PubMed · 647538
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J D Stenstrom, R J Raine. 1978-05-20. The nonmigrating pin.. https://pubmed.ncbi.nlm.nih.gov/647538/
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In this study, experimental allergic encephalomyelitis (EAE) rats and rats exhibiting EAE expressing high circulating anti-nerve growth factor antibody were daily monitored for clinical signs and chronic relapses. Eighty-five days after EAE induction, blood, spinal cord and brain stem were used for histological examination, nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) evaluation. The results showed that NGF-deprived rats display more severe clinical signs of disease. These effects were associated with a significant reduction of NGF in the brain stem and spinal cord but not of BDNF, which decreased only in spinal cord. These observations provide additional support to the hypothesis of a protective NGF role in rats exhibiting EAE.
The impact of hypoxia on somatostatin (SS) secretion from the median eminence (ME) of the hypothalamus and the possible glucocorticosteroid involvement in modulating secretion, were investigated in adult male rats exposed to hypoxia. SS levels were measured by specific radioimmunoassay during acute and prolonged hypoxia as well as after bilateral adrenalectomy (ADX) with or without a replacement with dexamethasone (DEX). The results were as follows: (a) acute hypoxia (5 km altitude, 10.8% O(2)) for 2 and 24 h markedly increased SS content in ME, but acute severe hypoxia (7 km, 8.2% O(2) for 24 h) markedly decreased SS level in ME. (b) Chronic hypoxia (10.8% O(2)) from 5 to 25 days exposure did not significantly affect SS content of ME. (c) ADX alone increased SS content of ME and this increase was further enhanced after 2 h exposure to hypoxia. (d) The increased SS in ME of ADX rats was blocked by replacement with DEX (500 microg/rat i.p.). The data presented suggest that acute hypoxia stress may increase or decrease SS content of ME in rats, depending on the severity and duration of the hypoxia and that the stimulatory action of hypoxia on SS content of ME be may in part mediated by the increased corticosterone levels during hypoxia.
BACKGROUND: Iron-dependent free radicals formation has been related to greater damage in cerebral ischemia. The authors analyzed whether increased body iron stores were associated with early neurologic worsening and excitatory amino acid release in patients with acute ischemic stroke. METHODS: Ferritin, total iron, and glutamate concentrations in plasma and CSF were measured on admission in 100 consecutive patients with a cerebral infarction of <24 hours' duration. The authors diagnosed progressing stroke when the Canadian Stroke Scale score decreased one or more points between admission and 48 hours. Cranial CT was performed on admission and repeated on days 4 to 7 of hospitalization. RESULTS: Ferritin concentrations in plasma (median 391, range 119 to 500 versus 148, 21 to 399 ng/mL) and in CSF (17.4, 6.8 to 82, versus 4.8, 0.6 to 14 ng/mL) were significantly higher in the 45 patients with subsequent progressing stroke than in those with nonprogressing stroke (p < 0.001). There was a positive correlation between ferritin and glutamate concentrations in plasma (r = 0.81, p < 0.001) and CSF (r = 0.64, p < 0.001). Plasma ferritin concentrations >275 ng/mL in plasma (OR, 33.5; 95% CI, 4.7 to 235) and >11 ng/mL in CSF (OR, 11.4; 95% CI, 3. 1 to 41) were independently and significantly related to early neurologic worsening. The effect was reduced by >60% after controlling for glutamate concentrations, but remained significant. CONCLUSIONS: High plasma and CSF ferritin concentrations within the first 24 hours from the onset of ischemic stroke are associated with early neurologic deterioration. Increased body iron stores may contribute to stroke progression by enhancing the cytotoxic mechanisms in cerebral ischemia.