Literature DB >> 15983455

Anaphylactic shock: a form of distributive shock without inhibition of oxygen consumption.

Pascale Dewachter1, Valérie Jouan-Hureaux, Patricia Franck, Patrick Menu, Nicole de Talancé, Faiez Zannad, Marie-Claire Laxenaire, Dan Longrois, Paul Michel Mertes.   

Abstract

BACKGROUND: 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.
METHODS: 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.
RESULTS: 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 x 100 g(-1) x min(-1) to 24.3 +/- 5 ml x 100 g(-1) x 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).
CONCLUSIONS: 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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Year:  2005        PMID: 15983455     DOI: 10.1097/00000542-200507000-00010

Source DB:  PubMed          Journal:  Anesthesiology        ISSN: 0003-3022            Impact factor:   7.892


  2 in total

1.  Impaired Myocardial Mitochondrial Function in an Experimental Model of Anaphylactic Shock.

Authors:  Walid Oulehri; Olivier Collange; Charles Tacquard; Abdelouahab Bellou; Julien Graff; Anne-Laure Charles; Bernard Geny; Paul-Michel Mertes
Journal:  Biology (Basel)       Date:  2022-05-10

2.  The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats.

Authors:  Jie Song; Mamoru Tanida; Toshishige Shibamoto; Tao Zhang; Mofei Wang; Yuhichi Kuda; Yasutaka Kurata
Journal:  PLoS One       Date:  2016-03-21       Impact factor: 3.240

  2 in total

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