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Copyright of EMC-Anesthesie--Reanimation is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To bring together the most recent data concerning the physiology of nociceptors at a time when there has been significant progress in the understanding of these.Data sources: References were obtained from computerised bibliographic data banks (Medline and others) and the authorsˈpersonal documents.Data synthesis: Nociceptive impulses are generated at the periphery in unmyelinated fibres called nociceptors, the responses of which depend on the tissue environment. Numerous mediators can activate, sensitise or “wake up” nociceptors : kinins (bradykinin, kallidin and their metabolites), pro-inflammatory cytokines (TNFα, IL-6, IL-1β, IL-8), anti-inflammatory cytokines (IL-4, IL-6, IL-10, IL-12, IL-13), prostanoids (PGE2, PGI2), lipo-oxygenases (leucotrienes such LTB4 or 15-HETE), the “central mediators of the immune response” (NF-κB), growth factors such as neurotrophins (NGF, BDNF, NT-3 and NT-4/5), peptides (substance P, CGRP, Neurokinin A), nitric oxide, histamine, serotonin, proteases, excitatory amino acids, adrenergic amines and opioids. The release of neuromediators by primary afferent fibres in the spinal cord may be summarised by successively considering calcium channels, presynaptic receptors, excitatory amino acids and peptides.Conclusion: Sensitisation phenomena are not exclusively peripheral but also central in origin and these are interlinked. [Copyright &y& Elsevier]

Background: Only few noninvasive methods have the potential to quantitate renal blood flow (RBF) in humans. Positron emission tomography (PET) is a clinical imaging method that can be used to measure the tissue blood flow noninvasively. The purpose of this study was to validate PET measurement of RBF using 15O-labeled water (H215O), a tracer that allows repeated measurements at short time intervals. Methods: RBF was measured in six pigs by PET and by radioactive microspheres (MS). Three measurements were performed in each pig at baseline (BL), during vascular expansion and dopamine infusion (DA; 20 microg. kg-1. min-1 intravenously), and during angiotensin II (Ang II) infusion (50 ng. kg-1. min-1 intravenously). RBF was estimated from aortic and renal tracer kinetics using a model adapted from the blood flow model described by Kety and Smith. Results: PET and MS values correlated strongly (y = 0.79x + 42, r = 0.93, P < 0.0001) over the RBF range from 100 to 500 mL. min-1. 100 g-1. Pharmacologically induced changes were significant and were measured equally well by PET and MS: 38 and 39%, respectively, below BL (P < 0.005 and P < 0.05) under Ang II, and 47 and 48%, respectively, above BL (P < 0.005 and P < 0.01) under DA. A Bland and Altman representation showed a low average difference of -17 +/- 45 mL. min-1. 100 g-1 (mean +/- SD). Conclusion: To our knowledge, this study provides the first validation of RBF measurement by PET using H215O over a large range of RBF values (100 to 500 mL. min-1. 100 g-1), which correspond to RBF values in both healthy subjects and in patients suffering from chronic renal failure. [ABSTRACT FROM AUTHOR]

Introduction Les troubles de la marche et le freezing – blocage survenant à l’initiation ou en cours de mouvement – sont fréquents et invalidants aux stades avancés de la maladie de Parkinson. Leur réponse aux traitements usuels (dopathérapie et stimulation des noyaux subthalamiques [NST]) est le plus souvent insatisfaisante. La stimulation des noyaux pédonculopontins (NPP) a été récemment proposée comme alternative thérapeutique pour la prise en charge des formes non-répondantes. Les circuits cérébraux sous-jacents, tout comme les mécanismes d’action de cette cible, restent cependant largement méconnus. Matériel et méthode La présente étude se proposait de mieux circonscrire la physiopathologie des troubles dopa-résistants et leur modulation par la stimulation bilatérale des NPP chez des patients doublement implantés (NST/NPP ; n = 3), au moyen de la technique de tomographie par emission de positons (TEP-H2O15), lors d’une tâche d’imagerie motrice de la marche. Les patients ont été scannés stimulation des NPP en marche et à l’arrêt, sous stimulation chronique des NST, à jeun de traitement dopaminergique. Résultats Lors de la réalisation de la tâche mentale, une hypoactivation frontale associée à une hyperactivation pariétale étaient constatées chez les patients, stimulation des NPP éteinte, comparativement aux données obtenues chez des témoins appariés en âge et en genre. Des activations dans l’aire motrice supplémentaire, les noyaux gris centraux, le cervelet et le mésencéphale (NPP, noyaux cunéiformes) étaient par ailleurs retrouvées, stimulation des NPP allumée. Discussion–conclusion La restauration conjointe d’activité de structures fronto-striatales, du cervelet et du mésencéphale sous stimulation bilatérale des NPP pourrait donc contribuer à améliorer la marche parkinsonienne. [ABSTRACT FROM AUTHOR]