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- Björkman, Sven, et al.
(författare)
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Thermic and tremorogenic effects of thyroliberin (TRH) in reserpine-treated mice--the non-involvement of GABA-ergic mechanisms.
- 1981
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Ingår i: Journal of Pharmacy and Pharmacology (JPP). - : Oxford University Press (OUP). - 0022-3573 .- 2042-7158. ; 33:9, s. 580-585
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Tidskriftsartikel (refereegranskat)abstract
- Administration of thyroliberin (TRH) to reserpinized mice causes tremor and counteracts the hypothermia in a dose-dependent fashion. The thyroliberin response is inhibited by gamma-hydroxybutyric acid (GHB) and baclofen, but not by other, more specific GABA-ergic agents, such as THIP, gamma-acetylenic GABA, and sodium valproate. Picrotoxin neither potentiates nor inhibits the thyroliberin actions. Nor are the thyroliberin effects dependent on cholinergic, monoaminergic or histaminergic mechanisms. The results repudiate a current hypothesis, that the peptide actions may be mediated by GABA-ergic pathways in the brain.
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| 2. |
- Koskinen, Lars-Owe D., Professor, 1955-, et al.
(författare)
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Regional cerebral, ocular and peripheral vascular effects of naloxone and morphine in unanesthetized rabbits.
- 1983
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 119:3, s. 235-241
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Tidskriftsartikel (refereegranskat)abstract
- Effects of morphine and naloxone were investigated on cerebral, ocular and peripheral blood flow in unanesthetized rabbits. Blood flow measurements were performed with the labelled microsphere method. Cervical sympathotomy was performed on one side the day before the flow determination. Naloxone 2 mg/kg b.w. i.v. had no consistent effect on cerebral, ocular or peripheral blood flow or on mean arterial blood pressure. Morphine 2 mg/kg b.w. i.v. caused a rise in PaCO2 of 0.9 kPa and tended to increase cerebral blood flow in all parts investigated. In the hippocampal region, caudate nucleus and collicles the increase in flow was about 30% which is more than expected from the rise in PaCO2. Blood flow in the retina increased while the other parts of the eye showed no consistent changes in blood flow. Morphine reduced the blood flow in the duodenum by 60%. Mean arterial blood pressure did not change after morphine. No effect of the cervical sympathotomy was detected on cerebral or ocular blood flow before or after morphine or naloxone. Thus, we found no evidence for a tonically operating opioid system controlling cerebral, ocular or peripheral blood flow. However, exogenously administrated opiate can influence blood flows in these areas.
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| 3. |
- Koskinen, Lars-Owe D., Professor, 1955-, et al.
(författare)
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Thyrotropin-releasing hormone (TRH) causes sympathetic activation and cerebral vasodilation in the rabbit.
- 1984
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 122:2, s. 127-136
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Tidskriftsartikel (refereegranskat)abstract
- The effects of TRH on regional blood flow were studied in rabbits under urethane anesthesia. Four types of experiments were performed with the following results. (1) I.v. injection of 2 mg/kg b.w. TRH in animals with unilateral cervical sympathotomy caused a rise in mean arterial blood pressure from 10.0 +/- 0.5 to 13.3 +/- 0.5 kPa. Total cerebral blood flow, measured with labeled microspheres, increased from 75 +/- 5 to 126 +/- 16 g/min/100 g tissue on the intact side. There was a similar increase on the side with sympathotomy. The greatest increase, about 70%, was observed in cortical gray matter, caudate nucleus and thalamic region. There were marked reductions in blood flows in the spleen, gastric mucosa, skin and skeletal muscle. Mydriasis occurred on the side with an intact sympathetic supply. (2) I.v. infusion of 0.06 mg/kg b.w. per min TRH in animals with unilateral cervical sympathotomy and stabilized blood pressure increased total cerebral blood flow from 84 +/- 10 to 139 +/- 7 g/min/100 g. Blood flows to the masseter muscle, submandibular gland and facial skin but not to the eye or tongue were markedly reduced on the side with an intact sympathetic supply while little or no effect was observed on the side with sympathotomy. (3) Unilateral peripheral stimulation of the sympathetic chain at 1 Hz after bilateral sympathotomy caused a reduction in blood flows in the tongue, masseter muscle, submandibular gland and facial skin in animals with stabilized blood pressure. No potentiation of the stimulation effect was observed during TRH infusion. (4) The arteriovenous difference in oxygen saturation in the brain decreased from 39.1 +/- 2.8 to 26.4 +/- 3.7% after i.v. injection of 2 mg/kg b.w. TRH. The results indicate that TRH caused cerebral vasodilation in excess of that required by possible changes in cerebral metabolism. The vasoconstriction in the head region and the mydriasis was caused mainly by an increase in the activity of the cervical sympathetic nerves.
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