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Effects of L-NMMA and indomethacin on arteriolar vasomotion in skeletal muscle microcirculation of conscious and anesthetized hamsters.

The purpose of this study was to determine the influence of NG-monomethyl-L-arginine (L-NMMA) and indomethacin (INDO), respectively inhibitors of nitric oxide synthase and cyclooxygenase, on spontaneous arteriolar activity (vasomotion) in the skeletal muscle of awake and anesthetized hamsters. Unanesthetized hamsters, implemented with the skin fold chamber window, displayed vasomotion, whose frequency and amplitude were quantified by power spectrum analysis. Intravenous administration of L-NMMA significantly increased vasomotion frequency and did not change the amplitude at the lower dose, but in order 3 arterioles amplitude decreased significantly. With higher doses L-NMMA caused constriction of order 1-2 vessels, frequency decreased and amplitude increased, and the arteriolar vasodilator response to acetylcholine decreased significantly. During anesthesia topically applied L-NMMA significantly decreased diameter and caused the appearance of vasomotion in order 1-2 arterioles. INDO did not affect vasomotion in unanesthetized hamsters and did not initiate vasomotion during anesthesia leading to the conclusion that prostaglandins do not regulate vasomotion. Vasomotion is not directly related to nitric oxide (NO) in conscious animals while NO blockage stimulates vasomotion in smaller arterioles of anesthetized hamsters without vasomotion; however, the simultaneous inhibition of cyclooxygenase and NO had no effect on arteriolar diameter during anesthesia. It is concluded that vasomotion is regulated by a mechanism that modulates smooth muscle cell activity through the endothelium.