[A new treatment modality in mandibular fractures: microplates and screws].
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Biomedical subjects
Publications and source records attributed to P Gauthier.
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Electrical stimulation of the periaqueductal gray substance (PAG) of the rostral midbrain of the rat produced biphasic or monophasic pressor responses depending on the duration of the stimulus train. Marked increases in plasma noradrenaline (NA) and adrenaline (A) levels accompanied the pressor responses, indicating the participation of the adrenal medulla. Depletion of central catecholamines (CA) by intraventricular administration of 6-hydroxydopamine (6-OHDA) did not affect the primary vasomotor component but markedly depleted adrenal CA levels and attenuated the adrenomedullary component of the response to brain stimulation. The intraperitoneal administration of p-chlorophenylalanine (pCPA) not only depleted brain serotonin (5-HT) levels but also reduced brain CA levels significantly. The adrenaline (A) levels were reduced in the adrenal glands of these rats and the adrenal secretory response to brain stimulation was attenuated. In contrast, the selective destruction of central 5-HT neurons by intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) in rats pretreated with desmethylimipramine (DMI) did not influence either the pressor nor the plasma CA responses to brain stimulation. Furthermore, the adrenal glands of these rats were normal. The results suggest that: (i) the central catecholaminergic neurons play an important role in the regulation of the adrenal glands but are not essential for the activation of the sympathetic vasoconstrictor fiber system: (ii) the pressor and plasma CA responses to PAG stimulation are not dependent on the central serotonergic system.
Bilateral anodal lesions performed with stainless steel electrodes placed either in the anterior medial (AMH) or lateral (ALH) hypothalamus, or in the ventromedial nucleus (VMH), induced in unrestrained rats the rapid development of arterial hypertension, tachycardia and death. Similarly placed cathodal lesions performed with platinum electrodes failed to elicit the cardiovascular syndrome. The electrical stimulation of the AMH, ALH or VMH caused an increased in the arterial blood pressure in anesthetized rats. This pressor response was characteristically biphasic and consisted of a sharp increase in arterial pressure at the onset of the stimulation, followed by a second elevation at the end of the stimulation. The hypertension evoked either by lesions or by stimulations of the hypothalamus, appeared to depend largely on a neurally mediated release of adrenal medullary catecholamines, and to some extent on the activation of the sympathetic vasoconstrictor fibers. Bilateral adrenalectomy, or adrenal demedullation, prevented the hypertension evoked by lesions, and selectively blocked the important secondary phase of the pressor response elicited by stimulation, but did not affect the primary phase. The latter was specifically eliminated by the destruction of the sympathetic vasomotor axons with 6-hydroxydopamine (6-OHDA). On the other hand, the tachycardia evoked by lesions or stimulations of the medial hypothalamus, resulted from an increase in sympathetic neural discharges to the heart, and it was abolished either by beta-receptor blockade with sotalol or by chemical sympathectomy with 6-OHDA. In contrast, the tachycardia occurring after lesions of the lateral hypothalamus was entirely due to circulating adrenal medullary catecholamines and it was eliminated by adrenalectomy. It is concluded that acute hypertension and tachycardia produced by anodal lesions performed with stainless steel electrodes results from the excitation of the hypothalamus, possibly due to the irritative action of the metallic ions deposited at the lesion sites. The observations of cardiovascular responses entirely due to adrenomedullary secretions suggests that the control of the adrenal medulla is at least partially distinct from that of the sympathetic vasoconstrictor and cardiac fibers, at the rostral hypothalamic level.
Electrical stimulation of the diencephalon and rostral mesencephalon produced a biphasic pressor response consisting of an initial sharp rise followed by a more prolonged elevation in blood pressure. Active sites from which comparable responses could be evoked were found in the ventral medial and lateral hypothalamus, in the region of the parafascicularis nucleus, and in the central gray matter and the tegmentum of the mesencephalon. Together with the biphasic pressor response brain stimulation also increased plasma catecholamine (CA) concentrations 10-fold. Either bilateral adrenalectomy or demedullation selectively abolished the secondary phase of the pressor response and greatly reduced the plasma CA response to stimulation. After chemical destruction of the terminals of the sympathetic neurones by intravenous administration of 6-hydroxydopamine (6-OHDA), the primary pressor phase was eliminated whereas the secondary phase as well as plasma CA concentration reached higher levels than in normal rats. 6-OHDA treatment combined with adrenalectomy completely abolished both pressor and CA responses. The results demonstrate that adrenomedullary mechanisms capable of increasing blood pressure significantly can be activated by electrical stimulation of different sites in the diencephalon and mesencephalon.
