Cerebral and peripheral blood flow effects of TRH in the rat—A role of vagal nerves

Koskinen, Lars-Owe D.

doi:10.1016/0196-9781(89)90171-x

Cited by 21 publications

(12 citation statements)

References 31 publications

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“…TRH has been shown to cause a cerebral vasodilatation in various species (Koskinen, 1989;Hugoson-Seligsohn & Koskinen, 1989;Seligsohn, 1992c). The cerebrovasodilator effect of the peptide does not seem to be due to an increase in cerebral metabolism (Koskinen & Bill, 1984;Koskinen & Sperber, 1986;Hugoson-Seligsohn & Koskinen, 1989).…”

Section: Effects Of L-name and Trh In The Brainmentioning

confidence: 99%

Effects of N^G‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Seligsohn

Bill

1993

British J Pharmacology

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1 The effects of 300 mg kg-' of the nitric oxide (NO) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on the regional blood flow, on the flow response to 1 mg kg-' of thyrotropin-releasing hormone (TRH) and on cerebral blood flow autoregulation were studied in urethane anaesthetized rabbits subjected to unilateral sectioning of the cervical sympathetic chain. The blood flow measurements were performed by the tracer microspheres method. 2 The cerebral arteriovenous difference in oxygen saturation (CAVOD) was measured before and after the administration of L-NAME and TRH in order to ascertain whether the effects on cerebral blood flow that were observed were secondary to changes in cerebral metabolism. 3 L-NAME caused a significant decrease in blood flow in several cerebral regions; CBF,O, decreased to 72 ± 4% of control (P < 0.001). An increase in blood pressure and a concurrent decrease in heart rate and cardiac output were noted. 4 In the eye, L-NAME caused a reduction in uveal blood flow which was more pronounced on the sympathetically intact side; in the retina the blood flow decreased to 50% of control on both sides. 5 The administration of TRH in animals pretreated with L-NAME caused a significant increase in blood pressure and cerebral blood flow. 6 In L-NAME-treated animals the CBF was not affected when the mean arterial blood pressure was increased by ligation of the abdominal aorta. 7 The CAVOD increased from 56.0 ± 5.2 to 73.6 ± 3.5%, 20 min after the administration of L-NAME.In animals given 1 mg kg-' TRH after L-NAME the CAVOD decreased to 54.6 ± 4.6%, 5 min after the injection of TRH. 8 The results of the present study indicate that endogenous NO is involved in the regulation of regional blood flow and blood pressure in the anaesthetized rabbit. The reduction in cerebral blood flow that was caused by L-NAME was not due to a reduction in cerebral metabolism. An interaction between the NO synthesis/release/effect and the sympathetic nervous system was found in the uvea. There was no evidence for a major involvement of NO in the cardiovascular responses to TRH and autoregulation of cerebral blood flow was not abolished by L-NAME.

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Section: Effects Of L-name and Trh In The Brainmentioning

confidence: 99%

Effects of N^G‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Seligsohn

Bill

1993

British J Pharmacology

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“…Various tissues were autopsied and the radioactivity determined by gamma spectrometry. Blood flows were calculated as previously described (18).…”

Section: Methodsmentioning

confidence: 99%

“…The microsphere method was employed to measure regional blood flow (18 , where MAP (kPa) was measured during the microsphere injection and Q t = tissue blood flow (g min -1 per g tissue). In order to evaluate whether the changes in blood flow represent vasodilation or vasoconstriction the relative change in vascular resistance as the ratio between the changes in tissue vascular resistance at 0 and 5 minutes after soman intoxication was calculated.…”

Section: Blood-flow Measurementmentioning

confidence: 99%

Nimodipine Affects the Microcirculation and Modulates the Vascular Effects of Acetylcholinesterase Inhibition

