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Biomedical subjects

G A Glaubiger

Publications and source records attributed to G A Glaubiger.

5 recordsLinked to original sources
PubMed1976

Effect of a large dose of thyrotrophin releasing factor on pituitary and thyroid function in patients with Parkinsonism.

Thyrotrophin releasing factor (TRF) was given intravenously in doses of 0-5 mg and 20 mg to six patients with Parkinsonism treated with L-dopa. Plasma thyrotrophin (TSH), prolactin, lutenizing hormone (LH), follicle stimulating hormone (FSH), thyroxine (T4) and triiodothyronine (T3) were measured before and after TRF infusion. The observation that FSH and LH did not change in response to either dose of TRF confirmed specificity of the effects TRF for certain anterior pituitary functions. The plasma TSH and prolactin levels achieved after 20 mg TRF were considerably greater and were maintained longer than those after 0-5 mg TRF. However, despite a seven fold increase in the overall TSH response, the T4 and T3 responses to 20 mg TRF were not significantly greater than those to 0-5 mg TRF. The explanation for this discrepancy between immunoreactive TSH levels and apparent biologic effect is unclear.

Adult↗
PubMed1975

On-off response. Clinical and biochemical correlations during oral and intravenous levodopa administration in parkinsonian patients.

Seven parkinsonian patients who had severe on-off effects during chronic treatment with levodopa were studied. Marked swings in plasma dopa levels as well as in motor function followed each oral dose of levodopa. A constant intravenous infusion of levodopa resulted in stable plasma dopa concentrations and virtual disappearance of motor fluctuations. Notwithstanding steady plasma dopa levels, an abrupt decline in the antiparkinsonian response to levodopa attended postural tilting or cold pressore stimulation. Although these maneuvers were accompanied by a significant rise in plasma norepinephrine, the intravenous infusion of this catecholamine failed to influence the effect of levodopa on parkinsonian signs. The results suggest that central noradrenergic mechanisms as well as alterations in circulating dopa may contribute to the on-off response to levodopa.

Administration, Oral↗