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

Sublingual and intestinal mucosal blood flow and PCO2 were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual PCO2 (PsCO(2)) was measured by using a novel fluorescent optrode-based technique and compared with lingual measurements obtained by using a Stowe-Severinghaus electrode [lingual PCO2 (PlCO(2))]. Endotoxin caused parallel changes in cardiac output, and in portal, intestinal mucosal, and sublingual blood flow ((Q) over dot(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 (Q) over dot(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 PsCO(2) and PlCO(2) were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of PsCO(2) and PlCO(2) to shock levels, despite higher cardiac output and (Q) over dot(s), possibly due to blood flow redistribution and shunting. Changes in PlCO(2) and PsCO(2) 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.