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Ann Thorac Surg 1993;55:490-492
© 1993 The Society of Thoracic Surgeons
Department of Surgery, Montreal Heart Institute, and Department of Medicine, Royal Victoria Hospital, Montreal, Quebec, Canada
Accepted for publication June 8, 1992.
* Address reprint requests to Dr Carrier, Department of Surgery, Montreal Heart Institute, 5000 Belanger St East, Montreal, Que, Canada H1T 1C8.
Cyclosporine (CSA) causes an acute vasoconstriction of renal artery and a significant increase in renal endothelin release. Pentoxifylline, a vasodilator, has been suggested to prevent CSA toxicity. To study the effect of pentoxifylline treatment on CSA-related vasoconstriction and endothelin release, a model of renal autoperfusion in the dog was used. Oral pentoxifylline at the dose of 400 mg three times daily for 3 days was given to 15 dogs. Pure powder CSA (10 mg) was injected into the isolated renal artery perfused at constant flow; changes in perfusion pressure reflected variations in vascular resistance. In the pentoxifylline-treated group (15 dogs), the infusion of CSA caused an average increase of 27 ± 8 mm Hg in renal perfusion pressure, compared with 60 ± 10 mm Hg in a control group of 8 untreated animals (p
0.05). Plasma concentration of endothelin in the renal vein increased from an average of 1.2 ± 0.2 pg/mL before to 2.4 ± 0.5 pg/mL after CSA administration (p
0.05) in the control group, whereas it did not change significantly in the pentoxifylline-treated group. Thus, oral pretreatment with pentoxifylline significantly decreased the renal vasoconstriction and endothelin release due to CSA administration.
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