1,720,999 research outputs found
Cytokine production by human peripheral blood mononuclear cells exposed to low-frequency electromagnetic field
No full textWe evaluated the effects of a 50-Hz pulsed electromagnetic field with a peak magnetic field of 3 mT on the production of cytokines by resting peripheral blood mononuclear cells. Our results demonstrate no modification of interleukin-1β, interleukin-2, or interleukin-6 levels, evaluated 0, 24, and 48 h after exposure, compared with sham-exposed cells. Proliferation indices were also practically unchanged, suggesting the absence of any activating effect of the electromagnetic field. Indeed, concentrations of tumor necrosis factor-α and interferon-γ, evaluated during the same period after 12 h of EMF exposure, were significantly lower than those measured in supernatants of control cells. This was confirmed by evaluation of both cytokines during a 24-h exposure period and 24 h thereafter, in the supernatants of exposed and sham-exposed cells. Comparison between tumor necrosis factor-α biologic activity and the cytokine antigen present in our samples showed strong and reproducible correlation values, suggesting the absence of qualitative differences in this protein due to either proteolytic activity or electromagnetic field
Effects of metabolic stress and ischaemia on the bladder, and the relationship with bladder overactivity
No full textThe bladder wall becomes to ischaemic when intravesical pressure rises above capillary pressure. This will occur routinely in bladders with outflow obstruction. Experiments in vitro show that the detrusor normally uses anaerobic as well as aerobic metabolism. Anoxic conditions result in an initial reduction in contractility, but significant contractile ability persists. Substrate removal causes a slow progressive fall in contractility as glycogen stores deplete. Removal of substrate and oxygen causes rapid loss of contractile ability and permanently damages intrinsic nerves, although the detrusor recovers well. In vivo ischaemia in animal models results in bladder overactivity and the expression of apoptotic markers in intrinsic neurons in the bladder wall. In humans, bladders from patients with bladder instability show patchy denervation, suggesting that periodic ischaemia and neuronal death may predispose to overactivity
Neuropeptides and urinary bladder ischemia-reperfusion injury
No full textUrinary bladder decompensation following partial bladder obstruction is directly related to decreased tissue
perfusion, resulting in periods of hypoxia and ischemia. Hence, it is important to look for substances which could
counteract against the ischemia/reperfusion- induced neuronal damage in detrusor muscle and in such a way to
ameliorate the functional disorders of urinary bladder. Many neuropeptides have been found to be synthesized, stored
and released in the lower urinary tract. Some of them were reported to reduce ischemia-reperfusion injury. The purpose
of this study was to examine the efficacy of vasoactive intestinal peptide (VIP), somatostatin and Sandostatin®
(Novartis) to counteract the damage suffered by neurons in urinary bladder exposed in vitro to experimentally induced
ischemia-reperfusion in guinea-pig. We found that VIP (0.3 μM), somatostatin (300 nM) and sandostatin (1 to 300 nM)
improved significantly the response to electrical field stimulation during reperfusion as compared to the control,
utreated tissues. The antioxidant activity of VIP, somatostatin and sandostatin, assessed as their capability to scavenge
peroxyl radicals during linoleic acid oxidation corresponded to 6.4 ± 0.1, 6.7 ± 0.3 and 7.0 ± 0.6, respectively. The
antioxidant activity of the above mentioned peptides could underlie their neuroprotective action during reperfusion,
when a significant amount of free radicals has been formed
Effects of astrocytoma cells conditioned medium on differentiated neuroblastoma cells subjected to hypoxia and reperfusion
No full textThe effect of anoxia and glucose-free solutions on the contractile response of guinea-pig detrusor strips to intrinsic nerve stimulation and the application of excitatory agonists
No full textPurpose: To study the effects of anoxia and substrate depletion, both separately and combined, on the contractile responses of guinea-pig detrusor smooth muscle strips to activation of intrinsic nerves, application of agonists and depolarization with high potassium solution. Materials and Methods: Bladders were opened and the urothelium removed. Strips of detrusor were dissected and mounted for tension recording in small organ baths superfused with warmed solutions of known composition. Results: Anoxia caused a small initial reduction of the contractile responses which then remained constant for several hours. Glucose-free solutions resulted in a slow progressive decline in the responses to field stimulation, carbachol and high potassium solution, with substantial responses still present after five hours. The response to ATP, however, was unaffected. Removal of oxygen and glucose, mimicking ischaemia, caused abolition of all responses within an hour. After reintroduction of normal conditions responses reached their maximal extent of recovery within an hour. Recovery was almost complete for responses to ATP and carbachol, but less so for high K+ solutions. Very little recovery to stimulation of intrinsic nerves was seen. Conclusions: The results demonstrate that phasic contractions can be fuelled almost fully by oxidative phosphorylation or by anaerobic glycolysis, but that in conditions mimicking ischaemia the intrinsic nerves are more susceptible to ischaemic damage than the detrusor smooth muscle
Effect of anoxia-glucopenia and re-superfusion on intrinsic nerves of mammalian detrusor smooth muscle: importance of glucose metabolism
No full textTo investigate the effect of anoxia/glucopenia and re-superfusion on intrinsic nerves in the mammalian urinary bladder.
