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A Saarinen

Publications and source records attributed to A Saarinen.

5 recordsLinked to original sources

Effect of a slow release preparation of levodopa on Parkinson's disease in combination with a peripheral decarboxylase inhibitor.

Plasma concentrations of levodopa were determined after therapeutic oral levodopa-carbidopa doses. The wide fluctuations observed in plasma levodopa levels could be considerably reduced by the addition of a slow release levodopa preparation. This kind of combination medication was given to 15 parkinsonian patients, whose earlier therapy had proved inadequate. With the combination medication, levodopa-carbidopa, on an average 420 mg/42 mg combined with 950 mg of levodopa in slow release form, a statistically significant improvement in parkinsonian signs could be achieved without any worsening of the side effects. The results suggest that parkinsonian patients may tolerate much higher daily levodopa doses if the fluctuations in plasma levels of the drug can be diminished.

Adult

UDPglucuronic acid pyrophosphatase assay with the aid of alkaline phosphatase.

A simple and sensitive method has been described for the determination of UDPglucuronic acid pyrophosphatase activity. Pyrophosphatase-free alkaline phosphatase preparation is added to the reaction mixture in order to hydrolyze the phosphate esters (UMP and alpha-D-glucuronic acid 1-phosphate) produced by pyrophosphatase. The inorganic phosphate liberated is measured by a modification of Fiske and SubbaRow's method. The phosphatase coupled method is time saving, easy to perform and accurate. It can also be used for pyrophosphatase assays with other nucleotide substrates like UDPglucose, UDP-N-acetylglucosamine, NAD+, NADH, NADP+ and NADPH.

Alkaline Phosphatase

[Bromocryptine].

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Acromegaly

Anesthetics and thyrotropin secretion in the rat.

The effects of seven anesthetics (thiopentone, 50 mg/kg ip; pentobarbitone, 50 mg/kg ip; chloral hydrate, 300 mg/kg ip; urethane, 1,5 g/kg, 1/2ip, 1/2sc; ether; methoxyflurane, 1,5%; halothane, 2%) on basal serum TSH concentrations and on the cold-induced as well as the TRH-induced TSH responses were studied in Sprague-Dawley rats. The basal TSH level in female rats were decreased by ether and halothane at 30 min and somewhat increased by pentobarbitone and chloral hydrate. The cold-induced (4C, 30-60 min) TSH response of the warm-adapted male rats (30 C, 7 days) was decreased by all of the anesthetics studied, but the effect of pentobarbitone was not significant. The TRH-induced (50 ng iv) TSH response in female rats was totally abolished only by deep ether anesthesia but augmented by bariturates and chloral hydrate. It is concluded that all of the anesthetics studied can modify the secretion of TSH by their central effects. Ether in high concentration seems to be effective also at the pituitary level. The use of anesthetics may be a source of error when studying the neurotransmitter control of TSH-TRH secretion in the rat.

Anesthetics

Neurotransmitter control of thyrotropin secretion in the rat.

In rats adapted to a +30 degrees C temperature for one week, transfer to a temperature of +4 degrees C increased immunoassay-able serum TSH from 150-300 ng/ml to 800-2000 ng/ml in 30 min. Since this response, as well as the level of serum TSH without stimulation, were decreased by reserpine, phentolamine, phenoxybenzamine, disulfiram and diethyldithiocarbamate, noradrenaline may be involved in the stimulation of TSH secretion. TRH-induced TSH increased was not blocked by reserpine. 1-Dopa, a noradrenaline precursor, decreased the TSH response to cold; alpha-methyl-p-tyrosine increased the TSH level. Apomorphine decreased the level of serum TSH and inhibited the response to cold. The possibility of a dopaminergic inhibitory factor released from the hypothalamus is discussed. 5-HT has possibly a role in the regulation of TSH secretion, since its precursor 5-HTP decreased the response to cold. No indication was found that acetylcholine is involved.

Acetylcholine