Karlsson

Koch

Koskinen

2003

Upsala Journal of Medical Sciences

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The present investigation was undertaken in order to study whether microvascular effects of the calcium antagonist nimodipine induces changes that can explain an increased detoxification of the highly toxic cholinesterase inhibitor soman. Anaesthetised, tracheotomised and artificially ventilated rats were treated intra-peritoneally (ip) with nimodipine, 10 mg kg -1 or vehicle followed one hour later by the exposure to 45 µg kg -1 soman (iv). Nimodipine per se induced a vasodilation in the intestine, myocardium and other muscles. In the abdominal skin soman elicited a significant vasoconstriction that was turned into an increased blood flow after nimodipine pre-treatment. A slight vasoconstriction in diaphragm of soman intoxicated rats was turned into a significant vasodilation by nimodipine pre-treatment. In the intestinal parts no effect of soman was detected. However, in nimodipine pretreated animals soman induced a significant vasoconstriction. The capacity of soman detoxifying processes, i.e. enzymatic hydrolysis and covalent binding to different esterases, is unequally distributed throughout the body.Together with the knowledge of the detoxifying processes of cholinesterase inhibition the results support our theory, that nimodipine alters the peripheral blood flow in a beneficial way resulting in improved detoxification ability.

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“…and 1 h prior to killing on day 18. The dose of TRH to be administered was based on similar studies in the pregnant rat and rabbit and several studies in adult nonpregnant animals [3,16,[24][25][26], Pregnant mice were weighed and then killed with i.p. pentobarbitone (100 mg/kg).…”

Section: Animal Care and Euthanasiamentioning

confidence: 99%

Fetal Mouse Lung Ultrastructural Maturation Is Accelerated by Maternal Thyrotropin-Releasing Hormone Treatment

et al. 1996

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Maternal administration of thyrotropin-releasing hormone, alone or in combination with corticosteroid, accelerates functional, morphologic and biochemical fetal lung maturation. However, the dose-response relationship of maternal thyrotropin-releasing hormone treatment and acceleration of fetal lung ultrastructural maturation or disaturated phosphatidylcholine content has not been investigated. We administered (i.p.) saline or thyrotropin-releasing hormone (0.2, 0.4 or 0.6 mg/kg/dose) to the pregnant Balb/c mouse on days 16 and 17 (b.i.d.) and on day 18 of gestation (1 h prior to killing). Morphometric ultrastructural analysis and quantitation of disaturated phosphatidylcholine content was done on the 18-day gestation fetal lung. Maternal thyrotropin-releasing hormone treatment resulted in an increase in the number of lamellar bodies and depletion of glycogen in fetal lung type II cells, and an increase in the lung airspace to parenchymal ratio. In addition, a striking difference in the pattern of lung growth was noted in the thyrotropin-releasing-hormone-treated (0.4 and 0.6 mg/kg/dose) groups. These lungs had larger air spaces, thinner alveolar septae and more air-blood barriers. Maternal thyrotropin-releasing hormone treatment did not influence fetal lung disaturated phosphatidylcholine content. We conclude that in the mouse, maternal thyrotropin-releasing hormone treatment enhances fetal lung structural maturation and propose that thyrotropin-releasing hormone plays a role in mammalian fetal lung growth.

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Cerebral and peripheral blood flow effects of TRH in the rat—A role of vagal nerves

Cited by 21 publications

References 31 publications

Effects of N^G‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Effects of N^G‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Nimodipine Affects the Microcirculation and Modulates the Vascular Effects of Acetylcholinesterase Inhibition

Fetal Mouse Lung Ultrastructural Maturation Is Accelerated by Maternal Thyrotropin-Releasing Hormone Treatment

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Cerebral and peripheral blood flow effects of TRH in the rat—A role of vagal nerves

Cited by 21 publications

References 31 publications

Effects of NG‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Effects of NG‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Nimodipine Affects the Microcirculation and Modulates the Vascular Effects of Acetylcholinesterase Inhibition

Fetal Mouse Lung Ultrastructural Maturation Is Accelerated by Maternal Thyrotropin-Releasing Hormone Treatment

Contact Info

Product

Resources

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Effects of N^G‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

Effects of N^G‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone