Scorpion venom leads to gastrointestinal ischemia despite increased oxygen delivery in pigs

Shaul Sofer, Rubin Cohen, Yehuda Shapir, Ling Chen, Athos Colon, Steven M. Scharf

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


Objectives: Scorpion envenomation may be accompanied by metabolic acidosis even in the absence of hypoxia and cardiovascular derangement. We tested the hypothesis that venom causes ischemia of the gastrointestinal tract rather than failure of delivery of oxygen to the periphery. Design: Repeated measures, prospective study in experimental animals. Setting: University-affiliated hospital research laboratory. Interventions: In ten spontaneously breathing, intubated, sedated pigs, purified dried venom (Leiurus quinquestriatus), 0.05 mg/kg, was administered intravenously. Measurements were obtained before (baseline), and 5, 15, 30, 60, 120, 180, and 240 mins after injection. Measurements end Main Results: Variables measured included: mean arterial pressure (MAP), heart rate (HR), mean pulmonary arterial pressure, pulmonary artery occlusion pressure, cardiac output, stroke volume, right ventricular ejection fraction (rapid thermistor), left ventricular dimensions (echocardiography), arterial gas tensions, lactate and catecholamine concentrations, gastric interstitial mucosal pH (tonometry), as well as systemic and pulmonary vascular resistances. Within 5 mins after venom injection, there was a hyperdynamic state accompanied by significantly increased MAP (97 ± 18 to 136 ± 47 mm Hg, p < .0003), HR (70 ± 12 to 121 ± 24 beats/min, p < .00006), and cardiac output (1.08 ± 0.35 to 2.95 ± 0.53 L/min, p < .0003), with no change in stroke volume, or pulmonary artery occlusion pressure. Right ventricular ejection fraction increased from 38.1 ± 4.3 to 48.6 ± 9.0% (p < .0009) by 15 mine. No change in left ventricular function was observed. There were significant decreases in systemic vascular resistance and pulmonary vascular resistance following envenomation. Arterial and gastric mucosal pH significantly decreased from 7.40 ± 0.04 to 7.25 ± 0.07 (p< .0001) for arterial pH, and 7.33 ± 0.08 to 7.17 ± 0.13 (p < .00001) for gastric mucosal pH by 30 mins after envenomation. The decrease in arterial pH was not sufficient to account for the change in gastric mucosal pH, indicating gastric mucosal ischemia. Arterial lactate increased from 2.6 ± 1.4 to 7.4 ± 1.9 (p < .05 x 10-1). There were significant increases in serum epinephrine and norepinephrine values by 5 mins. All hemodynamic variables and catecholamine concentrations returned to baseline by 4 hrs. However, there was persistent arterial and gastric mucosal acidosis and increased lactate concentrations even at 4 hrs. Oxygen delivery remained normal or supernormal for 4 hrs following envenomation. However, despite this finding, systemic and gastric mucosal pH changes indicate impaired gastrointestinal oxygen delivery. Conclusions: Despite increased peripheral oxygen delivery, scorpion envenomation was associated with evidence of ischemia of the gastrointestinal tract. This association could be due to shunting of blood from metabolically active areas, possibly associated with massive catecholamine release, or a direct toxic effect of the venom on regional oxygen transport at the cellular level.

Original languageEnglish
Pages (from-to)834-840
Number of pages7
JournalCritical Care Medicine
Issue number5
StatePublished - 1 May 1997


  • Blood pressure
  • Cardiac output
  • Gastric pH
  • Gastric tonometry
  • Ischemia
  • Metabolic acidosis
  • Oxygen delivery
  • Scorpion venom

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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