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The effects of duration and compliance of seating surfaces on reactive hyperemia within the skin overlying the ischial tuberosities was determined in four normal, one paraplegic and one cerebral palsy subject. Reactive hyperemia was demonstrated thermographically after short durations (ie, 5, 10, and 15 minutes) of seating on a hard surface. The magnitude of hyperemic response increased significantly (p < .001 for 15 v 5 minutes; p = .019 for 15 v 10 minutes; p = .001 for 10 v 5 minutes) with increased duration of seating. In all six subjects studied, the maximum postseating blood flow continued to increase with up to 15-minute seating on a hard surface, and the mean maximum response was positively correlated with duration of seating (4 = 0.918, p < 0.001). Although there was good correlations between magnitudes of interface pressures measured and vascular responses within each individual, there was no such direct correlation between individuals.

Calcium uptake by sarcoplasmic reticulum vesicles from batrachotoxin- or surgically denervated muscle was measured by both isotopic and energy dispersal X-ray procedures. In the presence of inorganic phosphate, vesicles obtained from both chemically and surgically denervated muscle accumulated less calcium than control vesicles. Intravesicular calcium appeared to be present either as a crystalline or granular precipitate. Our results support the concept that batrachotoxin, by blocking both axonal transport and impulse activity, results in a chemical denervation of the muscle.

The numbers of motoneurons in the brachial lateral motor columns were determined from the 6th embryonic day through the 5th week posthatching in age-matched dystrophic and normal chickens. The overall magnitude of cell loss was not significantly different between the dystrophic and normal strains. However there was a trend toward more motoneurons in the brachial lateral motor columns of dystrophic embryos and posthatch chickens which was found to be statistically significant at the 8th and 9th days of embryonic life. These observations are taken to suggest that, in addition to strain differences unrelated to the dystrophic gene, there may exist a temporal delay in developmental neuron cell death in dystrophic chick embryos that may be secondary to the primary defect within the dystrophic muscle.