A ‘Non-Additive’ Characterization of ℘{\wp} -Adic Norms

For F a -adic field together with a -adic valuation, we present a new characterization for a map p:FnR- to be a -adic norm on the vector space F n . This characterization was motivated by the concept of tight maps — maps that naturally arise within the theory of valuated matroids and tight spans. As an immediate consequence, we show that the two descriptions of the affine building of SL n (F) in terms of (i) -adic norms given by Bruhat and Tits and (ii) tight maps given by Terhalle essentially coincide. The result suggests that similar characterizations of affine buildings of other classical groups should exist, and that the theory of affine buildings may turn out as a particular case of a yet to be developed geometric theory of valuated (and d-valuated) matroids and their tight spans providing simply-connected G-spaces for large classes of appropriately specified groups G that could serve as a basis for an affine variant of Gromov’s theory

Neonatal chronic sympathectomy in normotensive rats affects pial arteries: enhanced stiffness and reduced capacity to dilate

The functional implication of previously shown effects on pial wall morphology by sympathectomy was tested. Following either ganglionic or pre-ganglionic denervation in 1-week-old rats the passive arterial compliance was reduced in basal cerebral arteries of 20-week-old normotensive, but not of hypertensive animals. The magnitude of the denervation induced stiffness was similar to the alteration seen in spontaneously hypertensive rats when compared with normotensive animals. No difference was seen between the two types of denervation. Following ganglionic sympathectomy in 1-week old normotensive rats-and examined 19 weeks later-the increase in cerebral blood flow (measured with the [14C]butanol sampling technique) induced by high arterial CO2 concentration was attenuated compared with control, whereas basal cerebral blood flow of 20-week-old animals was not different from control. The results indicate a long-term role by the sympathetic nerves not only on vessel wall composition, but also on the regulatory capacity of the cerebral circulation

Endothelin is a potent constrictor of human intracranial arteries and veins

Endothelin, a peptide produced in endothelial cells, was found to be a potent constrictor of human pial arteries through a direct, slow action on the smooth muscle cell, with a pD2 value of 8.54. It was less potent as a constrictor in pial veins (pD2 7.80) and in branches of the middle meningeal artery and superficial temporal artery (pD2 7.61 and 7.77). The major component of the contractile response in the arteries comprises an effect on potential-operated calcium channels, as evidenced by tests with nimodipine. Endothelin may regulate intracranial vessels tonically during physiological as well as pathophysiological conditions

Neonatal pre-ganglionic sympathectomy affects morphometrically defined architecture in rat cerebral arteries

In order to clarify further the nature of the long-term influence on the cerebral vasculature by the sympathetic nerves, a bilateral cervical pre-ganglionic denervation was performed in 1-week-old rats. Four weeks later, morphometric determinations of the vascular dimensions revealed diminished media cross-sectional areas and luminal radii in the middle cerebral and posterior cerebral arteries, whereas these parameters were unaffected in the basilar artery. In the latter artery, however, a 40% increase in the cross-sectional area of the internal elastic membrane was found. No re-innervation of the denervated ganglia occurred during the course of the experiment. The results suggest that the long-term effect exerted by the sympathetic nerves is associated with the nerve activity, rather than being a true trophic influence

Vasoconstrictor effects in spinal cord of the substance P antagonist [D-Arg, D-Trp7,9 Leu11]-substance P (Spantide) and somatostatin and interaction with thyrotropin releasing hormone

The present study was undertaken to investigate the possible effects of Spantide [D-Arg1, D-Trp7,9 Leu11]-substance P, a substance P antagonist, and of somatostatin on spinal cord blood flow. The experiments were performed with the laser-doppler technique on the L1 spinal cord segment exposed by laminectomy. The effect of Spantide was also studied in the rat with the [14C]iodoantipyrine technique. In addition, experiments were performed on rabbit skeletal muscle in vivo after administration of Spantide to the local vasculature. In the experiments on spinal cord, approximately the same doses were employed as those earlier shown to be "neurotoxic". When the vehicle alone (0.9% saline) was administered intrathecally, a slight decrease of brief duration was noted in the blood flow. Spantide, however, caused a dose-dependent decrease, where 2 micrograms caused an immediate drop of the blood flow to approx. 20% of its normal value. A total circulatory arrest was found in several animals. In most cases, the flow was gradually normalized, whereas the effect persisted for up to 60 min in others. Virtually the same effect was exerted by somatostatin. The experiments using the iodoantipyrine technique confirmed the effect of Spantide. Here, the high resolution of this method showed that the gray matter was affected preferentially, with a complete ischemic state or a drastically reduced flow in 4 out of 5 animals 10 min after 2 micrograms of Spantide; one animal was unaffected, and this animal did not show any signs of motor impairment. The vasoconstriction of Spantide was not affected by simultaneous injections with substance P. However, after i.v. pretreatment with thyrotropin-releasing hormone, at a dose that previously has been reported to be protective against the neurodegenerative effects of Spantide, blood flow was markedly increased as compared to Spantide alone. Results from the experiments using intravital microscopy flow studies in the rabbit tenuissimus muscle revealed that Spantide at the doses used had no vasoconstrictor effect in the skeletal muscle of this species. The results suggest that previous demonstrations of motor impairment and "neurotoxic" actions of intrathecally injected substance P antagonists and somatostatin may be related to a marked decrease in spinal cord blood flow. Counteraction of the effect of Spantide by thyrotropin-releasing hormone may be explained by its effect to increase blood flow