METHODS: Strips of detrusor smooth muscle were dissected from monkey and human urinary bladder and mounted for tension recording in organ baths superfused with Krebs solution. Human, monkey, and guinea-pig urinary bladders were treated to evaluate glycogen contents by a biochemical method.
RESULTS: Detrusor strips from both monkeys and humans had to be exposed to anoxia-glucopenia for up to 2-2.5 hr to observe a progressive decline in the response to electrical field stimulation (EFS) of the intrinsic nerves, at variance with guinea-pig detrusor strips. In contrast, the response to direct activation of the smooth muscle with carbachol remained almost unaltered. Incubation of human and monkey detrusor strips with 2-deoxyglucose (2-DG) during 1 hr anoxia-glucopenia, however, caused a marked damage to the intrinsic nerves. The glycogen contents of both human detrusor specimens and monkey urinary bladders were 2.0- and 1.4-fold higher, respectively, than that found in guinea-pig urinary bladder; furthermore, untreated monkey detrusor sections showed a greater number of glycogen granules as compared to those subjected to anoxia-glucopenia and re-superfusion. In guinea-pig and in monkey detrusor sections glycogen granules were found in smooth muscle cells but not in neurons of intramural ganglia.
CONCLUSIONS: A higher susceptibility of guinea-pig as compared to monkey and human nerves has been demonstrated; it is suggested that anaerobic glucose metabolism during anoxia-glucopenia is crucial for the functional recovery of detrusor intrinsic nerves from damage caused by anoxia-glucopenia and re-superfusion
Effects of quercetin and rutin on vascular preparations: a comparison between mechanical and electrophysiological phenomena.
No full textBackground: Several studies have indicated that quercetin promotes relaxation of vascular smooth muscle both in vivo and in vitro. However, Saponara et al. [(2002) Br J Pharmacol 135:1819-1827] have demonstrated that quercetin is an activator of vascular L-type Ca2+ channels. Aim of the study: We investigated the mechanical and electrophysiological properties of quercetin and its rutoside, rutin, in an attempt to clarify how Ca2+ channel activation might be related to the myorelaxing activity. Methods: Aorta ring preparations and single tail artery myocytes were employed for functional and patch-clamp experiments, respectively. Results: Rutin was found to relax intact rat aorta rings, which had been precontracted with phenylephrine (pIC50 = 5.65±0.3 1) but in contrast had no effect on depolarised (60 mM K+) preparations or on those from which the endothelium had been removed. Furthermore, rutin did not affect L-type Ca2+ current recorded in rat tail artery myocytes. The quercetin-induced relaxation of intact rings precontracted with phenylephrine exhibited two components characterised by 6.23±0.38 and 4.66±0.09 pIC50, respectively. Removal of the endothelium abolished the first component, leaving the second unaltered. Moreover, quercetin was found to relax 60 mM K+ depolarised rings with a pIC50 of 4.59±0.03. The application of quercetin in isolated smooth muscle cells brought about a marked increase of L-type Ca2+ current (pEC50= 5.09±0.05). Unlike quercetin, Bay K 8644 contracted aorta rings preincubated with 10, 20 or 30 mM K+. The myotonic effect of Bay K 8644 was observed both in the absence or presence of 30 μM quercetin. The application of Bay K 8644 (10-100 nM) caused a further significant increase in L-type Ca2+ current in rat tail artery myocytes stimulated with 30 μM quercetin. Conclusions: Quercetin is a naturally occurring L-type Ca2+ channel agonist. This effect, however, is overwhelmed by quercetin-induced vasorelaxation taking place via pathways which are more relevant than L-type Ca2+ influx in the hierarchy of functional competencies
Vasoactive intestinal peptide protects guinea-pig detrusor nerves from anoxia/glucopenia injury
No full textVasoactive intestinal peptide (VIP) was tested for its capability to protect the intrinsic nerves of guinea-pig urinary bladder from damage due to anoxia/glucopenia and reperfusion. Guinea-pig detrusor strips were mounted for tension recording in small organ baths and the nerves were subjected to electric field stimulation. VIP (0.3 microM) improved significantly the response of strips to electrical field stimulation either during anoxia/glucopenia or thereafter during reperfusion, as compared to untreated tissues. The antioxidant activity of VIP assessed as its capability to scavenge peroxyl radicals during linoleic acid oxidation corresponded to 6.42+/-0.13 pIC(50) M, i.e. close to the concentration proved to protect strips against the anoxic--glucopenic and reperfusion damage
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