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Background and purpose:
We determined if chronic sympatho-inhibition with rilmenidine has functional significance for the kidney by altering responses of renal blood flow (RBF) and plasma renin activity (PRA) to stress and acute hypotension in rabbits with renovascular hypertension.Experimental approach:
RBF to each kidney and renal sympathetic nerve activity (RSNA) to the left kidney were measured in rabbits in which a renal artery clip induced hypertension (2K1C) and in sham-operated rabbits. After 2 weeks, a subcutaneous minipump was implanted to deliver rilmenidine (2.5 mg·kg−1·day−1) to 2K1C rabbits for 3 weeks.Key results:
After 5 weeks of renal artery stenosis, mean arterial pressure (MAP) was 23% higher and PRA 3-fold greater than in sham-operated rabbits. Blood flow and renal vascular conductance in the stenosed kidney were lower (−75% and −80%) compared with sham, and higher in the non-clipped kidney (68% and 39%). Responses of RBF and PRA to hypotension were similar in 2K1C and sham rabbits. Airjet stress evoked a greater increase in MAP in 2K1C rabbits than sham controls. Chronic rilmenidine normalized MAP, reduced RSNA and PRA, and did not reduce RBF in the stenosed kidney. Responses of RBF (clipped and non-clipped kidney), RSNA and PRA to hypotension and airjet were little affected by rilmenidine.Conclusions and implications:
Our observations suggest that chronic sympatho-inhibition is an effective antihypertensive therapy in renovascular hypertension. It normalizes MAP and reduces basal PRA without compromising blood flow in the stenosed kidney or altering responses of MAP, haemodynamics and PRA to acute hypotension and stress. 相似文献106.
The development of a vascular network in tissue-engineered constructs is a fundamental bottleneck of bioregenerative medicine, particularly when the size of the implant exceeds a certain limit given by diffusion lengths and/or if the host tissue shows a very active metabolism. One of the approaches to achieve the vascularization of tissue constructs is generating a sustained release of proangiogenic factors from the ischemic site. This work describes the formation and characterization of hyaluronic acid-chitosan (HA/CS) nanoparticles for the delivery of two pro-angiogenic growth factors: vascular endothelial growth factor (VEGF) and platelet derived growth factor (PDGF-BB). These nanoparticles were prepared by an ionic gelification technique, and different formulations were developed by encapsulating the growth factors in association with two stabilizing agents: bovine serum albumin or heparin sodium salt. These carriers were characterized with regard to their physicochemical properties, their stability in biological media, and their cytotoxicity in the C3a hepatoma cell line. The results show that nanoparticles around 200?nm can be prepared by this method. HA/CS nanoparticles were stable when incubated in EMEM cell culture medium or in water at 37°C for 24?h. Cell culture tests confirmed that HA/CS nanoparticles are not cytotoxic within the concentration range used for growth factor delivery. Moreover, HA/CS nanoparticles were able to entrap efficiently both growth factors, reaching association values of 94% and 54% for VEGF and PDGF, respectively. In vitro release studies confirm that PDGF-BB is released from HA/CS nanoparticles in a sustained manner over approximately 1 week. On the other hand, VEGF is completely released within the first 24?h. 相似文献
107.
