• A J Schneider, G J Teule, A D Kester, P van Halderen, A B Groeneveld, G A Heidendal, and L G Thijs.
• Circ. Shock. 1987 Jan 1; 22 (2): 141-54.

AbstractIn 16 anesthetized pigs the cardiovascular effects of prostaglandin E1 and methylprednisolone (MPS) during E. coli sepsis were studied. Gated blood pool scans and hemodynamic studies were simultaneously performed. A control group, group I (n = 4), received volume loading alone; groups II, III, and IV received (each n = 4) volume loading after intravenous administration of MPS, prostaglandin E1, and both MPS and prostaglandin E1, respectively. Groups were formed by randomization, such that the effects of prostaglandin E1 (0.1 microgram/kg/min) and MPS (30 mg/kg) could be analyzed separately and in combination. Eight animals treated with prostaglandin E1 were compared with eight animals not receiving prostaglandin E1. The same method was applied to the MPS group. E. coli infusion resulted in an abrupt increase in pulmonary arterial pressure while systemic blood pressure gradually fell. Cardiac output decreased. Gated blood pool studies showed an increase in right ventricular end-diastolic volume and a decrease in right ventricular ejection fraction. Consequently, right-to-left ventricular end-diastolic volume ratio increased. Pulmonary arterial pressure was lowered in the treatment groups compared to control group. During volume loading right ventricular ejection fraction improved in the prostaglandin E1 group but remained low in the MPS group. Compared to control group, cardiac output did not change and mean systemic arterial pressure significantly decreased in the prostaglandin E1 group. Treatment with prostaglandin E1, MPS, or both drugs and volume loading did not reveal any difference between the four groups with respect to cardiac output, right and left ventricular volumes, and left ventricular ejection fraction. The present study indicates that in a porcine model of E. coli septic shock with acute pulmonary hypertension, prostaglandin E1 and MPS treatment decrease pulmonary vascular resistance but also systemic vascular resistance. Prior to and during volume loading right ventricular ejection fraction increased in the prostaglandin E1 group. However, neither prostaglandin E1 nor MPS improved right ventricular performance and forward flow during volume loading.

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