N A Herity1, J D Allen, B Silke, A A Adgey. 1. Regional Medical Cardiology Centre, Royal Victoria Hospital, Belfast, Northern Ireland. nherity@cahgt.n-i.nhs.uk
Abstract
BACKGROUND: Existing porcine models of endotoxic shock poorly represent the human situation. AIMS: To assess whether the cardiovascular profile of a porcine model could be improved by refining the protocol. METHODS: In 30 pigs, right and left heart pressures and cardiac output were measured. Lipopolysaccharide (LPS) was administered as a bolus (n=12), as a 30 minute infusion (n=6) or as a 30 minute infusion along with inhaled NO and volume resuscitation (n=6) and six sham-treated pigs received normal saline. Haemodynamic values were measured over three hours. RESULTS: LPS increased pulmonary vascular resistance (PVR) (13.3 +/- 1.4 to 37.0 +/- 3.9kPa/l per sec, p<0.05) and reduced cardiac output (6.0 +/- 0.6 to 4.8 +/- 0.41/min). Mortality was 50% within 30 minutes. Inhaled NO and volume resuscitation controlled pulmonary vascular resistance (PVR) and preserved CO. Systemic vascular resistance (SVR) declined in the first hour (118.4 +/- 11.8 to 65.8 +/- 8.2kPa/l per sec, p<0.05) and remained low. CONCLUSIONS: Porcine models of endotoxaemia based on LPS administration are a poor model of human septic shock, but can be improved by regulating PVR and supporting CO which may contribute to future studies of septic shock
BACKGROUND: Existing porcine models of endotoxic shock poorly represent the human situation. AIMS: To assess whether the cardiovascular profile of a porcine model could be improved by refining the protocol. METHODS: In 30 pigs, right and left heart pressures and cardiac output were measured. Lipopolysaccharide (LPS) was administered as a bolus (n=12), as a 30 minute infusion (n=6) or as a 30 minute infusion along with inhaled NO and volume resuscitation (n=6) and six sham-treated pigs received normal saline. Haemodynamic values were measured over three hours. RESULTS:LPS increased pulmonary vascular resistance (PVR) (13.3 +/- 1.4 to 37.0 +/- 3.9kPa/l per sec, p<0.05) and reduced cardiac output (6.0 +/- 0.6 to 4.8 +/- 0.41/min). Mortality was 50% within 30 minutes. Inhaled NO and volume resuscitation controlled pulmonary vascular resistance (PVR) and preserved CO. Systemic vascular resistance (SVR) declined in the first hour (118.4 +/- 11.8 to 65.8 +/- 8.2kPa/l per sec, p<0.05) and remained low. CONCLUSIONS: Porcine models of endotoxaemia based on LPS administration are a poor model of humanseptic shock, but can be improved by regulating PVR and supporting CO which may contribute to future studies of septic shock
Authors: A F Suffredini; R E Fromm; M M Parker; M Brenner; J A Kovacs; R A Wesley; J E Parrillo Journal: N Engl J Med Date: 1989-08-03 Impact factor: 91.245