Anaphylactic Shock: A Form of Distributive Shock without Inhibition of Oxygen Consumption

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The pathophysiology of anaphylactic shock during anesthesia is incompletely characterized. It is described as distributive by analogy with septic shock (anaerobic metabolism, high tissue oxygen pressure [Ptio2] values). The Ptio2 profile and its metabolic consequences during anaphylaxis are not known.


Ovalbumin-sensitized anaphylactic shock rats (n = 11) were compared to nicardipine-induced hypotension rats (n = 12) for systemic hemodynamics, Ptio2, sympathetic nervous system activation, skeletal muscle blood flow, and interstitial lactate and pyruvate concentrations using combined microdialysis and polarographic Clark-type oxygen probes.


In both groups, the time course and the magnitude of arterial hypotension were similar. The ovalbumin group but not the nicardipine group displayed decreased skeletal muscle blood flow (from 45 ± 6.2 ml · 100 g−1·min−1 to 24.3 ± 5 ml·100 g−1·min−1; P < 0.0001) and Ptio2 values (from 42 ± 5 to 5 ± 2; P < 0.0001). The ovalbumin group had more intense sympathetic nervous system activation with higher plasma epinephrine and interstitial norepinephrine concentrations. For the ovalbumin group, there was skeletal muscle anaerobic metabolism (lactate concentration increased from 0.446 ± 0.105 to 1.741 ± 0.459 mm; P < 0.05) and substrate depletion (pyruvate concentration decreased from 0.034 ± 0.01 mm to 0.006 ± 0.002 mm; P < 0.05) leading to increased interstitial lactate/pyruvate ratios (from 17 ± 6 to 311 ± 115; P < 0.05).


This profile suggests decreased skeletal muscle blood flow and oxygen delivery. Persistent energy consumption results in decreased Ptio2 and substrate depletion through anaerobic glycolysis leading to complete failure of cellular energy production. This could explain rapid organ dysfunction and resuscitation difficulties.

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