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Electroencephalographic (EEG) recordings of experienced parachutists were done by means of telemetry before, during, and after jumps of up to 3500m. During free-fall and after stabilization, alpha rhythm was recorded from several alpha reactive subjects when they closed their eyes. No pathological EEG recordings were obtained during the different phases of the jump.
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Activities of single efferent fibres which innervate the laryngeal muscles in adult cats were studied during repetitive stimulation of the recurrent laryngeal nerve or the vagus nerve. The orthodromic response (primary response) can be followed by another response (secondary response) which has a latence consistant with the hypothesis of a central origin. This secondary response has an irregular incidence of occurrence, about 5.6 time for 100 stimulations. This secondary response: 1. Is present for 90% of the tested inspiratory or expiratory laryngeal fibres; 2. Depends on a central origin because it no longer occurs when the cervical vagus nerve is cut rostral to the site of stimulation; 3. Is not the consequence of the stimulation of afferent fibres because it is not altered by destruction of the centripetal vagal pathway (Fig. 4); 4. Can be obtained by the stimulation of other branches than those containing the recorded fibre (Fig. 2), so it is not necessarily the consequence of the antidromic invasion of this fibre; 5. Depends on a cholinergic synapse because it is more frequently observed after intra-arterial injection of acetylcholine (Fig. 6) and disappears after injection of Mecamylamine (an antinicotinic drug) (Fig. 7); 6. Persists after injection of strychnine and becomes more frequently observed; hence it does not seem to be associated with a disinhibitory mechanism; 7. Depends on a phenomenon of convergence because it occurred more frequently when the amplitude of stimulation was increased (Fig. 3); 8. Has a central delay which seems not to be consistent with an electrotonic origin; 9. Can be recorded from an inspiratory fibre when stimulating the remaining inspiratory or expiratory fibres. A secondary response can also be recorded from an expiratory fibre by stimulating the same or other expiratory fibres, but not after excitation of inspiratory fibres (Fig. 5). These results suggest: (1) a functional organisation into the pool of laryngeal motoneurones; (2) the possible existence of intrabulbar axonal collaterals in that pool.
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Coronary patients exercised on an ergometric bicycle before and after physical training. Plasma catecholamines were sampled simultaneously at the arterial and coronary sinus levels and assayed with a radioenzymatic method. The increase in the level of coronary sinus catecholamines exceeded the increase in the arterial level, indicating a liberation of catecholamines by the myocardium and an activation of the peripheral sympathetic fibers during exercise. With high work loads, these values no longer differed, suggesting that the additional increase in circulating catecholamines originate from extra-myocardial stores, presumably the adrenal medulla. Arterial catecholamine levels were significantly correlated with work loads, heart rate, changes in systolic blood pressure, and rate-pressure product. After physical training, arterial catecholamine increases for various work loads were lower; these lower elevations were associated with diminished responses in heart rate and systolic blood pressure, resulting in a lower rate-pressure product. Physical training results in diminished sympathetic responses for a given level of exercise, which could be associated with the clinical improvement of these patients.
