Document Detail


Cerebral vasoconstriction during sustained ventricular tachycardia induces an ischemic stress response of brain tissue in rats.
MedLine Citation:
PMID:  9826520     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Arterial hypotension can cause cerebral ischemia when the autoregulation of the cerebral circulation is exhausted. We hypothesized that sudden cerebral vasoconstriction induced by moderate hypotensive, but hemodynamically stable, sustained ventricular tachycardias (MHT-VT) further compromises cerebral blood flow (CBF) and induces an ischemic stress response of the brain. CBF-measurements and morphological studies were performed without and with blockade of alpha-adrenergic receptors in order to determine the impact of MHT-VF on brain perfusion and brain tissue. Using a model of MHT-VT, CBF was measured with colored microspheres in 71 rats during control conditions. after the onset of MHT-VT, after the onset of moderate hypotensive hypovolemia (MHH), and after additional non- selective (alpha-blockade with phentolamine and selective alpha1-blockade with prazosin, respectively (0.2-0.4 mg/kg body weight). Plasma catecholamine concentrations were measured in 18 additional rats during control conditions. during MHT-VT and during MHH. The occurrence of heat shock protein (hsp) 72 and activated microglia in the brain was analysed in 18 additional rats in controls, after MHT-VT and MHH. After 20 min of the respective induced hypotension, control conditions were restored for a period of 8 h, by stopping VT or by infusion of isotonic saline solution. CBF was 0.98+/-0.16 (mean+/-S.D.) ml/g/min during control conditions at an arterial pressure of 118+/-13 mmHg, 0.50+/-0.05 ml/g/min (P<0.05 v control) during MHT-VT (76+/-4 mm Hg) and 0.75+/-0.14 ml/g/min (P<0.05 v control and v MHT-VT ) during MHH (71 +/- 8 mm Hg). CBF was better preserved with non-selective alpha-blockade during MHT-VT (0.78+/-0.15 ml/g/min, P<0.05 v MHT-VT and control) as well as with selective alpha1-blockade (0.67+/-0.08 ml/g/min, P<0.05 v MHT-VT and control). Plasma catecholamines were elevated during MHT-VT (P<0.05 v control) but not during MHH (P = N.S. v control). hsp 72 and activated microglia were found in hippocampal regions only after MHT-VT (P<0.05 v control and MHH). These morphological changes were prevented by non-selective alpha-blockade. Stable sustained MHT-VT further reduce the already compromised CBF leading to morphological alterations in the brain which are characteristic of an early ischemic stress response. alpha-Blockade prevents alpha1-adrenergic vasoconstriction and attenuates cerebral hypoperfusion.
Authors:
A Hagendorff; C Dettmers; P Danos; M Hümmelgen; C Vahlhaus; C Martin; G Heusch; B Lüderitz
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  30     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1998 Oct 
Date Detail:
Created Date:  1998-12-16     Completed Date:  1998-12-16     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2081-94     Citation Subset:  IM    
Affiliation:
Department of Cardiology, University of Bonn, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Antagonists / pharmacology
Animals
Brain / blood supply,  drug effects,  physiopathology*
Brain Ischemia / etiology,  pathology,  physiopathology*
Cerebrovascular Circulation / drug effects,  physiology*
Epinephrine / blood
Hemodynamics
Hippocampus / pathology
Hypotension / physiopathology
Male
Microglia / pathology
Norepinephrine / blood
Phentolamine / pharmacology
Prazosin / pharmacology
Rats
Rats, Sprague-Dawley
Regional Blood Flow
Stress, Physiological / etiology,  physiopathology*
Tachycardia, Ventricular / physiopathology*
Vasoconstriction
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Antagonists; 19216-56-9/Prazosin; 50-60-2/Phentolamine; 51-41-2/Norepinephrine; 51-43-4/Epinephrine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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