Evidence that hemorrhagic hypotension is mediated by the ventrolateral periaqueductal gray region

Department of Basic and Pharmaceutical Sciences, Albany College of Pharmacy, Albany, New York 12208 Severe hemorrhage lowers arterial pressure by suppressing sympathetic activity. This study tested the hypothesis that the decompensatory phase of hemorrhage is mediated by the ventrolateral periaquedu...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2001-09, Vol.281 (3), p.747-R752
Hauptverfasser: Cavun, Sinan, Millington, William R
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container_title American journal of physiology. Regulatory, integrative and comparative physiology
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Millington, William R
description Department of Basic and Pharmaceutical Sciences, Albany College of Pharmacy, Albany, New York 12208 Severe hemorrhage lowers arterial pressure by suppressing sympathetic activity. This study tested the hypothesis that the decompensatory phase of hemorrhage is mediated by the ventrolateral periaqueductal gray (vlPAG), a region importantly involved in the autonomic and behavioral responses to stress and trauma. Neuronal activity in the vlPAG was inhibited with either lidocaine or cobalt chloride 5 min before hemorrhage (2.5 ml/100 g body wt) was initiated in conscious, unrestrained rats. Bilateral injection of lidocaine (0.5 µl of a 2% or 1 µl of a 5% solution) into the caudal vlPAG delayed the onset and reduced the magnitude of the hypotension produced by hemorrhage significantly. In contrast, inactivation of the dorsolateral PAG with lidocaine was ineffective. Cobalt chloride (5 mM; 0.5 µl), which inhibits synaptic transmission but not axonal conductance, also attenuated hemorrhagic hypotension significantly. Microinjection of lidocaine or cobalt chloride into the vlPAG of normotensive, nonhemorrhaged rats did not influence cardiovascular function. These data indicate that the vlPAG plays an important role in the response to hemorrhage. hemorrhage; cardiovascular regulation; lidocaine; cobalt
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In contrast, inactivation of the dorsolateral PAG with lidocaine was ineffective. Cobalt chloride (5 mM; 0.5 µl), which inhibits synaptic transmission but not axonal conductance, also attenuated hemorrhagic hypotension significantly. Microinjection of lidocaine or cobalt chloride into the vlPAG of normotensive, nonhemorrhaged rats did not influence cardiovascular function. 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Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cavun, Sinan</au><au>Millington, William R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence that hemorrhagic hypotension is mediated by the ventrolateral periaqueductal gray region</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2001-09-01</date><risdate>2001</risdate><volume>281</volume><issue>3</issue><spage>747</spage><epage>R752</epage><pages>747-R752</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><abstract>Department of Basic and Pharmaceutical Sciences, Albany College of Pharmacy, Albany, New York 12208 Severe hemorrhage lowers arterial pressure by suppressing sympathetic activity. This study tested the hypothesis that the decompensatory phase of hemorrhage is mediated by the ventrolateral periaqueductal gray (vlPAG), a region importantly involved in the autonomic and behavioral responses to stress and trauma. Neuronal activity in the vlPAG was inhibited with either lidocaine or cobalt chloride 5 min before hemorrhage (2.5 ml/100 g body wt) was initiated in conscious, unrestrained rats. Bilateral injection of lidocaine (0.5 µl of a 2% or 1 µl of a 5% solution) into the caudal vlPAG delayed the onset and reduced the magnitude of the hypotension produced by hemorrhage significantly. In contrast, inactivation of the dorsolateral PAG with lidocaine was ineffective. Cobalt chloride (5 mM; 0.5 µl), which inhibits synaptic transmission but not axonal conductance, also attenuated hemorrhagic hypotension significantly. Microinjection of lidocaine or cobalt chloride into the vlPAG of normotensive, nonhemorrhaged rats did not influence cardiovascular function. These data indicate that the vlPAG plays an important role in the response to hemorrhage. hemorrhage; cardiovascular regulation; lidocaine; cobalt</abstract><cop>United States</cop><pmid>11506988</pmid><doi>10.1152/ajpregu.2001.281.3.r747</doi></addata></record>
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subjects Animals
Blood Pressure - drug effects
Blood Pressure - physiology
Cobalt - administration & dosage
Heart Rate - drug effects
Heart Rate - physiology
Hemorrhage - complications
Hemorrhage - physiopathology
Hypotension - etiology
Hypotension - physiopathology
Hypotension - prevention & control
Lidocaine - administration & dosage
Male
Microinjections
Periaqueductal Gray - drug effects
Periaqueductal Gray - physiopathology
Rats
Synaptic Transmission - drug effects
Wakefulness - physiology
title Evidence that hemorrhagic hypotension is mediated by the ventrolateral periaqueductal gray region
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