The aim of this investigation was to study ways of inducing prolonged contingent negative variations (CNV) in human subjects. Fourteen subjects underwent the following experimental procedure: 1st day: 2 CNVs in control conditions were recorded (16 successive trials, each with standard S1--S2 paradigm). 2nd day: 5 successive CNVs were recorded:(1) control; (2) labyrinthine stimulation before 1st, 5th, 9th and 13th trials with simple mental calculation performed between S1 and S2, i.e. during CNV; (3) mental calculation only; (4) labyrinthine stimulation only; (5) control. None of the three interference situations caused any significant changes in the mean and maximal CNV amplitudes measured between S1 and S2. On the other hand, the post-imperative part of the CNV was significantly (P less than 0.025) prolonged but only in the situation where 2 types of interference were applied at the same time. This increase disappeared with removal of the double interference. This change, which matches that observed spontaneously and reversibly in certain mental patients in the acute phase of their illness, seems to reflect a transient alteration of the psychophysiological state of the subject. The possibility of inducing these changes in a normal subject could serve as a means of determining the individual threshold of stress.
The response of the AV junction to adrenergic stimulation was studied in 35 anesthetized open-chest dogs before and after the injection of acetylstrophanthidin (5mug) directly into the AV node artery. An AV junctional rhythm was obtained under control conditions by injecting norepinephrine (n = 9) or isoproterenol (n = 8) into the AV node artery and by stimulation of the left stellate ganglion (n = 11) after selectively injecting propranolol into the sinus node artery. Acetylstrophanthidin brought about various degrees of conduction block from simple PR interval prolongation to complete heart block, and decreased the chronotropic response of the AV junction to adrenergic stimulation. In seven animals the appearance of a spontaneous second degree AV block did not reduce the AV junctional response to adrenergic stimulation. Acetylstrophanthidin also reduced the ventricular acceleration produced by adrenergic stimulation during atrial fibrillation. These results suggest that the anti-adrenergic effect of cardiac glycosides may not only be involved in the mechanism of AV conduction disturbances during digitalis intoxication, but may also play a role in slowing the ventricular rate during atrial fibrillation.
A natural antihistamine substance (NAS) present in bile has been investigated. It was found that the antihistamine activity was not due to proteins, lipids, pigments, or amino acids. On ion exchange chromatography and thin-layer chromatography, this activity was associated with bile acids. Many bile acids could, in varying degrees, inhibit this histamine induced guinea pig ileum contraction, desoxycholic acid being the most potent. However NAS activity could be separated from bile acids and their conjugates using a different solvent system. Furthermore, NAS showed a higher antihistamine activity than bile acids. This substance seems to be responsible for 15-20% of the activity of whole bile. The substance has not yet been identified.
The present study in dogs indicates that the peripheral sympathetic fibers develop mostly after birth and reach a full maturity at about 2 months of life. The norepinephrine content of the heart, spleen, intestine, salivary glands, and adrenal glands increased from birth to 56 days of age. In contrast, the content of the stellate ganglia decreased during this period. In most of the organs studied, the uptake of [3H] norepinephrine developed in parallel with the norepinephrine content, except in the right atrium and salivary glands where it was fully developed soon after birth. During development, the systemic blood pressure increased from 40 to 100 mm Hg. Bilateral adrenal vessel clamping failed to induce a fall in blood pressure in growing dogs which indicates that the adrenal medulla or the baroreceptors did not fully compensate for the lack of peripheral sympathetic fibers and for the lower blood pressure in newborn animals. Although cardiac norepinephrine content was still very low in 10-day-old animals, cardiovascular responses to direct and reflex sympathetic stimulation were similar to those observed in 56-day-old animals. These results indicate that the sympathetic nervous system becomes functional before the fibers reach their full maturity.
The aim of this study was to examine the influence of interfering stimuli on subjects' C.N.V. With a labyrinthic stimulation before association S1-S2 and arithmetic calculation task between S1 and S2, the C.N.V. showed a statistically significant variation (P less than 0.025): it became prolonged after the response to S2. Provocation of a prolonged C.N.V. could be used as criterion to determine an individual threshold of stress.
21 subjects were recorded during two experimental sessions: 1st session: 2 CNVs in control conditions; 2nd session: 1) control CNV, 2) CNV and arithmetic calculation, 3) CNV and labyrinthine stimulation, 4) CNV, arithmetic calculation and labyrinthine stimulation, 5) control CNV. The results obtained show a post-imperative extension of the CNV in the situation 2: arithmetic calculation (P less than 0.025) and 4: double interference (P less than 0.05).
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