No abstract available.
Animals ; Carbohydrate Metabolism* ; Hindlimb Suspension* ; Hindlimb* ; Insulin* ; Muscle, Skeletal* ; Rats* ; Receptor, Insulin*

OBJECTIVETo explore the protective effects of two types of ischemic postconditioning (IP) on intestinal mucosa barrier in rabbits with crush injury of the hind limb.

METHODSThis study was conducted between August and December 2008 in the Department of Trauma Surgery, Daping Hospital, Third Military Medical University, Chongqing, China. The model of crush injury to the hind limb of rabbits was firstly developed by a 25 kg object with the right hind limbs fixed by wooden splints, and then two types of IP were established, including occluding/opening the common iliac artery and vein alternatively (traditional IP, IP A) and binding/loosening the proximum of the injured hind limb alternatively (modified IP, IP B). Thirty-six male New Zealand white rabbits were randomly divided into three groups: IP A group, IP B group and control group, with 12 rabbits in each group. The serum levels of diamine oxidase (DAO) and intestinal fatty acid-binding protein (I-FABP) were detected at 2, 6, 12 and 24 hours after injury. Pathological changes of ileum were examined at 24 hours after injury.

RESULTSThe serum levels of I-FABP at 2, 6, 12 and 24 hours after injury in both IP A and IP B groups had a significant decrease, compared with control group. DAO levels also showed the same change trend at 2 and 6 hours after injury, but showed no significant difference between two IP groups. No difference in pathological changes of ileum was found among the three groups.

CONCLUSIONSIP can protect intestinal mucosa barrier function on the model of hind limb crush injury in rabbits. Meanwhile the modified IP B shows the same protection as the traditional IP A, and is worth applying in clinic.

Amine Oxidase (Copper-Containing) ; metabolism ; Animals ; Hindlimb ; injuries ; Intestinal Mucosa ; metabolism ; Ischemic Postconditioning ; Male ; Rabbits

Objective: To study the effects of vibration on the expression of mitochondrial fusion and fission genes and ultrastructure of skeletal muscle in rabbits. Methods: Thirty-two 3.5-month-old New Zealand rabbits were randomly divided into low-intensity group, medium-intensity group, high-intensity group and control group, with 8 rabbits in each group. The rabbits in the experimental group were subjected to hind limb vibration load test for 45 days. The vibration intensity of the high intensity group was 12.26 m/s(2), the medium intensity group was 6.13 m/s(2), and the low intensity group was 3.02 m/s(2) according to the effective value of weighted acceleration[a(hw (4))] for 4 hours of equal energy frequency. The control group was exposed to noise only in the same experimental environment as the medium-intensity group. The noise levels of each group were measured during the vibration load experiment. After the test, the mRNA expression of mitochondrial fusion gene (Mfn1/Mfn2) and fission gene (Fis1, Drp1) by RT-PCR in the skeletal muscles were measured and the ultrastructure of the skeletal muscles were observed in high intensity group. Results: The mRNA expression of mitochondrial in the skeletal muscle tissues of control group, low intensity group, medium intensity group and high intensity group were Mfn1: 3.25±1.36, 3.85±1.90, 4.53±2.31 and 11.63±7.68; Mfn2: 0.68±0.25, 1.02±0.40, 0.94±0.33 and 1.40±0.45; Fis1: 1.05±0.62, 1.15±0.59, 1.53±1.06 and 2.46±1.51 and Drp1: 3.72±1.76, 2.91±1.63, 3.27±2.01 and 4.21±2.46, respectively. Compared with the control group, the expressions of Mfn1 mRNA, Mfn2 mRNA and Fis1 mRNA in the high-intensity group increased significantly (P<0.05) , and the expressions of Mfn2 mRNA in the medium-intensity group and the low-intensity group increased significantly (P<0.05) . Compared with the control group, the ultrastructure of skeletal muscle of high intensity group showed mitochondrial focal accumulation, cristae membrane damage, vacuole-like changes; Z-line irregularity of muscle fibers, and deficiency of sarcomere. Conclusion: Vibration must be lead to the abnormal mitochondrial morphology and structure and the disorder of energy metabolism due to the expression imbalance of mitochondrial fusion and fission genes in skeletal muscles of rabbits, which may be an important target of vibration-induced skeletal muscle injury.
Animals ; Hindlimb/metabolism* ; Mitochondria/metabolism* ; Mitochondrial Dynamics ; Mitochondrial Proteins/pharmacology* ; Muscle, Skeletal ; Rabbits ; Vibration/adverse effects*