Audrey SL Low Mark Lunt Louise K Mercer James B Galloway Rebecca Davies Kath D Watson Deborah P Symmons William G Dixon Kimme L Hyrich 《Lancet》2013
BackgroundPeople with rheumatoid arthritis are at increased risk of cardiovascular morbidity and mortality, including stroke (cerebrovascular accident [CVA]). Anti-tumour necrosis factor (anti-TNF) therapy may influence the risk of CVA by reducing inflammation. The aim of the analysis was to study the association of anti-TNF therapy with risk of ischaemic CVA in rheumatoid arthritis.MethodsThe British Society for Rheumatology Biologics Registers-Rheumatoid Arthritis (BSRBR-RA) is an ongoing national prospective observational cohort study. Patients with rheumatoid arthritis recently started on anti-TNF therapy and a biologic-naive comparator group treated only with non-biologic disease modifying anti-rheumatic drugs (nbDMARDs) were recruited to the BSRBR-RA from 2001 to 2008. Patients were followed by physician and patient questionnaires and also linked to the national death register. Incident CVAs were identified from all three sources of follow-up. CVAs were validated against WHO criteria for CVA and further classified as ischaemic CVA using CT brain reports or if ischaemic CVA was reported as the underlying cause of death from death certificates according to International Classification of Diseases 10 (ICD-10) code I63. Patients with a previous CVA were excluded. Risk of ischaemic CVA was compared between the nbDMARD cohort and people ever exposed to anti-TNF using a Cox regression model. Missing baseline data were replaced by multiple imputation. Adjustment was made for confounders using propensity scores stratified by deciles.FindingsTo Oct 31, 2010, 130 verified incident ischaemic CVAs (21 in 3271 nbDMARD patients, 109 in 11 642 anti-TNF patients) had occurred during 11 973 and 61 226 person-years of observation, respectively (incidence rate 175 vs 178 per 100 000 person-years). After adjustment for confounders, there was no association between ever exposure to anti-TNF and ischaemic CVA risk (hazard ratio 0·88 [95% CI 0·46–1·71]).InterpretationExposure to anti-TNF therapy does not appear to be associated with risk of ischaemic CVA when compared with nbDMARD therapy. Further follow-up is needed to assess time-varying risk.FundingBritish Society for Rheumatology. 相似文献
108.
Two-photon excitation of potentiometric probes enables optical recording of action potentials from mammalian nerve terminals in situ 总被引:1,自引:0,他引:1
Fisher JA Barchi JR Welle CG Kim GH Kosterin P Obaid AL Yodh AG Contreras D Salzberg BM 《Journal of neurophysiology》2008,99(3):1545-1553
We report the first optical recordings of action potentials, in single trials, from one or a few (approximately 1-2 microm) mammalian nerve terminals in an intact in vitro preparation, the mouse neurohypophysis. The measurements used two-photon excitation along the "blue" edge of the two-photon absorption spectrum of di-3-ANEPPDHQ (a fluorescent voltage-sensitive naphthyl styryl-pyridinium dye), and epifluorescence detection, a configuration that is critical for noninvasive recording of electrical activity from intact brains. Single-trial recordings of action potentials exhibited signal-to-noise ratios of approximately 5:1 and fractional fluorescence changes of up to approximately 10%. This method, by virtue of its optical sectioning capability, deep tissue penetration, and efficient epifluorescence detection, offers clear advantages over linear, as well as other nonlinear optical techniques used to monitor voltage changes in localized neuronal regions, and provides an alternative to invasive electrode arrays for studying neuronal systems in vivo. 相似文献
109.
Further characterization of factor VIII-deficient mice created by gene targeting: RNA and protein studies 总被引:6,自引:7,他引:6
Bi L; Sarkar R; Naas T; Lawler AM; Pain J; Shumaker SL; Bedian V; Kazazian HH Jr 《Blood》1996,88(9):3446-3450
110.
We previously reported that 1 week of propranolol treatment (160 to 240 mg/d, orally) reduced resting metabolic rate (RMR) an average of 9% in healthy men. To determine whether this response was caused by the 25% reduction in serum triidothyronine (T3), rather than beta-adrenergic blockade, we examined the effect of nadolol on RMR in five healthy men. Nadolol is a nonselective beta-adrenergic antagonist that does not affect T3 production. After 6 to 10 days of nadolol treatment (240 mg/d), mean postabsorptive RMR declined 7% (P less than .01), with no significant change in serum T3 or thyroxine (T4) concentrations. This effect is significantly different from that of a hospitalized control group that received no drug and had no change in mean RMR, and was not different from the response to propranolol (previously published data). Nadolol slightly reduced the mean thermic response to a meal (12%), but this effect was not statistically significant. Mean postprandial RMR was 8% lower after nadolol treatment (P less than .01), mainly because of the reduced postabsorptive RMR, rather than a change in the response to the meal. These data suggest that beta-adrenergic activity makes a small but significant contribution to resting energy expenditure in man. 相似文献