SCORPION-VENOM LEADS TO GASTROINTESTINAL ISCHEMIA DESPITE INCREASED OXYGEN DELIVERY IN PIGS

Citation
S. Sofer et al., SCORPION-VENOM LEADS TO GASTROINTESTINAL ISCHEMIA DESPITE INCREASED OXYGEN DELIVERY IN PIGS, Critical care medicine, 25(5), 1997, pp. 834-840
Citations number
41
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
00903493
Volume
25
Issue
5
Year of publication
1997
Pages
834 - 840
Database
ISI
SICI code
0090-3493(1997)25:5<834:SLTGID>2.0.ZU;2-Q
Abstract
Objectives: Scorpion envenomation may be accompanied by metabolic acid osis even in the absence of hypoxia and cardiovascular derangement. We tested the hypothesis that venom causes ischemia of the gastrointesti nal 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. Intervent ions: In ten spontaneously breathing, intubated, sedated pigs, purifie d 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 and Mai n Results: Variables measured included: mean arterial pressure (MAP), heart rate (HR), mean pulmonary arterial pressure, pulmonary artery oc clusion pressure, cardiac output, stroke volume, right ventricular eje ction fraction (rapid thermistor), left ventricular dimensions (echoca rdiography), arterial gas tensions, lactate and catecholamine concentr ations, gastric interstitial mucosal pH (tonometry), as well as system ic and pulmonary vascular resistances. Within 5 mins after venom injec tion, there was a hyperdynamic state accompanied by significantly incr eased MAP (97 +/- 18 to 136 +/- 47 mm Hg, p < .0003), HR (70 +/- 12 to 121 +/- 24 beats/min, p < .00006), and cardiac output (1.88 +/- 0.35 to 2.95 +/- 0.53 L/min, p < .0003), with no change in stroke volume, o r pulmonary artery occlusion pressure. Right ventricular ejection frac tion increased from 38.1 +/- 4.3 to 48.6 +/- 9.0% (p < .0009) by 15 mi ns. No change in left ventricular function was observed. There were si gnificant decreases in systemic vascular resistance and pulmonary vasc ular resistance following envenomation. Arterial and gastric mucosal p H significantly decreased from 7.40 +/- 0.04 to 7.25 +/- 0.07 (p < .00 01) for arterial pH, and 7.33 +/- 0.08 to 7.17 +/- 0.13 (p < .00001) f or gastric mucosal pH by 30 mins after envenomation, The decrease in a rterial pH was not sufficient to account for the change in gastric muc osal pH, indicating gastric mucosal ischemia. Arterial lactate increas ed from 2.6 +/- 1.4 to 7.4 +/- 1.9 (p < .05 x 10(-8)). There were sign ificant increases in serum epinephrine and norepinephrine values by 5 mins. All hemodynamic variables and catecholamine concentrations retur ned to baseline by 4 hrs. However, there was persistent arterial and g astric mucosal acidosis and increased lactate concentrations even at 4 hrs. Oxygen delivery remained normal or supernormal for 4 hrs followi ng envenomation. However, despite this finding, systemic and gastric m ucosal pH changes indicate impaired gastrointestinal oxygen delivery. Conclusions: Despite increased peripheral oxygen delivery, scorpion en venomation was associated with evidence of ischemia of the gastrointes tinal tract. This association could be due to shunting of blood from m etabolically active areas, possibly associated with massive catecholam ine release, or a direct toxic effect of the venom on regional oxygen transport at the cellular level.