[Remodelling in atrial fibrillation].
Sixty spinal cord-injured male patients with VSD were recruited prospectively. Their mean age was 37 years (range 15-70 years). Baseline evaluation included a thorough medical history, clinical examination, blood pressure measurement, intravenous urogram, and videourodynamics. The patients received terazosin for a 90-day period. Videourodynamic evaluation after completion of the study included cystometrogram, sphincter electromyography, maximum urethral pressure gradient (MUPG), and measurement of post voiding residual (PVR) urine volume. The findings were compared with the pretreatment values.
NA may significantly increase CAP-evoked SP release through activation of α-adrenoreceptors, which may contribute to noradrenergic pain modulation.
A total of 625 centers in the United States and Canada.
The number of antihypertensive agents on the market has increased dramatically over the past 20 years. Many of these agents are used to treat children and adolescents with hypertension despite there being relatively limited data available supporting such use. Recent legislation has helped to increase the number of studies conducted in children, but many clinical questions remain unanswered.
Suburothelial venules showed spontaneous action potential and vasoconstriction activity while suburothelial arterioles were quiescent. Venular vasoconstriction was prevented by cyclopiazonic acid or nicardipine and decreased by 2-aminoethoxydiphenyl borate, niflumic acid or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. Venular smooth muscle cells and perivascular interstitial cells showed spontaneous Ca(2+) transients. Nicardipine decreased the amplitude and disrupted the synchronicity of Ca(2+) transients in and between the 2 cell populations. Residual Ca(2+) transients in nicardipine occurred asynchronously and were abolished by cyclopiazonic acid. Suburothelial arterioles constricted in response to transmural nerve stimulation. These nerve induced constrictions were suppressed by prazosin or the selective α(1A) blocker RS17053 but not by the α(1D) blocker BMY7378. Remaining constrictions were abolished by guanethidine.
The mean volume of the prostate was significantly higher in MetS patients than in patients without MetS (57 ± 32.65 mL compared with 46.00 ± 20.19 mL, p=0.036). The control group demonstrated an 11-unit reduction in IPSS, whereas those with MetS showed a reduction in the symptom score of only 6 units (p<0.001). Regarding the components of MetS separately, triglyceride (p<0.001), fasting blood sugar (p=0.001), and waist circumference (p=0.028) significantly affected the clinical progression of BPH. The observational nature of this study may be a limitation in comparison with an interventional study.
Quantitative mappings were established between drug physicochemical properties (PCPs) and parameter values of a physiologically based, mechanistically realistic, in silico liver (ISL). The ISL plugs together autonomous software objects that represent hepatic components at different scales and levels of detail. Microarchitectural features are represented separately from the mechanisms that influence drug metabolism. The same ISL has been validated against liver perfusion data for sucrose and four cationic drugs: antipyrine, atenolol, labetalol, and diltiazem. Parameters sensitive to drug-specific PCPs were tuned so that ISL outflow profiles from a single ISL matched in situ perfused rat liver outflow profiles of all five compounds. Quantitative relationships were then established between the four sets of drug PCPs and the corresponding four sets of PCP-sensitive, ISL parameter values; those relationships were used to predict PCP-sensitive, ISL parameter values for prazosin and propranolol given only their PCPs. Relationships were established using three different methods: 1) a simple linear correlation method, 2) the fuzzy c-means algorithm, and 3) a simple artificial neural network. Each relationship was used separately to predict ISL parameter values for prazosin and propranolol, given their PCPs. Those values were applied in the ISL used earlier to predict the hepatic disposition details for each drug. Although we had only sparse data available, all predicted disposition profiles were judged reasonable (within a factor of 2 of referent profile data). The order of precision, based on a similarity measure, was 3 > 2 > 1.
NO plays a role in a variety of in vitro models of angiogenesis, although confounding effects of NO on non-endothelial tissues make its role during in vivo angiogenesis unclear. We therefore examined the effects of NO on two physiological models of angiogenesis in mouse skeletal muscle: (1) administration of prazosin (50 mg l-1) thereby increasing blood flow; and (2) muscle overload from surgical ablation of a functional synergist. These models induce angiogenesis via longitudinal splitting and capillary sprouting, respectively. Administration of NG-nitro-L-arginine (L-NNA) abolished the increase in capillary to fibre ratio (C:F) in response to prazosin administration, along with the increases in luminal filopodia and large endothelial vacuoles. L-NNA prevented luminal filopodia and vacuolisation in response to extirpation, but had no effect on abluminal sprouting, and little effect on C:F. Comparison of mice lacking endothelial (eNOS-/-) and neuronal NO synthase (nNOS-/-) showed that longitudinal splitting is eNOS-dependent, and Western blotting demonstrated an increase in eNOS but not inducible NOS (iNOS) expression. These data show that there are two pathways of physiological angiogenesis in skeletal muscle characterised by longitudinal splitting and capillary sprouting, respectively. NO generated by eNOS plays an essential role in splitting but not in sprouting angiogenesis, which has important implications for angiogenic therapies that target NO.