The effect of vacuum-assisted closure therapy on the pig femoral artery vasomotor responses.

Vacuum-assisted closure (VAC) is frequently used to treat wound infections. The aim of the present study was to evaluate the effect of VAC therapy on blood vessels. Vasodilatation and vasoconstriction were studied in isolated ring segments of the pig femoral artery after continuous VAC therapy of an inguinal wound for 12 hours. Vasoconstriction induced by endothelin-1 (ET-1), which is mainly an endothelin type A receptor agonist (Emax = 181 +/- 2% of potassium), and the endothelin type B receptor agonist, sarafotoxin 6c (Emax = 30 +/- 1%), were significantly increased after VAC therapy (ET-1; 325 +/- 3% and sarafotoxin 6c; 69 +/- 1%). The norepinephrine-, phenylephrine-, and angiotensin II-induced vasoconstrictions were not affected by VAC therapy. Acetylcholine induced an endothelium-dependent dilatation that was enhanced after VAC therapy (Rmax = 38 +/- 1% of norepinephrine-preconstriction after sham and 47 +/- 1% after VAC therapy, p < 0.05). The dilatory response was mediated by nitric oxide (Rmax = 39 +/- 1%), prostaglandins (5 +/- 1%) and endothelium-derived hyperpolarizing factor (16 +/- 1%), which were all significantly increased after VAC therapy. In conclusion, VAC therapy for 12 hours enhances an endothelin type A and type B receptor-mediated vasoconstriction. This may be compensated for by a more efficacious endothelium-dependent vasodilatation. No spontaneous bleeding, perforation, dissection, or other macroscopic change could be observed in the arteries exposed to VAC therapy.