Bauxite deposits are widespread in NW Sardinia. They formed during the middle Cretaceous, in consequence of a period of emergence of the Mesozoic carbonate shelf. In the Nurra area the geometries derived by the Middle Cretaceous tectonic phases controlled the ore typologies. Two bauxite profiles, laying on different bedrocks, were sampled. The bauxitization proceeded from the surface downward, with the accumulation of Al 2 O 3 and residual 'immobile' elements (Al, Ti, HFSE), and corresponding mobility and loss of SiO 2 and Fe 2 O 3 . Epigenetic kaolinite formed close to faults and joints, probably as a result of silicification, introduced by low temperature hydrothermal solutions. Rare earth elements, especially LREE, are concentrated in Fe-rich bauxite horizons, probably due to scavenging by goethite. REE-enrichment is not observed in the boehmite-rich horizons. Very high REE contents are observed in a Fe-depleted horizon due to the occurrence of REE accessory minerals, probably of the bastnä site group. Conservative indices, including TiO 2 /Al 2 O 3 and Ti/Cr ratios, and Eu anomalies (Eu/Eu*), suggest that the deposits formed by weathering of sediments derived from mafic rocks of the Hercynian basement. This, in turn, implies that the basement was exposed during middle Cretaceous.
In the present study the possible derangement of the autonomic system and its influence in life threatening arrhythmias were analysed during paroxysmal activity. In hemispherectomized rats a paroxysmal activation of the hypothalamic and mesencephalic cardioarrhythmogenic triggers was performed by topical application of penicillin-G. Blood gas parameters and electrical activity of the thalamus, hypothalamus, vagal nerve fibre, ECG and arterial blood pressure were simultaneously monitored in basal conditions and repeated after the appearance of paroxysmal activity. Temporal correlation analysis was carried out. Results showed that during activation of these triggers, the spontaneous vagal nerve fibre activity significantly increased and triggered the appearance of cardiac arrhythmias which could become life threatening and induce animal death when blood gas and electrolytic parameters were simultaneously impaired. These experiments suggest that fatal evolution of the heart impairment is related not only to an autonomic cardiac trigger, but also to a concomitant metabolic derangement, which most likely shares the same autonomic origin.
The potential for cardiac arrhythmia was studied in an experimental focal epilepsy induced in hemispherectomized rats by topical application of buffered penicillin G onto the thalamus. The epileptic burst triggered cardiac and hemodynamic responses, as simultaneously monitored by arterial pressure, and hypothalamic and heart activity. During interictal epileptic activity, the single burst triggered a short-latency cardiac arrhythmia, characterized by sinus bradyarrhythmia and junctional rhythm, and lengthening of intervals between sphygmic waves with significant reduction of diastolic pressure. When the epileptic burst stopped, the cardiac activity resumed normal rhythm, and diastolic pressure returned to basal value. During ictal epileptic activity, the sinus and junctional bradyarrhythmic episodes lasted longer, and supraventricular extrasystoles, sinus arrest, and bigeminal ventricular extrasystoles were observed. Both systolic and diastolic pressures decreased from 120/85 to 100/65 mm Hg. The end of the ictal episode always marked resumption of normal cardiac rhythm and systemic pressure. Considering the absence of metabolic complications (blood-gas analytic parameters and acid-base balance being controlled) and the short latency of the cardiac and hemodynamic responses, it is suggested that during paroxysmal hypothalamic activity the observed cardiac arrhythmias and the hemodynamic modifications were neurogenic in origin. A role for cardiovascular alterations in sudden unexplained epileptic death is postulated.
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