Effects of hypertonic solutions and of mercuric chloride on the uptake of [ 14C]glucose analogues by rabbit brain Intracarotid perfusion of hypertonic solutions of urea, NaCl or acetamide increased the brain uptake index (BUI) of glucose analogues by rabbit brain, while isotonic urea was without effect. Lactamide, whether isotonic or hypertonic, decreased the BUI of glucose analogues. The increased BUI produced by the other hypertonic solutions could be inhibited by unlabeled substrate, unlabeled glucose or by phloridzin, and may reflect stimulated carrier-mediated transport of monosaccharides into brain. Although the increases could also have been due to altered cerebral blood flow, radioautography showed no gross evidence of such alterations. The BUI of 2-2-deoxy-~-[l-~~C]glucose was decreased by intracarotid injection of 0.01mM HgC12, to the same level seen following maximal inhibition with unlabeled 2-deoxy-~glucose, while 0 . 0 8~ HgC1, gave BUl's above this level. The lower concentration of HgC1, probably inhibited carrier-mediated monosaccharide transfer, while the higher concentration appeared to increase passive diffusion into the brain as well.
During an acute increase in ICP produced by balloon inflation three different phases could be observed. In the first phase (ICP 40-50 mm Hg) the latencies of R 1 and R 2 showed an initial decrease followed by increase in latency. In the second phase (ICP 50-70 mm Hg) R 2 disappeared, whereas R 1 showed marked alterations, prolongation of the latency and duration, and a decreasing amplitude. In the third phase no response could be evoked. The pathophysiological observations correlated with the morphological alterations. Two ischaemic zones with BBB damage which "transsected" the mesodiencephalic and pontomesencephalic border were found. The results suggest that the disappearance of R 2 depends on rostral damage, whereas alteration of R 1 is caused by a pontomesencephalic lesion.
To evaluate the interrelationships between anterior pituitary function and the antidiuretic system in patients harbouring hypothalamo-hypophyseal tumorous lesions, combined anterior pituitary stimulation tests were performed in the pre (n = 192 patients) and postoperative (n = 151 patients) state. Basal and stimulated plasma antidiuretic hormone, serum as well as urinary osmolality and diuresis were analyzed to determine the residual functional capacity of the antidiuretic system. In 106 patients with non-prolactin (PRL) secreting tumours basal and stimulated PRL secretion of the residual anterior pituitary was studied pre- and postoperatively. It was found that in the preoperative state latent (n = 12 patients) or manifest (n = 10 patients) types of diabetes insipidus (DI) were related to a significant decrease of maximal stimulated levels of thyroid stimulating hormone as well as basal and maximal stimulated levels of follicle stimulating hormone relative to patients without DI. In the postoperative state DI lasting longer than 10 days (n = 51 patients) was associated with decreased basal and maximal stimulated concentrations of cortisol, luteinizing and follicle stimulating hormone, whereas basal and maximal stimulated levels of PRL were significantly increased compared to those patients without DI (n = 61 patients). Decompression (n = 65 procedures) via the transnasal route was related with a lower frequency of the more severe types of DI (n = 7 patients) and a significant decrease of basal and maximal PRL levels in patients with non-PRL secreting tumours. The transcranial approach (n = 86 procedures) caused a higher rate of severe DI types (n = 33 patients) and an increase of PRL secretion from the residual anterior pituitary lobe. Patients without DI or DI of mild severity (n = 50), as a group, had a significant decrease of basal and maximal PRL levels compared with preoperative values (preoperative: basal = 14.3 +/- 1.5 ng/ml, max = 31.4 +/- 1.5 ng/ml, postoperative: basal = 9.6 +/- 1.1 ng/ml, max = 24.9 +/- 2.9 ng/ml). In patients with severer degrees of DI (n = 40) PRL levels were significantly increased, respectively (preoperative: basal = 15.3 +/- 3.1 ng/ml, max = 23.9 +/- 7.6 ng/ml, postoperative: basal = 19.7 +/- 3.4 ng/ml, max = 38.6 +/- 7.9 ng/ml). It was concluded that in the surgical treatment of non-PRL secreting hypothalamo-hypophyseal lesions the results of early postoperative assessment of basal and stimulated PRL levels may predict the type of postoperative DI.(ABSTRACT TRUNCATED AT 400 WORDS)
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