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| The Role of Nitric Oxide in Vasodilation in Upstream Muscle during Intermittent Pneumatic Compression |
| Source: Chen LE, Liu K, Qi WN, et al: Journal of Applied Physiology 92(2): 559-566, 2002 |
| Summary: This study examined the effects of intermittent pneumatic compression on uncompressed upstream muscles. Subjects were divided into two groups. Group 1 examined what effect L-NMMA (a nitric oxide synthase inhibitor) had on the IPC-induced vasodilation of the uncompressed cremaster muscle. Group 2 examined the effects of IPC application on the expression of eNOS mRNA and eNOS protein of the cremaster muscle. IPC on the legs resulted in vasodilation of the uncompressed cremaster muscle. It also caused an increase of 2 and 2.5 times its normal levels of eNOS mRNA in the uncompressed cremaster muscle. IPC induced vasodilation was significantly reduced, abolished or reversed with the concurrent infusion of L-NMMA (NOS inhibitor). Nitric oxide from eNOS can create vasodilation, reduce leukocyte adhesion, and inhibit platelet activation and aggregation, thereby increasing blood flow and enhancing fibrinolysis and antithrombotic activity. Authors speculate that one source of NO generation by IPC application could be a result of external compression causing elevated shear stress in the blood vessel’s walls due to increased blood flow velocity in the deep veins. This stimulates endothelial cells lining the blood vessel walls to release NO, which then modulates blood flow. Another possible source of NO is that it is produced by compression of the skeletal muscles by IPC cuffs, since eNOS is present in skeletal muscle fibers. This is the first study to connect IPC induced vasodilation and eNOS expression in skeletal muscles. Study results suggest that the increased release of NO (and related compounds) is a major pathway for vasodilation induced by IPC. |