mouth to normal young men. Propantheline (45 mg) significantly lowered basal growth hormone concentrations at 0800 hr, 12 hr after administration. Propantheline (30 mg) tended (p = 0.08) to lower growth hormone concentrations at 1200 hr, 16 hr after administration. Cortisol and prolactin levels were not changed 12, 16 and 20 hr after propantheline (30 mg) nor 12 hr after propantheline (45 mg).

Adult↗
PubMed1981

Neuroendocrine and neurochemical measurements in depression.

The authors performed dexamethasone suppression tests (DST), TRH infusions, 72-hour urine collections, and lumbar punctures on a group of male depressed patients. Approximately 60% of the patients were DST positive and 33% had a blunted TSH response. Two biologic variables, the 8 a.m. postdexamethasone cortisol and the postprobenecid CSF 5-hydroxyindoleacetic acid (5-HIAA), accounted for over half of the variance in the behavioral measure, the Hamilton score. Plasma cortisol elevation was associated with high 3-methoxy-4-hydroxyphenyl glycol (MHPG) excretion; TSH blunting was associated with low urinary MHPG excretion. Comprehensive biologic measures showed certain significant interrelationships and correlations with the severity of depression.

Adult↗
PubMed1980

Increased content of immunoreactive prostaglandin E in cerebrospinal fluid of patients with schizophrenia.

Immunoreactive prostaglandin E (I-PGE) and thromboxane B2 (I-TxB2) were measured in cerebrospinal fluid from patients with schizophrenia and from control subjects. Schizophrenics had higher I-PGE concentrations than healthy controls, patients classified as neurotics, and patients admitted for neurological investigation. I-TxB2 concentrations were similar in all four groups. These preliminary results are consistent with the hypothesis that at least in some forms of schizophrenia there may be an alteration of PG synthesis or metabolism.

Adult↗
PubMed1980

Epinephrine dispositon in control and asthmatic subjects.

Epinephrine (Epi) disposition in the human body was investigated in asthmatic and control subjects. After intravenous infusion of labeled catecholamines, asthmatics excreted less label than controls but the ratio of unchanged to changed catecholamines was similar in both groups. Further studies investigated retention of Epi in the lung after a bolus injection of labeled Epi and inulin. While in the controls the apparent volume of distribution of Epi was larger than that of inulin, in asthmatics the volumes were similar. The distribution volumes of both Epi and inulin were larger in asthmatics than in controls and the mid-expiratory maximal flow correlated negatively with both volumes. The results indicate that disposition of Epi is altered in bronchial asthma and may be related to pathological processes in the lung.

Adult↗
PubMed1978

Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs.

Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.

Acetylcholine↗
PubMed1978

Effect of histamine on cyclic AMP levels in control and antigen-sensitized guinea pig lungs.

The effect of histamine on cyclic AMP was investigated in control and antigen-sensitized guinea pig lungs. Although histamine elevated the cyclic AMP levels in a dose-dependent manner in both groups, the response was consistently smaller in the sensitized lungs. In vivo pretreatment of control guinea pigs with histamine decreased the subsequent effect of exogenous histamine on cyclic AMP. Phosphodiesterase activity was not different in the two groups and it was not affected by histamine. These results indicate that the process of antigen sensitization results in an altered cyclic AMP response to histamine.

Animals↗
PubMed1978

Relationships among digital clubbing, disease severity, and serum prostaglandins F2alpha and E concentrations in cystic fibrosis patients.

Nine patients with cystic fibrosis but without digital clubbing (Group A) were matched, prospectively, by sex and approximate age to 9 cystic fibrosis patients with digital clubbing (Group B) and to 9 normal persons (control subjects). Patients in Group B had significantly (P less than 0.05) lower clinical scores and forced vital capacity than did those in Group A, indicating more severe pulmonary disease in the former; however, other spirometer tests of pulmonary function revealed no differences between Groups A and B. The degree of digital clubbing had significant (P less than 0.05) linear relationships to forced vital capacity (r = -0.73) and clinical scores (r = 0.853) for Groups A and B. Plasma concentrations of prostaglandins F2alpha and E were significantly increased (P less than 0.05) in both Group A (X +/- SE, 0.48 +/- 0.03 and 0.87 +/- 0.10 ng per ml, respectively) and Group B (X +/- SE, 0.68 +/- 0.04 and 1.81 +/- 0.16 ng per ml, respectively) compared to the control group (X +/- SE, 0.14 +/- 0.01 and 0.39 +/- 0.02 ng per ml, respectively). Group B had significantly larger concentrations than did Group A; however, plasma concentrations of prostaglandin 15-keto-13, 14-dihydro metabolite were not different in Groups A and B, and were significantly smaller than in the control group. These studies suggest that the degree of digital clubbing in cystic fibrosis is related to the severity of the pulmonary involvement and that the prostaglandin system may play an important role in this disease.

Adolescent↗