Biomedical subjects
Publications and source records attributed to I Chowers.
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Previous experiments from this laboratory using the hypothalamic island have demonstrated that the adrenocortical discharge following sciatic nerve stimulation is mediated by neural pathways only. With the purpose of identifying the neural structures involved, this response was studied in rats with bilateral lesions in the medial forebrain bundle (MFB), mammillary peduncle (MP), fasciculus longitudinalis dorsalis (FLD), midbrain reticular formation MRF) and the medial geniculate body (GM). Lesions in the MFB, MP and MRF have inhibited the adrenocortical response following sciatic nerve stimulation. These and other data indicate that the above structures are involved in the mediation of this response and that the afferent pathway enters the mediobasal hypothalamus anteriorly.
Previous studies from this laboratory have demonstrated that in rats with hypothalamic islands the adrenocortical response to photic and acoustic stimulation was partially inhibited indicating that they were at least to a certain degree neurally mediated, though ether stress produced normal adrenocortical responses. With the purpose of determining to what extent afferent somatosensory connections to the hypothalamus participate in the activation of adrenocortical responses following sciatic nerve stimulation, the effects of this stimulus applied through chronically implanted electrodes were studied on the plasma corticosterone levels in pentobarbital anaesthetized intact animals and in rats with hypothalamic islands. Ether stress or sciatic nerve stimulation for 2 min in intact rats produced a rise of plasma corticosterone to 32.1 plus or minus 1.2 and 32.1 plus or minus 1.8 mug/100 ml, respectively. However, in animals with hypothalamic islands the corresponding values were 29.2 plus or minus 1.8 and 12.4 plus or minus 0.8 mug/100 ml, respectively. The latter value was not significantly different from the basal corticosterone levels (13.0 plus or minus 1.2 mug/100 ml) found in rats 15 min after pentobarbital anaesthesia, the time when the sciatic stimulus was applied. The present data indicate that the adrenocortical discharge following sciatic nerve stimulation is completely inhibited by hypothalamic deafferentation and therefore depends entirely on the activation of the afferent neural pathways to the hypothalamus.
Studies from this laboratory have demonstrated that the adrenocortical response following sciatic nerve stimulation is completely inhibited in rats with hypothalamic islands, indicating that this response depends entirely on the activation of afferent neural pathways to the hypothalamus. With the purpose of identifying the site of entry of these neural pathways into the mediobasal hypothalamus the effects of partial hypothalamic deafferentations were studied. It was found that in rats with posterior or posterolateral deafferentation the adrenocortical responses were similar to those obtained in intact rats, while anterior and anterolateral deafferentation resulted in a reduction of 62.3 and 53.3%, respectively. These results would indicate that the sciatic impulses which activate the adrenocortical response involve neural afferents which enter the mediobasal hypothalamus by an anterior pathway.
Rabbits exposed for one hour to a temperature of 40degrees Cand 35-37% humidity showed elevated plasma osmolality and pH. Most of the animals were not able to withstand the heat. Dexamethasone-treated rabbits under the same conditions withstood the heat better and their plasma pH and osmolality remained constant. Metopirone-treated rabbits withstood the heat and showed a rise in plasma osmolality and a slight change in plasma pH. The highest rise in rectal temperature was observed in the metopirone-treated rabbits. Only the untreated animals were unable to regain pre-exposure rectal temperature. The results suggest that high levels of glucocorticosteroids enhance neurogenic and metabolic mechanisms which have protective functions during acute exposure to heat.
Thyrotropin (TSH)-stimulation tests were performed on 21 patients with solitary hot nodules in the thyroid gland. Twelve of the patients were euthyroid and nine were hyperthyroid. The average age of the euthyroid patients was 38 +/- 14 (SD) years, and that of the hyperthyroid patients, 55 +/- 8 years. Prior to TSH stimulation, the scanograms of the euthyroid patients showed 131I uptake only in the nodules, while after the TSH test, almost equal uptake was observed in both lobes. The scanograms of the hyperthyroid patients that showed 131I uptake only in the area of the nodules prior to the TSH test showed no appreciable change after TSH stimulation.
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