Document Detail


Cardiovascular responses to oxygen inhalation after hemorrhage in anesthetized rats: hyperoxic vasoconstriction.
MedLine Citation:
PMID:  17056674     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxygen inhalation is recommended for the initial care of trauma victims. The improved survival seen in early hemorrhage is normally associated with an increase in blood pressure. Although clinical use of oxygen can occur late after hemorrhage, the effects of late administration have not been specifically examined. Anesthetized rats were studied using an isobaric hemorrhage model with target pressures of either 70 or 40 mmHg. At various times after hemorrhage, the feedback control of the blood pressure was stopped and the inspired gas was changed from room air to 100% oxygen. The results show that shortly after hemorrhage to 70 mmHg, oxygen inhalation results in an increase in mean arterial blood pressure of 60 +/- 3 mmHg, which is associated with a large increase in total peripheral resistance from 0.89 +/- 0.05 to 1.25 +/- 0.1 peripheral resistance units. The blood pressure response is essentially unchanged with time, and it is not altered by a 10-min exposure to N(G)-nitro-l-arginine methyl ester. At a target pressure of 40 mmHg, the initial blood pressure response to oxygen is the same, but it gradually decreases as the animal develops a lactic acidosis. We conclude that the therapeutic value of oxygen needs to be separately evaluated for late hemorrhage.
Authors:
James L Atkins; Ken B Johnson; Frederick J Pearce
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2006-10-20
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  292     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-02-08     Completed Date:  2007-03-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H776-85     Citation Subset:  IM    
Affiliation:
Division of Military Casualty Research, Walter Reed Army Institute of Research, 503 Robert Grant Ave., Silver Spring, MD 20910, USA. james.atkins@na.amedd.army.mil
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MeSH Terms
Descriptor/Qualifier:
Acidosis, Lactic / chemically induced,  physiopathology
Administration, Inhalation
Animals
Blood Pressure / drug effects
Carbon Dioxide / blood
Cardiovascular System / drug effects*,  physiopathology
Disease Models, Animal
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
Hemorrhage / blood,  drug therapy*,  physiopathology
Hyperoxia / blood,  physiopathology*
Lactic Acid
Male
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors
Oxygen / administration & dosage*,  blood,  therapeutic use
Rats
Rats, Sprague-Dawley
Respiration, Artificial
Risk Assessment
Time Factors
Vascular Resistance / drug effects
Vasoconstriction / drug effects*
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 124-38-9/Carbon Dioxide; 50-21-5/Lactic Acid; 50903-99-6/NG-Nitroarginine Methyl Ester; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase

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


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