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LETTER TO THE EDITOR

The following is the abstract of the article discussed in the subsequent letter:

Sublingual and intestinal mucosal blood flow and PCO₂ were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual PCO₂ (Ps) 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)]. 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 and Pl were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of Ps and Pl to shock levels, despite higher cardiac output and _s, possibly due to blood flow redistribution and shunting. Changes in Pl and Ps 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.

REPLY

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

James A. Kruse

Critical Care Services
Bassett Hospital
Cooperstown, New York