Document Detail


Changes in adenine nucleotides during hemorrhagic shock and reperfusion.
MedLine Citation:
PMID:  9024829     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Certain tissues are known to be susceptible to shock-induced damage: liver, small bowel mucosa, and small bowel wall. This study was done to assess the changes in adenine nucleotides induced by hemorrhagic shock. Male Sprague-Dawley rats (n = 21; 300-350 g) were anesthetized with sodium pentobarbital (50 mg/kg, ip) and mechanically ventilated. The external jugular vein and common carotid artery were cannulated. Laparotomy was done. Hemorrhagic shock was induced by withdrawing blood into a heparinized syringe until a mean arterial blood pressure of 40 mm Hg was obtained and was maintained for 30 min by continued withdrawals. Shed blood was then reinfused through the venous catheter. No additional fluid was administered. The animals were observed for another 60 min. Throughout the procedure, biopsies were taken of liver and small bowel. The small bowel biopsies were separated into mucosal and wall fractions. Nucleotides were extracted. ATP, ADP, AMP, adenosine, inosine, xanthine, and hypoxanthine were measured with gradient HPLC. Cellular ATP concentrations decreased significantly during shock (P < 0.05). Liver ATP dropped from 8.93 +/- 0.55 to 2.91 +/- 0.16 micromol/g dry tissue (mean +/- SEM) (33%), small bowel mucosal ATP from 9.40 +/- 1.04 to 3.26 +/- 0.21 (35%), and small bowel wall ATP from 5.47 +/- 0.36 to 2.74 +/- 0.18 (50%). The nucleotide response to shock in small bowel mucosa was closer to that of liver than to that of small bowel wall. After reperfusion, ATP levels were partially restored in liver, small bowel mucosa, and small bowel wall, but not to preshock values. All of the metabolites (adenosine, inosine, hypoxanthine, and xanthine) increased during shock (P < 0.05), and did not return to preshock levels after reperfusion. The abnormalities in ATP and its metabolites, and their persistence after reperfusion, suggest a possible mechanism for the production of postshock damage.
Authors:
C W Van Way; A Dhar; R Reddy; L Evans; B Wogahn; T S Helling
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of surgical research     Volume:  66     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  1996 Dec 
Date Detail:
Created Date:  1997-03-05     Completed Date:  1997-03-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  159-66     Citation Subset:  IM    
Affiliation:
Department of Surgery, University of Missouri at Kansas City, School of Medicine 64111, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenine Nucleotides / metabolism*
Animals
Intestine, Small / metabolism
Liver / metabolism
Male
Nucleotides / metabolism
Rats
Rats, Sprague-Dawley
Reperfusion Injury / metabolism
Shock, Hemorrhagic / metabolism*
Time Factors
Chemical
Reg. No./Substance:
0/Adenine Nucleotides; 0/Nucleotides

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


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