Document Detail

Hypoxia-hypotension decreases pressor responsiveness to exogenous catecholamines after severe traumatic brain injury in rats.
MedLine Citation:
PMID:  11505138     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To quantify the phenylephrine pressor responsiveness after severe brain injury combined with hypoxia-hypotension, and to study the respective roles of brain injury and hypoxia-hypotension in the observed alteration. DESIGN: Randomized study. SETTING: Accredited animal laboratory. SUBJECTS: Adult Sprague Dawley rats. INTERVENTIONS: Anesthetized animals were assigned to control, brain injury, hypoxia-hypotension, and brain injury combined with hypoxia-hypotension groups. Brain injury was induced with an impact-acceleration device. During the 15-min hypoxia-hypotension, arterial oxygen pressure was decreased to 40 torr (5.3 kPa) and mean arterial pressure to 30 mm Hg. Thirty-six of the 53 included rats were alive at the end of hypoxia-hypotension (nine animals per group). In an additional group (Hypo, n = 8), mean arterial pressure was lowered to the level observed in brain injury combined with hypoxia-hypotension with pentobarbital infusion. Sixty minutes after injuries (T60), animals received 0.1, 1, and 10 microg/kg phenylephrine in a random order. Pressor responsiveness to phenylephrine was defined as maximal postinjection minus preinjection mean arterial pressure. MEASUREMENTS AND MAIN RESULTS: During hypoxia-hypotension, mortality was higher and residual restored blood volume was lower (p <.01) in the animals with brain injury and hypoxia-hypotension compared with hypoxia-hypotension alone. At T60, mean arterial pressure (mm Hg) was lower (p <.01) in the brain injury group (83 +/- 22) compared with controls (110 +/- 10) and in brain injury combined with hypoxia-hypotension (76 +/- 18) compared with controls and hypoxia-hypotension (107 +/- 14). Pressor responsiveness (mm Hg) to 1 and 10 microg/kg phenylephrine was less (p <.05) in brain injury combined with hypoxia-hypotension (15 +/- 6 and 44 +/- 8) and hypoxia-hypotension (15 +/- 3 and 44 +/- 8) compared with controls (26 +/- 2 and 57 +/- 11). No significant difference was observed for phenylephrine pressor responsiveness between controls and the Hypo group (25 +/- 5 and 66 +/- 7). CONCLUSIONS: Combination of brain injury and hypoxia-hypotension induces a severe hemodynamic alteration associated with a decreased pressor responsiveness to phenylephrine. Transient hypoxia-hypotension is responsible for the depressed alpha-1 adrenergic reactivity.
S Holtzer; B Vigué; C Ract; K Samii; P Escourrou
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Critical care medicine     Volume:  29     ISSN:  0090-3493     ISO Abbreviation:  Crit. Care Med.     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-08-15     Completed Date:  2001-09-06     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1609-14     Citation Subset:  AIM; IM    
Laboratoire de Physiologie (upress EA 2704), Université Paris-Sud, Faculté de médecine de Bicêtre, Le Kremlin Bicêtre, France.
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MeSH Terms
Adrenergic alpha-Agonists / pharmacology*,  therapeutic use
Blood Glucose
Brain Injuries / complications,  drug therapy*
Hemodynamics / drug effects
Hypotension / complications,  drug therapy*
Hypoxia, Brain / complications,  drug therapy*
Intracranial Pressure
Phenylephrine / pharmacology*,  therapeutic use
Pressoreceptors / drug effects*
Rats, Sprague-Dawley
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Blood Glucose; 59-42-7/Phenylephrine

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

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