Key result
Dystrophic ischiatic arteries were less sensitive to serotonin than normal arteries, while sensitivity to noradrenaline was similar, contradicting the view that muscle necrosis is due to anoxia.
Why the study?
Do isolated ischiatic arteries from dystrophic chickens exhibit different pharmacological responses to serotonin and noradrenaline compared to normal chickens?
Do isolated ischiatic arteries from dystrophic chickens exhibit different pharmacological responses to serotonin and noradrenaline compared to normal chickens?
Dystrophic avian arteries show reduced sensitivity and tension generation in response to serotonin compared to normal arteries, which does not support the hypothesis that muscle fibre necrosis in avian dystrophy is caused by muscle anoxia.
Challenges anoxia hypothesis for necrosis in avian dystrophy model; leaves open relevance to mammalian or human disease.
The pathogenesis of the human muscular dystrophies is unknown, and several competing hypotheses have been proposed. The vascular hypothesis states that muscle fibre necrosis occurs in dystrophy as a result of transient muscle ischemia. Although abnormalities of the vascular system may be demonstrated in dystrophy, their role in pathogenesis remains obscure. The responses to serotonin (5-HT) and noradrenaline (NA) were examined in isolated ischiatic artery preparations from normal and genetically dystrophic chickens. The tension generated in response to 5-HT was greater in arteries from normal chickens than in arteries from dystrophic chickens, whereas responses to NA were similar. Analysis of the concentration-response relationships demonstrated that the dystrophic ischiatic artery was less sensitive to 5-HT than was the normal artery, although the sensitivity to NA was similar in both vessels. The results of this study are not consistent with the view that muscle fibre necrosis in avian dystrophy is a consequence of muscle anoxia. These data do demonstrate pharmacological differences between dystrophic avian arteries and arteries from normal chickens, but their presence may represent merely the expression of dystrophy in vascular smooth muscle.
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Howlett et al. (1986) studied Muscular dystrophy. Genetically dystrophic chickens vs. Normal chickens was evaluated on Tension generated in response to serotonin (5-HT) and noradrenaline (NA). Dystrophic ischiatic arteries were less sensitive to serotonin than normal arteries, while sensitivity to noradrenaline was similar, contradicting the view that muscle necrosis is due to anoxia.
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