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ispartof: AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION vol:101 issue:9 pages:897-904 ispartof: location:United States status: published

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© 2014, Springer-Verlag Berlin Heidelberg. The purpose of this study was to assess, in the murine kidney, the mechanisms underlying the endothelium-dependent control of vascular tone and whether or not, in a severe model of hypertension and renal failure, KCa channels contribute to its regulation. Wild-type (BL) and double-transgenic female mice expressing human angiotensinogen and renin (AR) genes received either control or a high-salt diet associated to a nitric oxide (NO) synthase inhibitor treatment (BLSL and ARSL). Changes in renal perfusion pressure (RPP) were measured in isolated perfused kidneys. BLSL and AR were moderately hypertensive without kidney disease while ARSL developed severe hypertension and renal failure. In the four groups, methacholine induced biphasic endothelium-dependent responses, a transient decrease in RPP followed by a cyclooxygenase-dependent increase in RPP. In the presence or not of indomethacin, the vasodilatations were poorly sensitive to NO synthase inhibition. However, in the presence of cyclooxygenase and NO synthase inhibitors, apamin, and/or TRAM-34, blockers of KCa2.3 and KCa3.1, respectively, abolished the decrease in RPP in response to either methacholine or the two activators of KCa2.3/KCa3.1, NS309, and SKA-31. Thus, KCa2/3 channels play a major role in the regulation of murine kidney perfusion and this mechanism is maintained in hypertension, even when severe and associated with kidney damage.

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International audience; The repair of the finger flexor tendons can be complicated by the appearance of ruptures and peritendinous adhesions. Ruptures are often treated with tendon grafts. Peritendinous adhesions can require tenolysis. Following these two surgical procedures, there is a risk of new adhesions and rupture. Rehabilitation after this secondary surgery consists of a tailored, closely supervised protocol. Protocols used by the team at the Physical Medicine and Rehabilitation Department of the Regional Rehabilitation Institute and the team at the Plastic and Reconstructive Surgery Department of the Emile-Gallé Surgical Center of Nancy (France) are described. A close collaboration between these teams of surgeons and physical therapists is essential. After tendon grafting, protected early motion helps to move the transplant immediately while still protecting it. After tenolysis, immediate (several times a day) and extended rehabilitation ensures that the mobility obtained intraoperatively is maintained. It is performed in a specialized rehabilitation center during the first three postoperative weeks. The goal is to prevent new adhesions from forming while taking into account tendon's fragility.; La réparation des tendons fléchisseurs des doigts peut être compliquée par la survenue de ruptures et d’adhérences péritendineuses. Le traitement des ruptures repose souvent sur des greffes et les adhérences péritendineuses peuvent nécessiter de recourir à des ténolyses. Dans les suites de ces deux gestes chirurgicaux, il existe un risque de nouvelles adhérences et de rupture. La rééducation après cette chirurgie secondaire est basée sur un protocole adapté et une surveillance attentive. Les protocoles utilisés par l’équipe de médecine physique et réadaptation de l’Institut régional de réadaptation de Nancy, en collaboration avec l’équipe de chirurgie plastique et reconstructrice, SOS main du Centre chirurgical Emile-Gallé de Nancy, sont décrits. Cette collaboration étroite entre les chirurgiens et l’équipe de rééducation est primordiale. Après greffe, la prise en charge repose sur des mobilisations précoces protégées permettant de mobiliser d’emblée la greffe tout en la protégeant. Après ténolyse, la rééducation immédiate pluriquotidienne et prolongée est le garant du maintien des mobilités obtenues en cours d’intervention. Elle est réalisée en structure de rééducation spécialisée pendant les trois premières semaines postopératoires. L’objectif est d’éviter la formation de nouvelles adhérences tout en tenant compte de la fragilité tendineuse.

Monocyte-derived foam cells figure prominently in rupture-prone regions of atherosclerotic plaque. As urokinase/urokinase-receptor (u-PA/u-PAR) is the trigger of a proteolytic cascade responsible for ECM degradation, we have examined the effect of atherogenic lipoproteins on monocyte surface expression of u-PAR and u-PA. Peripheral blood monocytes, isolated from 10 healthy volunteers, were incubated with 10 to 200 microg/ml of native or oxidised (ox-) atherogenous lipoproteins for 18 h and cell surface expression of u-PA and u-PAR was analysed by flow cytometry. Both LDL and Lp(a) induced a dose-dependent increase in u-PA (1.6-fold increase with 200 microg/ml of ox-LDL) and u-PAR [1.7-fold increase with 200 microg/ml of ox-Lp(a)]. There is a great variability of the response among the donors, some of them remaining non-responders (absence of increase of u-PA or u-PAR) even at 200 microg/ml of lipoproteins. In positive responders, enhanced u-PA/u-PAR is associated with a significant increase of plasmin generation ( .9-fold increase with 200 microg/ml of ox-LDL), as determined by an amidolytic assay. Furthermore, monocyte adhesion to vitronectin and fibrinogen was significantly enhanced by the lipoproteins [respectively 2-fold and 1.7-fold increase with 200 microg/ml of ox-Lp(a)], due to the increase of micro-PAR and ICAM-1, which are receptors for vitronectin and fibrinogen. These data suggest that atherogenous lipoproteins could contribute to the development of atheromatous plaque by increasing monocyte adhesion and trigger plaque weakening by inducing ECM degradation.