| 1. |
- Koskinen, Lars-Owe D., Professor, 1955-
(författare)
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Effects of TRH on cerebral and peripheral blood flows : role of submesencephalic brain stem centres
- 1986
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 128:2, s. 277-288
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Tidskriftsartikel (refereegranskat)abstract
- The localization of the origin of the cardiovascular effects elicited by thyrotropin-releasing hormone (TRH) was attempted in this study. The radioactively labelled microsphere method was employed for measurement of regional cerebral (rCBF) and peripheral blood flow in albino rabbits anaesthetized with urethane. The effect of 50 micrograms and 2 mg kg-1 TRH (administered i.v.) on rCBF and peripheral blood flow was evaluated in animals with the brain stem sectioned (BSS) at the level of pons-mesencephalon. The cerebral vasodilating effect of TRH was abolished or attenuated, while the peripheral vasoconstriction and increase in mean arterial blood pressure (MAP) was unaffected. Cordotomy at the CI level caused a marked fall in MAP and abolished the pressor response to TRH. In animals infused with angiotensin II, in order to normalize the decreased MAP after cordotomy, TRH caused a marked increase in rCBF. Administration of 50 ng and 5 micrograms TRH into the fourth ventricle caused a marked peripheral vasoconstriction and pressor response. The same amounts of TRH administered into the mesencephalic aqueduct caused a marked increase in rCBF and peripheral vasoconstriction. The results indicate that TRH elicits the pressor and peripheral vasoconstrictor responses from a submesencephalic brain stem region. The increase in rCBF caused by TRH is probably mediated by a somewhat higher submesencephalic level.
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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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Regional glucose metabolism in the rabbit brain in control and TRH-treated animals
- 1986
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Ingår i: Acta Physiologica Scandinavica. - : Wiley-Blackwell. - 0001-6772 .- 1365-201X. ; 126:3, s. 349-353
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Tidskriftsartikel (refereegranskat)abstract
- The local cerebral metabolism in urethane anaesthetized control and TRH-treated rabbits was studied with the [14C]2-deoxyglucose method. In the controls, the glucose use was found to be highest in regions known to have a high blood flow and low in regions with low flow. The glucose consumption was, calculated using the constants found by Kennedy et al. in monkeys, 23.5 +/- 6.0 mumol 100 g-1 min-1 in parietal cortex. The TRH was infused at a dose of 0.06 mg kg-1 min-1 which is known to cause vasodilation in the brain. No marked influence of the peptide on the glucose use was detected. It was concluded that the previously reported cerebral vasodilation caused by TRH is not due to an increase in cerebral metabolism.
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| 4. |
- Koskinen, Lars-Owe D., Professor, 1955-
(författare)
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The influence of muscarinic and prostaglandic mechanisms on regional cerebral and peripheral blood flows and on the vascular effects of thyrotropin releasing hormone (TRH).
- 1994
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 152:4, s. 399-406
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Tidskriftsartikel (refereegranskat)abstract
- TRH has pronounced vascular effects. The final transmitter mechanisms of these effects are not fully understood. The present study was conducted in order to elucidate whether these effects are mediated by prostaglandic or muscarinic mechanisms. Muscarinic blockade augmented the vasoconstricting- and pressor effect of TRH; vasodilation in the brain was attenuated only in the caudate nucleus. Indomethacin provoked a decrease in regional cerebral blood flow and in the gastric mucosal blood flow. No effect of indomethacin was observed on the vascular effects of TRH. It is concluded that the cerebral vasodilating and peripheral vasoconstricting effects of TRH are not mediated by prostaglandins. Muscarinic mechanisms are involved in the vasodilating effect of TRH only in the caudate nucleus.
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| 5. |
- 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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| 6. |
- Seligsohn, E. E., et al.
(författare)
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Effects of alpha 2-adrenoceptor blockade and thyrotropin-releasing hormone (TRH) on the cardiovascular system in the rabbit.
- 1991
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 143:2, s. 187-194
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Tidskriftsartikel (refereegranskat)abstract
- The effects of two different doses of thyrotropin-releasing hormone on regional blood flows were studied in urethane-anaesthetized rabbits pretreated with the alpha 2-adrenergic antagonists yohimbine and idazoxan. The effects of yohimbine were also studied using unanaesthetized rabbits. Blood flow measurements were performed using the tracer microsphere method. Thyrotropin-releasing hormone was injected i.v. at a dose of either 0.1 mg kg-1 or 2.0 mg kg-1. Yohimbine and idazoxan did not modify the effect of thyrotropin-releasing hormone on mean arterial blood pressure. In the anaesthetized animals, blockade of the alpha 2-adrenoceptors resulted in a vasoconstriction in several peripheral organs and the vasoconstriction increased after thyrotropin-releasing hormone administration. Pretreament with yohimbine reduced total cerebral blood flow moderately and in such animals thyrotropin-releasing hormone elicited only minor cerebral blood flow effects. Pretreatment with idazoxan did not reduce the total cerebral blood flow and in such animals it increased from 53 +/- 1 to 75 +/- 4 g min-1 100 g-1 (P less than 0.01) after the administration of the lower dose of thyrotropin-releasing hormone and from 64 +/- 5 to 112 +/- 17 g min-1 100 g-1 (P less than 0.01) after the higher dose. In the conscious animals, yohimbine caused an increase in mean arterial blood pressure and heart rate. Vascular resistance increased in several organs. The cerebral blood flow decreased in white matter (P less than 0.05) and the caudate nucleus (P less than 0.05). The results indicate that there is a yohimbine-sensitive mechanism involved in the cerebrovasodilating effect of thyrotropin-releasing hormone in anaesthetized rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
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