Statistical treatment of oxygenation-related data in muscle tissue.

Muscle oxygenation is determined not only by the flow and oxygen content of the supplying blood but also by the density of the capillary network, the heterogeneity of the distribution of the capillaries and the properties and distribution of the muscle fibres. The distribution of the capillaries is adequately analysed by the method of capillary domains, which also allows to link capillaries to individual fibres. Thus, capillarisation can be linked to cell properties like fibre cross-sectional surface area and perimeter, and oxygen consumption of the individual muscle fibres.

Region-specific adaptations in determinants of rat skeletal muscle oxygenation to chronic hypoxia.

Chronic exposure to hypoxia is associated with muscle atrophy (i.e., a reduction in muscle fiber cross-sectional area), reduced oxidative capacity, and capillary growth.

The influence of flow redistribution on working rat muscle oxygenation.

We applied a theoretical model of muscle tissue O2 transport to investigate the effects of flow redistribution on rat soleus muscle oxygenation. The situation chosen was the anaerobic threshold where redistribution of flow is expected to have the largest impact. In the basic situation all capillaries received an equal proportion of the total flow through the tissue, resulting in 4.

Maintenance of heterogeneity of capillary spacing is essential for adequate oxygenation in the soleus muscle of the growing rat.

Objectives: Normal muscle growth is accompanied by capillary proliferation, which usually lags behind the increase in muscle size, causing a decline in mean capillary density (CD). It is not known, however, how the capillary distribution is affected and what impact it has on the oxygenation of the muscle.

Methods: The capillarization of soleus muscles of rats (64-425 g) was determined with the method of capillary domains.

Calbindin-D28K dynamically controls TRPV5-mediated Ca2+ transport.

In Ca(2+)-transporting epithelia, calbindin-D(28K) (CaBP(28K)) facilitates Ca(2+) diffusion from the luminal Ca(2+) entry side of the cell to the basolateral side, where Ca(2+) is extruded into the extracellular compartment. Simultaneously, CaBP(28K) provides protection against toxic high Ca(2+) levels by buffering the cytosolic Ca(2+) concentration ([Ca(2+)](i)) during high Ca(2+) influx. CaBP(28K) consistently colocalizes with the epithelial Ca(2+) channel TRPV5, which constitutes the apical entry step in renal Ca(2+)-transporting epithelial cells.