The aim of the present study was to investigate the expressions of calpain and calpastatin in the myocardium of simulated weightlessness rats, and to elucidate the underlying mechanism of cardiac troponin I (cTnI) degradations. Tail-suspended (SUS) rats were used as a simulated weightlessness model on the ground. The myocardium of rats was homogenized, and the expressions of calpain-1, calpain-2, calpastatin and cTnI were analyzed by Western blotting technique. Calpastatin expression was significantly decreased in 2- and 4-week SUS groups compared with that in the synchronous controls (P<0.05). Calpain-2 expression was slightly decreased, whereas calpain-1 expression was unaltered in SUS groups. However, calpain-1/calpastatin and calpain-2/calpastatin ratios were increased after tail-suspension, being significantly higher in 2- and 4-week SUS groups than those in the synchronous controls (P<0.05, P<0.01). Cardiac TnI degradation was significantly increased after tail-suspension (P<0.01), but cTnI degradation in both SUS and control groups was significantly inhibited by a non-specific inhibitor of calpain, PD150606 (P<0.01). These results suggest that an increase in calpain activity may enhance cTnI degradation in the myocardium of tail-suspended rats.
Animals ; Calcium-Binding Proteins ; metabolism ; Calpain ; metabolism ; Hindlimb Suspension ; Myocardium ; metabolism ; Proteolysis ; Rats ; Troponin I ; metabolism ; Weightlessness Simulation

The purpose of this study was to determine the effect of releasing of immobilization on glycogen metabolism of hindlimb muscle after 7days use of a hindlimb casting in mice. The experimental group was divided into control group and recovery groups after removal of left hindlimb casting. The recovery groups, were subivided into the 0, 3rd and 5th day after removal of left hindlimb casting. The results were as follows; 1. The degree of atrophy of hindlimb muscles by 7 days immobilization was measured by ratio of muscle to body weight in plantaris and soleus muscles. The muscle to body weight ratios of plantaris and soleus muscles were decreased by 88% and 74%, respectively on the day of cast removal. The ratios of the both muscles were increased to the level of the control values on the 3rd and 5th day removal of casting. 2. A significant reduction of the glycogen concentration in gastrocnemius muscle occurred after 7 days hindlimb immobilization. The glycogen concentration in gastrocnemius muscle was decreased by 63% on the day of cast removal. The glycogen concentration was recovered to the values of the control group on the 3rd and 5th day after removal of hindlimb casting. 3. The level of muscle glycogen concentration of 25% glucose ingested control group was almost twice that of the normal diet control group. The muscle glycogen concentration of glucose ingested group was significantly less by 81% after 7 days of immobilization compared with the respective control gmup. The concentration recovered to the values of control on the 3rd and 5th day after removal of hindlimb casting. In contrast, there was no significant difference in the liver glycogen concentration between the immobilized grop and the cast removed group in which was removed. 4. The effects of releasing of hindlimb immobilization on plasma glucose, insulin concentration and insulin
Animals ; Atrophy ; Blood Glucose ; Body Weight ; Diet ; Glucose ; Glycogen ; Hindlimb Suspension ; Hindlimb ; Hypokinesia ; Immobilization ; Insulin ; Liver Glycogen ; Metabolism ; Mice ; Muscle, Skeletal ; Muscles

The purpose of this animal experiment was to evaluate the changes of bone mineral density in paralyzed limbs, and to assess the effects of electrically stimulating muscle contraction upon bone mineral density (BMD) in paralyzed limbs during the four week period immediately following spinal cord injury (SCI). Ten rabbits were used for the study, spinal cords were totally transected at the T11 spine level. The paralyzed quadriceps femoris of one limb was contracted by electrical stimulation for 60-minutes daily, while the other side was not stimulated as a control. The BMD of each lower limb was measured by Dual Photon Absorptiometry before and four weeks after acute SCI. BMD of both limbs decreased in all rabbits four weeks after SCI. The decrease in BMD for stimulated and non-stimulated limbs was 6.130 +/- 3.212% and 9.098 +/- 3.831%, respectively during the four-week period after SCI. The BMD of stimulated limbs decreased significantly less than that of the non-stimulated limbs. Electrically induced muscular contraction reduced bone mineral loss in the paralyzed limb during the early stage of SCI in the rabbit.
Animal ; Bone Density* ; Electric Stimulation Therapy* ; Hindlimb* ; Male ; Paralysis/therapy* ; Paralysis/metabolism* ; Rabbits

