Protective skeletal muscle arteriolar vasomotion during critical perfusion conditions of osteomyocutaneous flaps is not mediated by nitric oxide and endothelins.

Abstract

After flap surgery, vasomotion, defined as oscillation of the arteriolar diameter, may protect tissue during critical perfusion conditions. The mechanisms that regulate vasomotion are still unclear; therefore, we studied the incidence of vasomotion in peripheral tissue and whether nitric oxide or endothelins are involved in regulation of vasomotion. In Sprague-Dawley rats, an osteomyocutaneous flap was prepared. To induce critical perfusion conditions, we reduced arterial blood flow supplying the flap to 0.15 ml/min. Seven animals received NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide-synthase inhibitor, and six animals bosentan, an endothelin A/B receptor antagonist. Microcirculation of muscle, skin, subcutis and periosteum was assessed by intravital microscopy before and after drug application. In all animals, reduction of arterial blood supply induced arteriolar vasomotion in muscle (100%), but not in periosteum, subcutis and skin. Vasomotion was found to be affected by neither L-NAME (frequency 2.6+/-0.2 versus 2.4+/-0.2 cycles/min; amplitude 67+/-19 versus 55+/-20%; share of dilation period in vasomotion cycle 59+/-2 versus 58+/-3%) nor bosentan (1.8+/-0.1 versus 1.7+/-0.1 cycles/min; 60+/-10 versus 64+/-6%; 50+/-2 versus 53+/-1%). Our study indicates that during critical perfusion conditions, arteriolar vasomotion develops only in muscle, not in skin, subcutis and periosteum, and that nitric oxide and endothelins are not involved in the regulation of this protective vascular response.