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.

Corticosterone synthesis and serum levels at the end of the perinatal period a study of the effects of stress, diazepam and polyethylene glycol treatments.

The effects of stress (intraperitoneal injections onece daily for three days), diazepam (Faustan, Germed) and polyethylene glycol (Macrogolum, Spofa) on the corticosterone production rate (BPR) and concurrent changes in serum corticosterone levels (BSL) were investigated in 4-day-old male rats. Stress stimulation increased the BSL but the BPR was affected only slightly and the difference was not statistically significant. A low dose of diazepam (1 mg/kg) prevented the stress-induced rise in BSL and decrease of BPR, in comparison to stressed animals. On the contrary, high doses of diazepam (10 mg/kg) increased the BSL, while BPR corresponded to control values. Polyethylene glycol (0.12 g/kg; substance of this class is contained in the diazepam vehiculum) decreased the BSL, but the BPR was increased above control values; a higher dose of this substance (1.2 g/kg) yielded only scattered, non-significant results. It is concluded that in preweaned animals 1. the changes in BSL may be associated with minor or transient changes in BPR which indicate small changes in brainpituitary adrenocorticotropic activity, 2. changes in peripheral corticosterone metabolism can play an exceptionally important role in the regulation of glucocorticoid activity in very young rats, 3. a comparison of controls with stressed animals which had received low doses of diazepam indicate a relatively high steady state activity of adrenal cortex and its regulation in 4-day-old control rats.

Cholinesterase reactivators - contribution to the study of their metabolic effects.

Cholinesterase reactivators - trimedoxim, methoxim and obidoxim - injected in the dose of 20 mg/kg s.c., increase muscle glycogen concentration in normal, but not in adrenalectomized rats. This effect may be in connection with simoultaneously found rise of serum corticosteron level. Trimedoxim decreases adrenaline, methoxim and obidoxim noradrenaline concentration in adrenals.

Effect of sodium intake on aldosterone and corticosterone production, the serum sodium concentration and body weight in infant rats during weaning period.

1. The effect of a low salt (LS, 0.3% NaC1) and control (HS, 1% NaC1) diet on in vitro aldosterone and corticosterone production, the serum corticosterone level, the serum sodium concentration and adrenal and body weight was studied in 30-day-old male rats, some of which were weaned prematurely at the age of 15 days (PW) and some left with the female up to the end of the experiment (NW). 2. Aldosterone production in the control (HS-NW) animals was 1.07+/-0.07 mug/100 mg adrenal/hour (mean +/-S.E.M.), in HS-PW animals 0.6+/-0.07 (P less than 0.01), while in LS-NW and LS-PW animals it rose to 1.59+/-0.1 and 1.81+/-0.14 respectively. The effect of the salt regimen was significant in both the NW group (P less than 0.01) and the PW group (P less than 0.01). Premature weaning did not inhibit aldosterone production in LS-PW animals. 3. Corticosterone production in animals fed on the control diet was 1.81+/-0.16 mug corticosterone/100 mg adrenal/hour in HS-NW rats and 0.91+/-0.09 in the HS-PW group (P less than 0.01). On the low salt diet it fell to 1.4+/-0.11 in LS-NW rats (HW-NW) vs LS-NW: P less than 0.01) and to 0.4+/-0.06 in LS-PW animals (HS-PW vs LS-PW: P less than 0.01). The difference between LS-NW and LS-PW was likewise statistically significant (P less than 0.01). Changes in production were not accompanied by parallel changes in the serum corticosterone level, where an analysis of variance showed no significant difference. 4. The low salt diet reduced the serum sodium concentration in both NW and PW animals (HS-NW 132.9+/-0.86 mEd HS-PW 132+/-0.86, LS-PW 128.5+/-1.16: P less than 0.01). The differences between NW and PW animals were not significant. 5. A low salt intake also reduced the body weight both of animals left with the female (HS-NW vs LS-NW: P less than 0.01) and of prematurely weaned animals (HS-PW vs LS-PW: P less than 0.01). Early weaning significantly affected body weight in LS animals only, the body weight of LS-PW animals being significantly lower than that of LS-NW animals (P less than 0.02). 6. The results show that infant rats are hypersensitive to a low salt intake at the end of the weaning period and that this phenomenon is not mediated by lower reactivity of the zona glomerulosa and of its regulation.