This experiment was designed to explore the correlation between the mechanism of immobilization-induced skeletal muscle atrophy and the apoptosis of muscular cells. The models of skeletal muscle atrophy induced by immobilization for different length of time were established according to Sievanen II methods. 24 rabbits, each of them having one hind leg fixed by the tubal plaster and the other one free as control, were randomly divided into four groups depending on time of fixation (3, 7, 14, and 28 days respectively). The animals were sacrificed by the end of fixation. TdT-mediated d-UTP nick end labeling (TUNEL) was used to investigate the apoptotic muscle cells in the animal's bone. By comparing the apoptotic muscle cells with the morphology of the skeletal muscle, the correlation between cell apoptosis and skeletal muscle atrophy were analyzed. Apoptotic muscle cells did appear after immobilization in the atrophied skeletal muscle. In various groups, some cells with false positive stained TUNEL were found in the atrophic muscle, which could be distinguished from apoptotic cells by their characteristics. In conclusion, cell apoptosis participates in the process of skeletal muscle atrophy induced by immobilization; the amount of apoptotic cells is strongly associated with the time of immobilization, its peak appears on the 14th day of immobilization; the distribution of apoptotic skeletal muscle cell varies with the time of fixation. The severity of skeletal muscle atrophy is associated with the degree of the muscle cell apoptosis.
Animals ; Apoptosis ; physiology ; Immobilization ; In Situ Nick-End Labeling ; Muscle, Skeletal ; pathology ; Muscular Atrophy ; etiology ; Rabbits

6-week old rats were subjected to sciatic nerve resection and the right hindlimbs were then under a low stress environment. Bone mineral density (BMD) of different regions and geome-morphological parameters of femurs were measured. The results showed that the increase in the diameter, subperiosteal area and bone mineral density of femurs were suppressed obviously under low stress environment. But the sensitivity of BMD of different regions of the femur to the low stress environment was different. The suppression of the increase in femoral BMD was composed of an early impairment in the gain of BMD at the femoral metaphysis, which is rich in trabecular bone, and a sustained reduction in the gain of BMD at the femoral diaphysis, which is rich in cortical bone. The results of geome-morphology suggested that the early reduction in the increase of BMD at the metaphysis was due to an enhancement of bone resorption, whereas the suppression of gain in cortical bone mass and size is the result of a sustained reduction of periosteal bone formation.
Animals ; Bone Density ; physiology ; Bone Resorption ; etiology ; Female ; Femur ; pathology ; Immobilization ; Rats ; Rats, Sprague-Dawley ; Sciatic Nerve ; physiology ; surgery ; Stress, Mechanical ; Weight-Bearing ; physiology

In our previous study, we demonstrated that immobilization stress blocked estrogen-induced luteinizing hormone(LH) surge possibly by inhibiting the synthesis and release of gonadotropin-releasing hormone (GnRH) at the hypothalamic level and by blocking estrogen-induced prolactin (PRL) surge by increasing the synthesis of dopamine receptor at the pituitary level in ovariectomized rats. The present study was performed to determine whether immobilization stress affects pituitary LH responsiveness to GnRH, and whether endogenous opioid peptide (EOP) and dopamine systems are involved in blocking LH and PRL surges during immobilization stress. Immobilization stress was found to inhibit basal LH release and to completely abolish LH surge. However, the intravenous application of GnRH agonist completely restored immobilization-blocked LH surge and basal LH release. Treatment with naloxone did not exert any effect on immobilization-blocked LH surge but increased basal LH release during immobilization stress. Pimozide did not affect immobilization-blocked LH surge or basal LH release. Naloxone also decreased immobilization-induced basal PRL release, but had no effect on immobilization-blocked PRL surge. Immobilization-increased basal PRL levels were augmented by pimozide treatment and immobilization-blocked PRL surge was dramatically restored by pimozide. We conclude that immobilization stress does not impair pituitary LH response to GnRH, and that the immobilization stress-induced blockage of LH surge is probably not mediated by either the opioidergic or the dopaminergic system. However, immobilization-blockade of PRL surge may be partly mediated by the dopaminergic system.
Animal ; Estradiol/*pharmacology ; Female ; Gonadorelin/*pharmacology ; Immobilization ; Luteinizing Hormone/*secretion ; Naloxone/pharmacology ; Opioid Peptides/physiology ; Ovariectomy ; Prolactin/*secretion ; Rats ; Rats, Sprague-Dawley ; Receptors, Dopamine/physiology ; Stress/*metabolism

To compare the effects of ketamine and tiletaminezolazepam (TZ) drugs widely used for the chemical restraint and immobilization of primates, on various physiological parameters and blood gas values in cynomolgus monkeys (Macaca facicularis). Rectal temperature, heart rate, respiration rate and blood gas analysis were measured before treatment and at 1, 10, 20, 30, 40, 50 and 60 min after administration. Additionally, in both groups, induction and maintenance times were compared. Heart rate, respiration rate, rectal temperature, pH and pCO2 were not significant different in the two groups. However, pO2 in the ketamine-treated group was significantly lower at 30 and 40 min than in the TZ-treated group. The induction time was short in both groups, and the maintenance time was longer in the TZ-treated group (67.8+/-6.5 min) than in the ketamine-treated group (42.3+/-6.7 min). However, decreased rectal temperatures must be watched and prevented following TZ administration to cynomolgus monkeys. It was considered that ketamine may be useful for short duration anesthesia including handling, physical examination, blood sampling and TZ may be useful for prolonged anesthesia including minor surgery and other surgical procedure.
Animals ; Body Temperature/drug effects ; Carbon Dioxide/blood ; Excitatory Amino Acid Antagonists/*pharmacology ; Female ; Heart Rate/drug effects ; Hydrogen-Ion Concentration ; Immobilization/*physiology ; Ketamine/*pharmacology ; Macaca fascicularis ; Male ; Partial Pressure ; Respiratory Mechanics ; Restraint, Physical/*methods ; Tiletamine/*pharmacology ; Time Factors

The clinical treatment of joint contracture due to immobilization remains difficult. The pathological changes of muscle tissue caused by immobilization-induced joint contracture include disuse skeletal muscle atrophy and skeletal muscle tissue fibrosis. The proteolytic pathways involved in disuse muscle atrophy include the ubiquitin-proteasome-dependent pathway, caspase system pathway, matrix metalloproteinase pathway, Ca-dependent pathway and autophagy-lysosomal pathway. The important biological processes involved in skeletal muscle fibrosis include intermuscular connective tissue thickening caused by transforming growth factor-β1 and an anaerobic environment within the skeletal muscle leading to the induction of hypoxia-inducible factor-1α. This article reviews the progress made in understanding the pathological processes involved in immobilization-induced muscle contracture and the currently available treatments. Understanding the mechanisms involved in immobilization-induced contracture of muscle tissue should facilitate the development of more effective treatment measures for the different mechanisms in the future.
Atrophy ; Autophagy ; Calcium ; metabolism ; Caspases ; metabolism ; Connective Tissue ; metabolism ; pathology ; Contracture ; etiology ; metabolism ; pathology ; therapy ; Fibrosis ; Humans ; Immobilization ; adverse effects ; Joints ; Lysosomes ; metabolism ; Matrix Metalloproteinases ; metabolism ; Muscle, Skeletal ; metabolism ; pathology ; Proteasome Endopeptidase Complex ; metabolism ; Proteolysis ; Signal Transduction ; physiology ; Transforming Growth Factor beta1 ; metabolism ; Ubiquitin ; metabolism