Thermographic study of in vivo modulation of vascular responses to phenylephrine and endothelin-1 by dexamethasone in the horse
Article first published online: 5 JAN 2010
2006 EVJ Ltd
Equine Veterinary Journal
Volume 38, Issue 2, pages 119–126, March 2006
How to Cite
Cornelisse, C. J., Robinson, N. E., Berney, C. A., Eberhart, S., Hauptman, J. E. and Derksen, F. J. (2006), Thermographic study of in vivo modulation of vascular responses to phenylephrine and endothelin-1 by dexamethasone in the horse. Equine Veterinary Journal, 38: 119–126. doi: 10.2746/042516406776563251
- Issue published online: 5 JAN 2010
- Article first published online: 5 JAN 2010
- vascular function
Reasons for performing study: In vitro, glucocorticoids potentiate vasoconstriction of equine digital vessels to catecholamines and this has been implicated as a mechanism of glucocorticoid-induced laminitis. This observation has never been confirmed in vivo.
Objectives: To study the effects of glucocorticoid therapy on vasoconstrictor responsiveness in the horse in vivo.
Methods: In a blinded, randomised cross-over experiment, 9 horses were treated with either dexamethasone (0.1 mg/kg bwt i.v. q. 24 h) or saline i.v. for 6 days. The changes in local average skin temperature before (baseline) and after intradermal injections of the α1-adrenoceptor agonist phenylephrine (PHE; 10−4, 10−5, 10−6, 10−7 and 10−8 mol/l), endothelin-1 (ET-1; 10−5, 10−6, 10−7, 10−8 and 10−9 mol/l) or ET-1 plus a blocker (BQ-123 10−6 mol/l; RES-701 10−6 mol/l; and L-NAME 10−4 mol/l) were investigated with a thermograph.
Results: Dexamethasone (DEX) decreased baseline skin temperatures, suggesting reduced blood flow as a consequence of an increase in vasomotor tone. This was accompanied by potentiation of the response to PHE as demonstrated by a left shift in the dose-response curve and a decrease in the EC50. Dexamethasone did not potentiate ET-1, but the interplay with the lower baseline temperature resulted in a significantly lower skin temperature for this vasoconstrictor after DEX. The different ET-1 blockers had no effect on ET-1 modulated skin temperatures.
Conclusions: Dexamethasone decreases skin perfusion. This is accompanied by a potentiated α1-adrenoceptor agonist response and a greater response to ET-1.
Potential relevance: Glucocorticoid therapy probably decreases perfusion of the equine hoof. During disease states that already are characterised by hypoperfusion and/or increased levels of circulating catecholamines, glucocorticoid therapy could, according to the vascular model of laminitis, tilt the balance in favour of laminitis.