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  • Open Access

Epinephrine induces tissue perfusion deficit in porcine endotoxin shock: evaluation by regional CO2 content gradients and L/P ratios

  • 1,
  • 2,
  • 2 and
  • 3
Critical Care20048 (Suppl 1) :P178

  • Published:


  • Gastric Wall
  • Gastric Tissue
  • Endotoxin Shock
  • Splanchnic Blood Flow
  • Splanchnic Perfusion


We hypothesized that epinephrine (EPI) as opposed to norepinephrine (NE) has selective adverse effects on visceral perfusion when used to treat hypotensive endotoxin shock. We specifically wanted to test the hypothesis that perfusion deficiency could be detected by regional venous to arterial CO2 content gradients (as opposed to pCO2 gradients).

Materials and methods

We measured regional venous lactate and pyruvate concentrations as well as regional CO2 exchange over three locations of the hastrointestinal tract (stomach, small intestine and colon) in a porcine model of prolonged hypotensive (mean arterial pressure [MAP] < 60 mmHg) endotoxin shock with 4 hours of treatment with either EPI (n = 6) or NE (n = 6) aiming at MAP > 70 mmHg. The data are presented as median (interquartile range). Friedman's test was used for within the group analysis of statistical significance.


In 5/6 EPI-treated animals, the splanchnic blood flow decreased regardless of the direction of change in cardiac output (CO). Meanwhile, NE increased splanchnic perfusion concomitantly with CO. Four hours of EPI infusion increased markedly the venous to arterial pCO2 gradient over gastric tissue (39 [37–49] mmHg,P < 0.05) and to a lesser extent over small intestinal tissue (19 [12–25] mmHg, P < 0.05) and colonic tissue (18 [15–24] mmHg,P < 0.05). The CO2 content gradient, however, increased markedly only over gastric tissue (10.8 [10.7–12.1] ml/dl, P < 0.05).


EPI, unlike NE, induced an overall relative reduction of splanchnic blood flow and specifically reduced gastric wall perfusion as evaluated by regional CO2 content gradients. The lactate gradient and L/P ratio over the gastric wall increased accordingly. These findings suggest that EPI should not be used as a first-line vasopressor in septic shock.

Figure 1

Authors’ Affiliations

University of Pittsburgh Medical Center, Pennsylvania, USA
Kuopio University Hospital, Finland
Tampere University Hospital, Finland


© BioMed Central Ltd. 2004