Do hormonal (stress) and vascular (ischaemia) factors contribute to reflex muscle atrophy induced by chronic nociceptive stimulation in rats?

1. Reflex muscle atrophy was induced in rats by fracturing the metatarsal bones of one hind paw and injecting 0.02 ml turpentine oil into the planta under shortlasting ether anaesthesia. The atrophy thus evoked in the soleus and extensor digitorum longus (EDL) was compared with the contralateral muscles. 2. There was a twelvefold increase of plasma corticosteroid levels one hour after application of the above nociceptive stimulus and the levels were still somewhat enhanced at 3 days. Neither bilateral adrenalectomy nor administration of corticosteroid hormones or cold stress affected the development of reflex atrophy. 3. Restriction of the arterial blood supply (ligature of the common iliac artery) led to a slowly progressing atrophy with a maximum 10 days after the ligature. Reflex atrophy introduced at different times after ligature was not enhanced. 4. These results are interpreted as evidence that neither general stress (and the effect of catabolic hormones) nor local restriction of muscle blood flow (by reflex vasospasm, for example) are likely to play any appreciable role in the mechanism of reflex muscle atrophy.