title: Gastric intramural PCO2 during peritonitis and shock.
abstract: OBJECTIVE
  To define whether increases in gastric intramural tissue CO2 and H+ increase during experimentally induced peritonitis with circulatory shock as they do under conditions of hemorrhagic shock and cardiac arrest.
  
  
  METHODS
  Peritonitis was induced in Sprague-Dawley rats by cecal ligation and fecal spillage.
  
  
  RESULTS
  Over an interval of 260 +/- 20 min in 5 animals, there was a progressive reduction in mean aortic pressure from 153 +/- 12 to 40 +/- 20 mm Hg and a decline in cardiac index from 429 +/- 135 to 178 +/- 7 ml/min. This was associated with increases in gastric intramural [H+] from 34 +/- 5 to 217 +/- 93 mmol/L (p = 0.001). Arterial blood lactate content concurrently increased from 0.9 +/- 0.1 to 4.6 +/- 0.7 mmol/L (p = 0.001). Only a late increase in gastric intramural PCO2 from 45 +/- 5 to 128 +/- 38 mm Hg (p = 0.01) was observed.
  
  
  CONCLUSIONS
  In contrast to the gastric acid base changes that accompany hemorrhagic shock, in which there is an early and prominent increase in both PCO2 and [H+] in close relationship to decreases in cardiac output and arterial pressure, there was a prominent increase in gastric [H+] but only a delayed rise in gastric intramural PCO2. Arterial blood lactate and central venous oxygen saturation were earlier indicators of perfusion failure. Since the bicarbonate concentration in the stomach wall was substantially greater than that of simultaneously measured arterial blood, this has bearing on the current clinical method of gastric tonometry which assumes that arterial blood bicarbonate is equivalent to gastric wall bicarbonate.
authors.affiliation: Department of Pediatrics, University of health Sciences, Chicago Medical School, North Chicago, IL 60064-3095.
authors.forename: V S
authors.initials: VS
authors.lastname: Desai
authors.forename: M H
authors.initials: MH
authors.lastname: Weil
authors.forename: W
authors.initials: W
authors.lastname: Tang
authors.forename: G
authors.initials: G
authors.lastname: Yang
authors.forename: J
authors.initials: J
authors.lastname: Bisera
mesh_terms: D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D006439:Hemodynamics / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D007511:Ischemia / Q000378:metabolism*; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D010100:Oxygen / Q000097:blood; D010538:Peritonitis / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012772:Shock, Septic / Q000378:metabolism*; D013270:Stomach / Q000098:blood supply
chemical_list: D001639:Bicarbonates; D007773:Lactates; D002245:Carbon Dioxide; D019344:Lactic Acid; D010100:Oxygen