Disuse muscle atrophy of lower limbs in hemiplegic patients

Activation of the vasoactive intestinal peptide 2 receptor modulates normal and atrophying skeletal muscle mass and force

“…To evaluate the functionality of the VIP receptors expressed in skeletal muscle and to validate the observation that only VPAC2R is expressed in skeletal muscle, skeletal muscles in organ bath were stimulated with either the VPACR-nonselective agonist VIP, the VPAC1R-selective agonist [K 15 ,R (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27), or the VPAC2R-selective agonist Ro-25-1553, and cAMP generation was evaluated. As can be seen in Fig.…”

“…Glucocorticoid-induced skeletal muscle atrophy was performed as described in MATERIALS AND METHODS. The VPAC1R agonist [K 15 ,R 16 ,L 27 ]VIP(1-7),GRF(8-27)-NH2, VPAC2R agonist RO-25-1553, ␤2-adrenergic receptor agonist clenbuterol (positive control), and physiological saline (vehicle control) were administered via twice daily subcutaneous injection at the indicated doses in combination with theophylline (except clenbuterol). Theophylline (30 mg/kg) was administered twice daily intraperitoneally to potentiate the action of the VPAC1R and VPAC2R agonists.…”

“…The results of treating mice undergoing corticosteroidinduced atrophy with the VPAC1R-selective agonist [K 15 ,R 16 Treatment with Ro-25-1553 resulted in a 40 and 35% inhibition of dexamethasone-induced TA and MG muscle mass loss, respectively, at the 0.1 mg⅐kg Ϫ1 ⅐day Ϫ1 dosage but had no effect at the 0.3 mg⅐kg Ϫ1 ⅐day Ϫ1 dose. The reason for the lack of dose response in this model but not the other atrophy models is at present unclear but may be a model-specific effect because this model, unlike the two disuse models, denervation and casting, is physi- Fig.…”

“…Skeletal muscle atrophy can be initiated by a variety of stimuli including, for example, disuse, nerve damage, and glucocorticoid use (2,15,17,19,31,37,40). Atrophy induces multiple changes in skeletal muscle that are independent of the atrophy-inducing stimuli, including decreased protein synthesis, increased protein degradation, alterations in contractile and metabolic enzyme protein isozymes, loss of vasculature, and remodeling of the extracellular matrix (2,5,6,22,24,25,27).…”

Analysis of Ultrasonographic Architectural Properties of Muscles of Chronic Stroke Patients during Different Muscle Activities

“…Muscle atrophy in stroke patients is caused by damage to the central nervous system and the resulting failure to use the paretic side for a prolonged period of time; it decreases muscle fiber diameters and changes muscle morphology 23) . Our present study showed that muscle thickness, pennation angle, and fascicle length significantly decreased both at rest and during MVIC as muscle spasticity increased (p<0.001).…”