# Effects of Induced Endotoxaemia on Global Cardiovascular, Oxygenation and Haematologic Variables and the Integrity of the Endothelial Glycocalyx in the Horse

## TL;DR

This study examines how endotoxaemia affects cardiovascular and blood parameters in horses, finding typical early changes but no evidence of glycocalyx damage.

## Contribution

The study provides new insights into the cardiovascular effects of endotoxaemia in horses without observing glycocalyx degradation.

## Key findings

- Endotoxaemia caused significant increases in cardiac index, oxygen delivery, and lactate levels in horses.
- Systemic vascular resistance and diastolic blood pressure decreased significantly after endotoxin administration.
- No changes in glycocalyx degradation products were observed despite cardiovascular alterations.

## Abstract

Endotoxaemia is a significant cause of morbidity and mortality in equids due to perfusion impairment and possible destruction of the glycocalyx.

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.

In vivo experiments

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).

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.

Short‐term experimental endotoxaemia under isoflurane induced anticipated cardiovascular changes but did not alter glycocalyx shedding products in this study.

The current study demonstrated characteristic and well‐documented early hyperdynamic changes in cardiovascular parameters accompanied by concurrent hypotension, increased pulse pressure variation, leucopenia, and hyperlactatemia consistent with acute endotoxaemia. Notwithstanding, no consistent increase in glycocalyx‐shedding products was observed during this approximately 2.5 h period of endotoxaemia.