Haemodynamic and metabolic effects of resuscitation with Ringer’s ethyl pyruvate in the acute phase of porcine endotoxaemic shock
Ethyl pyruvate has been shown to possess anti-inflammatory and free radical scavenging properties. However, the haemodynamic effects of ethyl pyruvate have not been studied in detail. We investigated the systemic, regional and microcirculatory haemodynamic and metabolic effects of resuscitation with Ringer’s ethyl pyruvate solution (REPS) vs. Ringer’s acetate (RA) in an acute model of porcine endotoxaemic shock. Methods:
Fourteen anaesthetized pigs received an infusion of endotoxin that was increased stepwise over 30 min to a rate of 2.5 g/kg/h. After 60 min of endotoxaemia, the animals were resuscitated with either ethyl pyruvate 40 mg/kg, given as REPS, or the equivalent volume of RA, administered over 10 min. Thereafter, an infusion of either ethyl pyruvate 40 mg/kg/h, given as REPS, or the equivalent volume of RA, was started, and the maintenance fluid was reduced so that the total amount of fluid given was kept constant. The experiment was terminated after 300 min of endotoxaemia. Results:
Endotoxin infusion led to a hypodynamic state that was reversed by fluid resuscitation after 60 min. Progressive deterioration ensued and, after 300 min, all animals were again hypodynamic. No differences in response to treatment were found between the groups with regard to systemic haemodynamics, renal artery or portal vein flow or microcirculatory flow in the liver, kidney, ileal serosa or mucosa. Metabolic acidosis and increased arterial blood lactate developed in both groups, but, in the REPS group, the base excess was significantly lower from 150 min and the anion gap was significantly higher at 150 and 210 min. Conclusion:
We could not demonstrate any difference between REPS and RA for resuscitation in this model of acute porcine endotoxaemic shock.
Document Type: Research Article
Affiliations: 1: Department of Anaesthesiology and Intensive Care, Karolinska University Hospital and Department for Clinical Science Intervention and Technology, Karolinska Institutet, Huddinge, Stockholm 2: Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Publication date: 2006-11-01