HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 98/1/108    most recent 00243.2004v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Guzman, J. A. Articles by Kruse, J. A. Search for Related Content PubMed PubMed Citation Articles by Guzman, J. A. Articles by Kruse, J. A.

Lingual, splanchnic, and systemic hemodynamic and carbon dioxide tension changes during endotoxic shock and resuscitation

Division of Pulmonary, Critical Care, and Sleep Medicine, Wayne State University School of Medicine, Detroit, Michigan

Submitted 4 March 2004 ; accepted in final form 28 July 2004

Sublingual and intestinal mucosal blood flow and PCO₂ were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual PCO₂ (Ps_CO2) was measured by using a novel fluorescent optrode-based technique and compared with lingual measurements obtained by using a Stowe-Severinghaus electrode [lingual PCO₂ (Pl_CO2)]. Endotoxin caused parallel changes in cardiac output, and in portal, intestinal mucosal, and sublingual blood flow (_s). Different blood flow patterns were observed during resuscitation: intestinal mucosal blood flow returned to near baseline levels postfluid resuscitation and decreased by 21% after vasopressor resuscitation, whereas _s rose to twice that of the preshock level and was maintained throughout the resuscitation period. Electrochemical and fluorescent PCO₂ measurements showed similar changes throughout the experiments. The shock-induced increases in Ps_CO2 and Pl_CO2 were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of Ps_CO2 and Pl_CO2 to shock levels, despite higher cardiac output and _s, possibly due to blood flow redistribution and shunting. Changes in Pl_CO2 and Ps_CO2 paralleled gastric and intestinal PCO₂ changes during shock but not during resuscitation. We found that the lingual, splanchnic, and systemic circulations follow a similar pattern of blood flow variations in response to endotoxin shock, although discrepancies were observed during resuscitation. Restoration of systemic, splanchnic, and lingual perfusion can be accompanied by persistent tissue hypercarbia, mainly lingual and intestinal, more so when a vasopressor agent is used to normalize systemic hemodynamic variables.

sublingual circulation; endotoxic shock; vasopressors