Responses of cerebral arterioles during chronic ethanol exposure

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Abstract

The purpose of this study was to examine the effects of ethanol exposure on responses of cerebral arterioles in vivo. Rats were fed liquid diets with or without ethanol for 2-3 mo. Using intravital microscopy, we measured diameter of cerebral arterioles in non-ethanol- and ethanol-fed rats in response to acetylcholine, histamine, ADP, the thromboxane analogue (U- 46619), and nitroglycerin. In non-ethanol-fed rats, acetylcholine, histamine, and ADP produced dose-related dilatation of cerebral arterioles. In ethanol- fed rats, however, acetylcholine produced vasoconstriction, and vasodilatation in response to histamine and ADP was impaired. Dilatation of cerebral arterioles in response to nitroglycerin and vasoconstriction in response to the thromboxane analogue (U-46619) were similar in non-ethanol- fed and ethanol-fed rats. Thus these findings suggest that chronic ethanol exposure impairs responses of cerebral arterioles to agonists, which produce dilatation via the release of an endothelium-derived relaxing factor. We speculate that impaired vasodilatation coupled with preservation of vasoconstriction in ethanol-fed rats may have important implications for the pathogenesis of stroke during chronic alcohol ingestion.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume262
Issue number3 31-3
StatePublished - 1992

Fingerprint

Arterioles
Ethanol
Vasoconstriction
Adenosine Diphosphate
Histamine
Acetylcholine
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Dilatation
Thromboxanes
Nitroglycerin
Vasodilation
Endothelium-Dependent Relaxing Factors
Eating
Stroke
Alcohols
Diet

Keywords

  • acetylcholine
  • adenosine 5'-diphosphate
  • alcoholism
  • brain
  • histamine
  • nitroglycerin
  • rats
  • stroke

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Responses of cerebral arterioles during chronic ethanol exposure",
abstract = "The purpose of this study was to examine the effects of ethanol exposure on responses of cerebral arterioles in vivo. Rats were fed liquid diets with or without ethanol for 2-3 mo. Using intravital microscopy, we measured diameter of cerebral arterioles in non-ethanol- and ethanol-fed rats in response to acetylcholine, histamine, ADP, the thromboxane analogue (U- 46619), and nitroglycerin. In non-ethanol-fed rats, acetylcholine, histamine, and ADP produced dose-related dilatation of cerebral arterioles. In ethanol- fed rats, however, acetylcholine produced vasoconstriction, and vasodilatation in response to histamine and ADP was impaired. Dilatation of cerebral arterioles in response to nitroglycerin and vasoconstriction in response to the thromboxane analogue (U-46619) were similar in non-ethanol- fed and ethanol-fed rats. Thus these findings suggest that chronic ethanol exposure impairs responses of cerebral arterioles to agonists, which produce dilatation via the release of an endothelium-derived relaxing factor. We speculate that impaired vasodilatation coupled with preservation of vasoconstriction in ethanol-fed rats may have important implications for the pathogenesis of stroke during chronic alcohol ingestion.",
keywords = "acetylcholine, adenosine 5'-diphosphate, alcoholism, brain, histamine, nitroglycerin, rats, stroke",
author = "William Mayhan",
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T1 - Responses of cerebral arterioles during chronic ethanol exposure

AU - Mayhan, William

PY - 1992

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N2 - The purpose of this study was to examine the effects of ethanol exposure on responses of cerebral arterioles in vivo. Rats were fed liquid diets with or without ethanol for 2-3 mo. Using intravital microscopy, we measured diameter of cerebral arterioles in non-ethanol- and ethanol-fed rats in response to acetylcholine, histamine, ADP, the thromboxane analogue (U- 46619), and nitroglycerin. In non-ethanol-fed rats, acetylcholine, histamine, and ADP produced dose-related dilatation of cerebral arterioles. In ethanol- fed rats, however, acetylcholine produced vasoconstriction, and vasodilatation in response to histamine and ADP was impaired. Dilatation of cerebral arterioles in response to nitroglycerin and vasoconstriction in response to the thromboxane analogue (U-46619) were similar in non-ethanol- fed and ethanol-fed rats. Thus these findings suggest that chronic ethanol exposure impairs responses of cerebral arterioles to agonists, which produce dilatation via the release of an endothelium-derived relaxing factor. We speculate that impaired vasodilatation coupled with preservation of vasoconstriction in ethanol-fed rats may have important implications for the pathogenesis of stroke during chronic alcohol ingestion.

AB - The purpose of this study was to examine the effects of ethanol exposure on responses of cerebral arterioles in vivo. Rats were fed liquid diets with or without ethanol for 2-3 mo. Using intravital microscopy, we measured diameter of cerebral arterioles in non-ethanol- and ethanol-fed rats in response to acetylcholine, histamine, ADP, the thromboxane analogue (U- 46619), and nitroglycerin. In non-ethanol-fed rats, acetylcholine, histamine, and ADP produced dose-related dilatation of cerebral arterioles. In ethanol- fed rats, however, acetylcholine produced vasoconstriction, and vasodilatation in response to histamine and ADP was impaired. Dilatation of cerebral arterioles in response to nitroglycerin and vasoconstriction in response to the thromboxane analogue (U-46619) were similar in non-ethanol- fed and ethanol-fed rats. Thus these findings suggest that chronic ethanol exposure impairs responses of cerebral arterioles to agonists, which produce dilatation via the release of an endothelium-derived relaxing factor. We speculate that impaired vasodilatation coupled with preservation of vasoconstriction in ethanol-fed rats may have important implications for the pathogenesis of stroke during chronic alcohol ingestion.

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KW - adenosine 5'-diphosphate

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KW - brain

KW - histamine

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KW - stroke

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