- Poster presentation
- Open Access
Haemodynamic and renal effects of clonidine in an ovine model of severe sepsis and septic acute kidney injury
© Calzavacca et al.; licensee BioMed Central Ltd. 2012
- Published: 14 November 2012
- Severe Sepsis
- Mean Arterial Pressure
- Cardiac Index
- Acute Kidney Injury
In sepsis, the sympathetic nerve activity (SNA) is differentially increased to individual organs . It has been suggested that inhibition of central sympathetic outflow with clonidine would improve outcome in sepsis  but the cardiovascular and renal effects of clonidine in sepsis are unknown. Accordingly, we sought to assess the effect of the central α2-agonist clonidine on renal function in an ovine model of severe sepsis.
Animals had renal and cardiac flow probes implanted to continuously measure the cardiac index (CI) and renal blood flow (RBF). Mean arterial pressure (MAP) was continuously monitored and hourly urine collection was performed. After the first 24 hours of sepsis every animal was randomly and blindly allocated to receive vehicle or clonidine 0.25 μg/kg/hour for 8 hours. Animals were followed for further 40 hours during recovery and, at least 2 weeks later, crossed over to the other arm of the study. Two-way repeated-measures ANOVA was performed and P < 0.05 was considered significant. Data are mean ± standard error of the average of 4 hours preceding each time point.
In experimental hyperdynamic sepsis, treatment with clonidine appears safe, but it does not improve the glomerular filtration rate.
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