Validation of a Pseudomonas aeruginosa porcine model of septic shock.

OBJECTIVES: To develop a standardized bacteraemic porcine model of septic shock with cardiovascular and immunological profiles similar to those observed in human clinical states. METHODS: Sepsis was induced by an intravenous challenge of 18 anaesthetized pigs with live Pseudomonas aeruginosa. The pulmonary arterial pressure was monitored and the bacterial infusion was stopped when the systolic pulmonary arterial pressure reached 45 mmHg. Septic shock was treated with fluid resuscitation and epinephrine infusion. The haemodynamic parameters and the rate of different inflammatory cytokines were recorded during 6 h of observation. RESULTS: The mean+/-SD cardiac output increased from 2.4+/-1.2 to 5.7+/-2.1 L/min while the mean+/-SD systemic vascular resistance index decreased from 1957+/-744 to 709+/-221 dyn/s/cm5/m2. The pharmacokinetic profile of the inflammatory cytokines was similar to the one observed in human studies. CONCLUSIONS: The control of the systolic pulmonary arterial pressure during a P. aeruginosa infusion leads to a hyperdynamic, reproducible cardiovascular profile similar to the one observed in human septic shock. Since the immunological profile of the inflammatory cytokines is also similar to the human one, this standardized porcine model appears to be appropriate for experimental research concerning sepsis.

Ropivacaine combined with various anti-arrhythmic drugs results in mild alterations in myocardial contractility in pigs.

PURPOSE: The present study was undertaken following the observation of a marked decrease in myocardial contractility after ropivacaine in a patient on amiodarone, in order to investigate the cardiovascular effects of combining ropivacaine with anti-arrhythmic drugs (AARD). METHODS: Anesthetized domestic pigs were treated with disopyramide, flecainide, atenolol, amiodarone, diltiazem or nicardipine at a dose leading to blood levels obtained in treated patients, then received 1 mg*kg(-1) ropivacaine. Blood pressure (BP), left venticular (LV) dP/dt max, sinus heart rate, and intraventricular conduction time were measured before and following the administration of AARD, and following ropivacaine at different time points. RESULTS: All tested AARD induced the expected hemodynamic and electrophysiologic effects. Following ropivacaine, a 20 to 35% decrease in LV dP/dt max of prolonged duration was observed with amiodarone only. A brief 10 to 20% decrease in mean BP was observed in all animals, except those treated with nicardipine who sustained an important and prolonged decrease in BP. All other variables were not significantly affected. DISCUSSION: The combination of ropivacaine with AARD was always associated with a slight drop in LV dP/dt max. The effect on mean BP was slight, except with nicardipine. Clinicians should be aware of the interactions of ropivacaine with AARD, especially amiodarone and nicardipine.