57 resultados para skeletal muscles
Resumo:
We have previously demonstrated that remote ischemic preconditioning (IPC) by instigation of three cycles of 10-min occlusion/reperfusion in a hindlimb of the pig elicits an early phase of infarct protection in local and distant skeletal muscles subjected to 4 h of ischemia immediately after remote IPC. The aim of this project was to test our hypothesis that hindlimb remote IPC also induces a late phase of infarct protection in skeletal muscle and that K(ATP) channels play a pivotal role in the trigger and mediator mechanisms. We observed that pig bilateral latissimus dorsi (LD) muscle flaps sustained 46 +/- 2% infarction when subjected to 4 h of ischemia/48 h of reperfusion. The late phase of infarct protection appeared at 24 h and lasted up to 72 h after hindlimb remote IPC. The LD muscle infarction was reduced to 28 +/- 3, 26 +/- 1, 23 +/- 2, 24 +/- 2 and 24 +/- 4% at 24, 28, 36, 48 and 72 h after remote IPC, respectively (P <0.05; n = 8). In subsequent studies, hindlimb remote IPC or intravenous injection of the sarcolemmal K(ATP) (sK(ATP)) channel opener P-1075 (2 microg/kg) at 24 h before 4 h of sustained ischemia (i.e., late preconditioning) reduced muscle infarction from 43 +/- 4% (ischemic control) to 24 +/- 2 and 19 +/- 3%, respectively (P <0.05, n = 8). Intravenous injection of the sK(ATP) channel inhibitor HMR 1098 (6 mg/kg) or the nonspecific K(ATP) channel inhibitor glibenclamide (Glib; 1 mg/kg) at 10 min before remote IPC completely blocked the infarct- protective effect of remote IPC in LD muscle flaps subjected to 4 h of sustained ischemia at 24 h after remote IPC. Intravenous bolus injection of the mitochondrial K(ATP) (mK(ATP)) channel inhibitor 5-hydroxydecanoate (5-HD; 5 mg/kg) immediately before remote IPC and 30-min intravenous infusion of 5-HD (5 mg/kg) during remote IPC did not affect the infarct-protective effect of remote IPC in LD muscle flaps. However, intravenous Glib or 5-HD, but not HMR 1098, given 24 h after remote IPC completely blocked the late infarct-protective effect of remote IPC in LD muscle flaps. None of these drug treatments affected the infarct size of control LD muscle flaps. The late phase of infarct protection was associated with a higher (P <0.05) muscle content of ATP at the end of 4 h of ischemia and 1.5 h of reperfusion and a lower (P <0.05) neutrophilic activity at the end of 1.5 h of reperfusion compared with the time-matched control. In conclusion, these findings support our hypothesis that hindlimb remote IPC induces an uninterrupted long (48 h) late phase of infarct protection, and sK(ATP) and mK(ATP) channels play a central role in the trigger and mediator mechanism, respectively.
Resumo:
The motor points of the skeletal muscles, mainly of interest to anatomists and physiologists, have recently attracted much attention from researchers in the field of functional electrical stimulation. The muscle motor point has been defined as the entry point of the motor nerve branch into the epimysium of the muscle belly. Anatomists have pointed out that many muscles in the limbs have multiple motor points. Knowledge of the location of nerve branches and terminal nerve entry points facilitates the exact insertion and the suitable selection of the number of electrodes required for each muscle for functional electrical stimulation. The present work therefore aimed to describe the number, location, and distribution of motor points in the human forearm muscles to obtain optimal hand function in many clinical situations. Twenty three adult human cadaveric forearms were dissected. The numbers of primary nerves and motor points for each muscle were tabulated. The mean numbers and the standard deviation were calculated and grouped in tables. Data analyses were performed with the use of a statistical analysis package (SPSS 13.0). The proximal third of the muscle was the usual part of the muscle that received the motor points. Most of the forearm muscles were innervated from the lateral side and deep surface of the muscle. The information in this study may also be usefully applied in selective denervation procedures to balance muscles in spastic upper limbs. Copyright © 2007 Via Medica.
Resumo:
The organisation of the human neuromuscular-skeletal system allows an extremely wide variety of actions to be performed, often with great dexterity. Adaptations associated with skill acquisition occur at all levels of the neuromuscular-skeletal system although all neural adaptations are inevitably constrained by the organisation of the actuating apparatus (muscles and bones). We quantified the extent to which skill acquisition in an isometric task set is influenced by the mechanical properties of the muscles used to produce the required actions. Initial performance was greatly dependent upon the specific combination of torques required in each variant of the experimental task. Five consecutive days of practice improved the performance to a similar degree across eight actions despite differences in the torques required about the elbow and forearm. The proportional improvement in performance was also similar when the actions were performed at either 20 or 40% of participants' maximum voluntary torque capacity. The skill acquired during practice was successfully extrapolated to variants of the task requiring more torque than that required during practice. We conclude that while the extent to which skill can be acquired in isometric actions is independent of the specific combination of joint torques required for target acquisition, the nature of the kinetic adaptations leading to the performance improvement in isometric actions is influenced by the neural and mechanical properties of the actuating muscles.
Resumo:
Myostatin is a negative regulator of skeletal muscle growth. We have previously reported that recombinant myostatin protein inhibits DNA and protein synthesis in C2C12 cells. Our objective was to assess if C2C12 cells express myostatin, determine its sub-cellular localization and the developmental stage of C2C12 cells in which myostatin mRNA and protein are expressed. To study the endogenous expression of myostatin, C2C12 myoblasts were allowed to progress to myotubes, and changes in the levels of endogenous myostatin mRNA expression were determined by RT-PCR. The myostatin protein and the two major myosin heavy chain (MHC) isoforms (MHC-I and -II) were determined by Western blot. Confirmation of the relative MHC expression patterns was obtained by a modified polyacrylamide gel electropheretic (PAGE) procedure. Imunofluorescence staining was employed to localize the site of myostatin expression and the relative distribution of the MHC isoforms. Co-expression of these proteins was studied using a dual staining approach. Expression of myostatin mRNA was found in myotubes but not in myoblasts. Myostatin protein was seen in most but not all, of the nuclei of polynucleated fibers expressing MHC-II, and myostatin was detected in the cytoplasm of myotube. The localization of myostatin protein in myotube nuclei was confirmed by Western blot of isolated nuclear and cytoplasmic fractions. Incubation of C2C12 myotubes with graded doses of dexamethasone dose-dependently increased the intensity of nuclear myostatin immunostaining and also resulted in the appearance of cytoplasmic expression. In conclusion, myostatin was expressed mostly in C2C12 myotubes nuclei expressing MHC-II. Its predominant