OBJECTIVE: To study the influence of the electric stimulation of denervated muscle atrophy. METHODS: Sixteen SD rats were made the model of denervated skeletal muscle in two lower limbs by cutting off the sciatic nerve and femoral nerve. The right gastrocnemius muscle was stimulated with JNR-II nerve amp; muscle recovery instrument by skin as the experimental side and the left was not treated as the control side. The muscle histology, ultrastructure, fibrillation potential amplitude, Na(+)-K(+)-ATPase and Ca(2+)-ATPase activities were observed 2 weeks and 4 weeks after operation. RESULTS: Electric stimulation could protect mitochondria and sarcoplasmic reticulum from the degeneration. The reduction rates of muscle cell diameter and cross section in the experimental side were slower significantly than those in control side. There was no influence on fibrillation potential amplitude in the both sides after electric stimulation. The reduction rates of Na(+)-K(+)-ATPase activity in the experimental side were slower 15.59% and 27.38% respectively than those in the control side. The reduction rates of Ca(2+)-ATPase activity in the experimental side were slower 4.83% and 21.64% respectively than those in the control side. CONCLUSION: The electric stimulation can protect muscle histology, electrophysiology and enzymic histochemistry of denervated skeletal muscle from the degeneration. The electric stimulation is an effective method to prevent and treat muscle atrophy.
OBJECTIVE To observe the ultrastructural changes and number of satellite cells in different muscles with different denervation interval and investigate the mechanism of denervation atrophy. METHODS Muscles of different denervation interval were harvested, which were 6 biceps brachii and 6 abductor digiti minimi. The ultrastructure of the samples were observed under transmission electron microscope. The number of nucleus and satellite cells were counted to calculate the percentage content of satellite cells. RESULTS In early stage of denervation, the myofilament and sarcomere of the majority were well oriented. The nucleoli of some muscle cell nucleus were enlarged and pale. Vacuolarization was also seen in some mitochondria. There was no obvious proliferation of collagen fiber around myofibers. After denervation of half a year, rupture and disorientation of myofilament was seen. The nucleus became smaller, dark stained, and some of them were condensed. There was proliferation of fibroblasts, adipose cells and collagen fibers around myofibers. Motor endplate was not recognized one year after denervation. In the early stage of denervation, satellite cell percentage of the two muscles was relatively high. It then declined with time. One year after denervation, satellite cells were scarcely detected. Comparison of the curves for satellite cell declination in two muscles revealed that the declination of the abductor digiti minimi was faster than that of biceps brachii. Decrease of the former started 3 months after denervation, while the latter started after 6 months. CONCLUSION Disappearing of motor endplate and proliferation of collagen fibers are main factors that affect the treatment outcome in late cases. Decrease of satellite cell number is another cause. The correlation of less satellite cell in abductor digiti minimi and poorer recovery of hand intrinsic muscles indicates that increment of satellite cells in long-term denervated muscles may be one of the effective measures to improve treatment outcome.
OBJECTIVE: To investigate the mechanism and to explore the measures of prevention and treatment of hypothermal vasoconstriction. METHODS: By the techniques of endothelial cell culture and scanning electron microscopy, and vasomotor functional test of isolated vascular vessels, the relation of hypothermal vasoconstriction and the release of endothelium-derived contractile and vasodilative factors were observed. RESULTS: Hypothermia obviously induced vasoconstriction of isolated vascular vessels, whether endothelium was intact or removed, the lower the temperature, the higher the vascular tension. Removal of endothelium could decrease the effect of vasoconstriction by hypothermia. The conditioned medium of bovine aortic endothelial cell could induce significantly vasoconstriction of isolated rat common neck arterial ring in hypothermia. It indicated that the bovine aortic endothelial cells secreted contractile factors into the medium. Reheating to 37 degrees C or vasodilator or reheating plus vasodilator did not obviously influence the hypothermia-induced vasoconstriction within 2 hours. When reheating to 50 degrees C, vascular tension was decreased, but only changed in range of 28% to 42%. CONCLUSION: Hypothermia vasoconstriction is relative to vasoconstrictor factors secreted by endothelium. Reheating to 37 degrees C or vasodilator does not antagonize the constriction of vascular vessels. Reheating to 50 degrees C only partially eliminates the constrict effect of blood vessels, so the prevention of hypothermia vasoconstriction should be emphasized.