Veterinary medicine and science · 2025
Effects of Induced Endotoxaemia on Global Cardiovascular, Oxygenation and Haematologic Variables and the Integrity of the Endothelial Glycocalyx in the Horse.
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Neudeck Stephan, Sauter Philipp K, Kutter Annette P N, Steblaj Barbara, Söbbeler Franz J, Reiners Julia, Freise Fritjof, Gutiérrez Bautitsta Alvaro J, Kästner Sabine B R
Аннотация
BACKGROUND: Endotoxaemia is a significant cause of morbidity and mortality in equids due to perfusion impairment and possible destruction of the glycocalyx.
OBJECTIVES: To evaluate our hypothesis that endotoxaemia induces changes in global cardiovascular and haematologic parameters and compromises glycocalyx integrity, evidenced by an early rise in plasma shedding products.
STUDY DESIGN: In vivo experiments METHODS: In a prospective, randomised, controlled experimental trial, endotoxaemia was induced with E. coli B55:O5 LPS 30 ng kg-1 over 30 min IV in six healthy adult horses ventilated with oxygen supplemented with isoflurane. Standard cardiovascular variables were recorded and calculated, and leucocyte counts, lactate, heparan sulphate and syndecan-1 concentration were determined at baseline (B) before endotoxin and at 0, 30, 60 and 120 min after endotoxin. Data were analysed using mixed models and adjusted by Tukey-Kramer (SAS Enterprise Guide Software 7.1).
RESULTS: After endotoxin (120 min), 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 kg cm-5, p < 0.001), diastolic arterial blood pressure (69 ± 14 vs. 38 ± 5 mmHg; p < 0.001), and leucocyte 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.
CONCLUSION: Short-term experimental endotoxaemia under isoflurane induced anticipated cardiovascular changes but did not alter glycocalyx shedding products in this study.
OBJECTIVES: To evaluate our hypothesis that endotoxaemia induces changes in global cardiovascular and haematologic parameters and compromises glycocalyx integrity, evidenced by an early rise in plasma shedding products.
STUDY DESIGN: In vivo experiments METHODS: In a prospective, randomised, controlled experimental trial, endotoxaemia was induced with E. coli B55:O5 LPS 30 ng kg-1 over 30 min IV in six healthy adult horses ventilated with oxygen supplemented with isoflurane. Standard cardiovascular variables were recorded and calculated, and leucocyte counts, lactate, heparan sulphate and syndecan-1 concentration were determined at baseline (B) before endotoxin and at 0, 30, 60 and 120 min after endotoxin. Data were analysed using mixed models and adjusted by Tukey-Kramer (SAS Enterprise Guide Software 7.1).
RESULTS: After endotoxin (120 min), 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 kg cm-5, p < 0.001), diastolic arterial blood pressure (69 ± 14 vs. 38 ± 5 mmHg; p < 0.001), and leucocyte 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.
CONCLUSION: Short-term experimental endotoxaemia under isoflurane induced anticipated cardiovascular changes but did not alter glycocalyx shedding products in this study.