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 |
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Sprache: | eng |
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Zusammenfassung: | 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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ISSN: | 0363-6119 1522-1490 |
DOI: | 10.1152/ajpregu.2001.281.3.r747 |