Macrocirculation Endotoxemia in Horses
Description
Endotoxemia is a significant cause of morbidity and mortality in equids [1,2] due to perfusion impairment and possible destruction of the glycocalyx [3]. In a prospective, randomized, controlled experimental trial, endotoxemia was induced with E. coli B55:O5 LPS 30 ng kg-1 over 30 minutes IV in six healthy adult horses ventilated with isoflurane in oxygen. Standard cardiovascular variables were recorded and calculated and leucocyte counts, lactate, heparan sulphate and syndecan-1, were determined at baseline (B) before endotoxin and at 0, 30, 60, 120 minutes after endotoxin. Data were analysed by a mixed model variance analysis and adjusted by Tukey-Kramer (SAS Enterprise Guide Software 7.1). After endotoxin (120 minutes), a significant increase (p ≤ 0.05) in cardiac index (43 ± 9 vs. 80 ± 15 ml kg-1 min-1, p < 0.01 ), in oxygen delivery index (8 ± 3 vs. 17 ± 4 ml min-1 kg-1, p <0.001), in pulse pressure variation (8 ± 3 vs. 17 ± 4, p < 0.01 and in lactate (1.55 ± 0,9 vs. 4.4 ± 0.52 mmol L-1, p < 0.0001) occurred with a decrease in systemic vascular resistance index (247 ± 87 vs. 83 ± 20 dynes s-1 cm-5, p <0.001), diastolic arterial blood pressure (69 ± 14 vs 38 ± 5 mmHg; p <0.001), and leukocyte counts (5.6 ± 1.3 vs. 1.5 ± 0.3 G l-1, p < 0.0001). No changes in the glycocalyx degradation products could be found. Short-term experimental endotoxemia under isoflurane induced anticipated cardiovascular changes, but did not alter glycocalyx shedding products in this study.