Animals ; Hindlimb ; blood supply ; Ischemic Preconditioning ; Lung ; metabolism ; Male ; P-Selectin ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

Microgravity is known to produce a number of neurological disturbances during space flight; however, the underlying mechanism of these disturbances is yet to be elucidated. There have been some reports about the increased oxidative stress under microgravity or simulated microgravity. In the present study, we investigated the process of oxidative stress induced by simulated microgravity in different areas of rat brain, which may shed light on the mechanism of neurological disturbances and further neuroprotective research in spaceflight. After adaption for 7 d, 40 healthy male Sprague-Dawley rats were matched for body weight and randomly assigned to control groups (7, 14, 21 and 28 d) and tail-suspended simulated microgravity groups (7, 14, 21 and 28 d). The tail-suspended groups were treated with 30 angels of tail suspension and the control groups were treated similarly to the tail-suspended groups but without tail suspension. After the required times, different structures of rat brain, including cerebellum, cerebral cortex and hippocampus, were harvested and frozen for the further determination. Griess assay, thiobarbituric acid reactive substance (TBARS) assay, competitive ELISA and ferric reducing ability of plasma (FRAP) assay were used for the observation of the changes of reactive nitrogen species (RNS), malondialdehyde (MDA), nitrotyrosine (NT) and total antioxidant capacity (TAC), respectively. As shown in the results, there were different changes in various brain regions after tail suspension compared with control groups. (1) In cerebellum, NT increased after 7 d tail suspension, decreased after 14 d and increased again after 28 d; MDA increased after 14 d; RNS increased and TAC decreased after tail suspension for 21 d; (2) Increase of NT after14 d tail suspension, increase of MDA and decrease of TAC after 21 d were found in cerebral cortex; (3) In hippocampus, RNS increased after tail suspension for 7 d, decreased after 14 d and increased again after 28 d; MDA increased after 21 d; NT increased after 28 d; TAC increased after 7 d and recovered after 21 d. These results suggest that simulated microgravity induced by tail suspension increases the level of oxidative stress in rat brain; however, there are different features in different areas of rat brain. During the response to simulated microgravity, rat brain tissues present a similar process from adaptive response to irreversible oxidative damage.
Animals ; Antioxidants ; metabolism ; Brain ; physiopathology ; Hindlimb Suspension ; Male ; Malondialdehyde ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Weightlessness Simulation

Animals ; Hindlimb ; blood supply ; Intestine, Small ; metabolism ; Ischemia ; metabolism ; prevention & control ; Ischemic Preconditioning ; Lung Injury ; metabolism ; Male ; Muscle, Skeletal ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism

OBJECTIVETo explore the role of myeloperoxidase (MPO) and tumor necrosis factor-α (TNF-α) in myocardial injury induced by hind-limb ischemia-reperfusion (IR) in rats.

METHODSRat models of bilateral hindlimb IR established using a tourniquet were randomized into 9 groups, including a normal control group normal, 2 ischemic groups with hindlimb ischemia for 2 and 4 h, and 6 IR groups with a 4-h ischemia followed by reperfusion for 0.5, 2, 4, 6, 12, and 24 h. The plasma and myocardial levels of MPO and TNF-α in each group were measured, and the myocardial expression of TNF-α was determined with immunohistochemistry.

RESULTSCompared with the normal control group, the rats with a 2-h ischemia showed significantly increased levels of MPO and TNF-α in the plasma and myocardium. Compared with those in rats with a 4-h ischemia, the plasma and myocardial MPO levels increased significantly at 0.5 and 2 h of reperfusion, respectively; the plasma TNF-α level increased significantly at 4 h of reperfusion and myocardial TNF-α level decreased obviously at 12 h; plasma levels of MPO and TNF-α both significantly decreased at 24 h. The plasma MPO and TNF-α and myocardial TNF-α reached the peak levels at 4 h of reperfusion, and the peak myocardial MPO level occurred at 6 h. Immunohistochemistry showed that TNF-α positivity moderately increased after hindlimb ischemia, and further increased at 4 h of reperfusion but obviously reduced at 24 h.

CONCLUSIONThe activation of systemic and local neutrophils and inflammatory cytokines may play an important role in myocardial injury induced by hindlimb IR in rats.

Animals ; Disease Models, Animal ; Hindlimb ; blood supply ; Ischemia ; metabolism ; Male ; Myocardium ; metabolism ; Peroxidase ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism