[NERVE SUPPLY OF THE LEVATORES COSTARUM AND MORPHOLOGICAL CONSIDERATIONS].
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BACKGROUND: Tumor necrosis factor alpha (TNF-alpha) has been implicated in loss of muscle mass in chronic obstructive pulmonary disease and other consumptive processes. TNF-alpha production would be related to inflammation arising from pulmonary disease itself or, alternatively, from smoking, and would be carried to the muscle through the blood stream. However, it has also been suggested that TNF-alpha may be expressed directly in muscle tissue. Regardless the site of production of TNF-alpha, its relation to subsequent muscle damage is unclear. OBJECTIVE: We studied the expression of TNF-alpha and an interleukin inhibitor of its production (IL-10) in the main respiratory muscles and a peripheral muscle in the dog. METHOD: Nine young, male Beagle dogs were included. From all animals we obtained a biopsy of the diaphragm (Dph) and external intercostal (ExtI) muscles and a leg muscle (internal vastus of the quadriceps, IntV). TNF-alpha and IL-10 gene expressions were measured through the analysis of messenger RNA levels, using reverse transcription and polymerase chain reaction. We also assessed sarcolemmal damage using intracellular fibronectin detection (immunohistochemistry). RESULTS: The expression of both cytokines showed wide interindividual variability. On the one hand, TNF-alpha (was very low in Dph and ExtI (0.02 0.03 and 0.05 0.06 a.u., respectively), but relatively high in the IntV (0.14 0.08 a.u.). IL-10 expression, on the other hand was low in the Dph (0.06 0.05 a.u.) and slightly higher in the ExtI (2.7 1.9 a.u., p < 0.01) and IntV (1.6 1.7 a.u.). Sarcolemmal damage was minimal in all three muscles and was related to TNF-alpha expression in the peripheral muscle (r = 0.682, p < 0.05). CONCLUSIONS: 1) TNF-alpha and IL-10 appear to be constitutively expressed within the skeletal muscle in dogs. 2) Basal TNF-alpha expression is lower in respiratory muscles than in peripheral muscles. 3) The expression in the latter is related to membrane damage.
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The effect of sleep state on ventilation and the mechanics of breathing was studied in nine normal adolescents by use of a respiratory inductive plethysmograph and surface electromyogram electrodes. Minute ventilation was state dependent (P less than 0.01), decreasing by a mean of 8% from wakefulness to nonrapid-eye-movement (NREM) sleep and increasing 4% from NREM to rapid-eye-movement (REM) sleep. These changes were caused by changes in respiratory rate. Tidal volume (VT) was not affected by sleep state (P greater than 0.10). The pattern of breathing during wakefulness was similar to that of REM sleep. During NREM sleep intercostal and diaphragmatic muscle activity increased by a mean of 34% and 11%, respectively, as compared with wakefulness, indicating an increase in the respiratory work load. This was accompanied by a substantial increase in rib cage contribution to VT. REM sleep was associated with a marked decrease in intercostal muscle activity (P less than 0.05) and a diminished rib cage contribution; VT was maintained due to a mean increase of 34% in diaphragmatic muscle activity (P less than 0.05).
Lorisid locomotor and postural behaviour exhibits a number of features that distinguish it clearly from other primates. The comparative myological study of the trunk in the slow loris (Nycticebus coucang) and the squirrel monkey (Saimiri sp.) presented here reveals differences that are related to unique aspects of lorisid positional behaviour. While quadrupedal running and leaping requires flexion and extension of the spine, slow climbing quadrupedalism in lorisids depends on spinal lateral flexion and rotation. The contrasting development of the epaxial musculature in the two species dissected reflects these different requirements. Bipedal suspension is a common posture in the lorisids during which rotation and dorsiflexion of the head is made possible by the robustly developed deep, dorsal, cervical musculature. The long lower lever arm in the M. rectus abdominis may play a significant role in the ventroflexion required to regain a quadrupedal stance.
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Displacements of the rib cage are determined by the intrinsic passive properties of the rib cage, rib cage musculature, pleural and abdominal pressures, and the diaphragm. The diaphragm's mechanical actions on the rib cage are inferred from a force-balance analysis in which the diaphragm is seen to cause expansion of the rib cage by pulling cephalad at its insertions on the lower ribs (insertional component) and by raising intra-abdominal pressure, which pushes outward on the diaphragm's zone of apposition to the rib cage (appositional component). Goldman and Mead suggested that the diaphragm, acting alone, could drive both the rib cage and abdomen on their passive characteristics. The force-balance analysis shows that the diaphragm's inspiratory action on the rib cage is less than predicted by Goldman and Mead, but that in the special circumstances of their experiment (low lung volumes), the appositional component is large and the rib cage can be driven close to its passive characteristics. The force-balance analysis is consistent with recent observations by other investigations and is incompatible with the model proposed by Macklem and colleagues and with the Goldman-Mead hypothesis. Experiments on three subjects produced data consistent with the force-balance analysis, showing that the inspiratory action of the diaphragm on the rib cage is greatest at low lung volumes.
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We examined the participation of expiratory muscles on breathing in the rat. The experiments were performed on 16 male rats in halothane [1.5%] or urethane [1.3 g/kg i.p.] anaesthesia. We recorded the electromyographic [EMG] activity of intercostal and abdominal muscles with a concentric needle electrode during quiet breathing, breathing against increased pressure in the airways and during the expiration reflex. In halothane anaesthesia the EMG expiratory phasic activity was observed only in internal intercostal muscles in 40% of spots examined during quiet breathing and in 58.5% when breathing against increased pressure. The EMG activity during the expiratory reflex was difficult to evaluate. In the abdominal muscles permanent EMG activity was found in 66% of trials. In urethane anaesthesia no phasic expiratory EMG activity was observed in intercostal or abdominal muscles. In abdominal muscles in 9% of trials a permanent activity was found.
Myogenin and MRF4 are skeletal muscle-specific bHLH transcription factors critical for muscle development. In addition to a variety of skeletal muscle defects, embryos homozygous for mutations in myogenin or MRF4 display phenotypes in the thoracic skeleton, including rib fusions and sternal defects. These skeletal defects are likely to be secondary because myogenin and MRF4 are not expressed in the rib cartilage or sternum. In this study, the requirement for myogenin and MRF4 in thoracic skeletal development was further examined. When a hypomorphic allele of myogenin and an MRF4-null mutation were placed together, the severity of the thoracic skeletal defects was greatly increased and included extensive rib cartilage fusion and fused sternebrae. Additionally, new rib defects were observed in myogenin/MRF4 compound mutants, including a failure of the rib cartilage to contact the sternum. These results suggested that myogenin and MRF4 share overlapping functions in thoracic skeletal formation. Spatial expression patterns of skeletal muscle-specific markers in myogenin- and MRF4-mutant embryos revealed early skeletal muscle defects not previously reported. MRF4-/- mice displayed abnormal intercostal muscle morphology, including bifurcation and fusion of adjacent intercostals. myogenin/MRF4-mutant combinations displayed ventral myotome defects, including a failure to express normal levels of myf5. The results suggested that the early muscle defects observed in myogenin and MRF4 mutants may cause subsequent thoracic skeletal defects, and that myogenin and MRF4 have overlapping functions in ventral myotome differentiation and intercostal muscle morphogenesis.
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