Objectives This work investigated the acute antinociceptive effect of a synthetic chalcone, 4-dimethylamino chalcone (DMAC), as well as its effects on vincristine-induced peripheral neuropathy (VIPN) in mice.Methods The inhibitory activity of myeloperoxidase was assessed by measuring HOCl formation. Formalin and hot plate tests were used to study the acute antinociceptive effect of DMAC. VIPN was induced through the administration of vincristine sulphate (0.1 mg/kg, i.p., 14 days). Then, DMSO, DMAC (10 or 30 mg/kg; i.p.), or pregabalin (10 mg/kg, i.p.) were administered for 14 consecutive days. Thermal hyperalgesia and mechanical allodynia were evaluated before and after VIPN induction and on days 1, 3, 7, and 14 of treatment. Neurodegeneration and neuroinflammation were assessed through immunohistochemistry for NF200, iNOS, and arginase-1 within the sciatic nerve.Key findings DMAC inhibited myeloperoxidase activity in vitro and presented an acute antinociceptive effect in both formalin and hot plate tests, with the involvement of muscarinic and opioid receptors. Treatment with 30 mg/kg of DMAC significantly attenuated thermal hyperalgesia and mechanical allodynia and prevented macrophage proinflammatory polarisation in VIPN mice.Conclusions Our results show that DMAC, acting through different mechanisms, effectively attenuates VIPN.

This study evaluated the analgesic and anti-inflammatory activities of Vitex polygama. Ethyl acetate and butanol fractions (10-30 mg/kg), obtained from the hydroalcoholic leaf extract, showed an antinociceptive effect in the acetic acid-induced abdominal writhing test, formalin test and modified hot plate test in mice, indicating a peripheral anti-inflammatory action. Ethyl acetate and butanol fractions were effective in inhibiting nitric oxide and TNF-α production, respectively, in RAW 264.7 macrophages. Both fractions (10-30 mg/kg) showed an acute analgesic effect in mice with vincristine-induced neuropathic pain exposed to a thermal stimulus. Through ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-UV-MS/MS) it was possible to identify seven major compounds: isoorientin, orientin, vitexin, isovitexin, O-p-hydroxybenzoyl orientin, O-caffeoyl-orientin, and di-caffeoylquinic acid. Orientin and isoorientin were isolated from ethyl acetate fraction and had their identity confirmed by nuclear magnetic resonance (NMR). Glucosyl flavones appear to be the main metabolites responsible for the anti-inflammatory and analgesic activities observed for V. polygama.

This study aimed to investigate the effects of the combined injectable contraceptive (CIC) containing estradiol valerate (EV) and norethisterone enanthate (NET-EN) on aorta function and morphology, as well as on redox status, of female Wistar rats. Female rats (9-10 weeks of age) received intramuscular injections of CIC (0.1 mg EV plus 1 mg NET-EN) or castor oil (control group, CTL) for 8 weeks, once a week. Food intake, body weight and systolic blood pressure were measured during the treatment period. Thoracic aortic segments were prepared for isometric tension recording and morphological analysis. Redox status was evaluated by total oxidant status (TOS) and lipid peroxidation (LP) on plasma and reduced glutathione (GSH) on whole blood. CIC group presented lower food intake and lower total weight gain compared to CTL group. There was no change in systolic blood pressure, vascular response of aorta to phenylephrine and acetylcholine and aorta thickness. Plasma TOS and LP values were reduced in CIC group, although GSH was not altered. It was shown that the longterm treatment with the CIC containing EV plus NET-EN does not induce endothelial dysfunction and histomorphometric changes of vascular wall, as well as improves redox status on female Wistar rats.

Endothelial dysfunction in obesity plays a key role in the development of cardiovascular diseases, and it is characterized by increased vascular tonus and oxidative stress. Thus, this study aimed to investigate the vasodilatory and antioxidant activities of Mandevilla moricandiana ethyl acetate fraction and subfractions. Vascular effects were investigated on aorta isolated from control and monosodium glutamate (MSG) induced-obese Wistar rats, and antioxidant activity was assessed by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and oxygen radical absorbance capacity (ORAC) methods. The ethyl acetate fraction (MMEAF) induced a concentration-dependent vasodilation on aortic rings through the NO pathway, with the involvement of histamine H1 and estrogen ERα receptors and showed potent antioxidant activity. In aorta of MSG obese rats, maximal relaxation to acetylcholine was increased in the presence of MMEAF (3 µg/mL), indicating that MMEAF ameliorated obesity-induced endothelial dysfunction. Quercetin and kaempferol aglycones and their correspondent glycosides, as well as caffeoylquinic acid derivatives, A-type procyanidin trimer, ursolic and oleanolic triterpenoid acids were identified in subfractions from MMEAF and seem to be the metabolites responsible for the vascular and antioxidant activities of this fraction.

This study aimed to investigate the effects of the combined injectable contraceptive (CIC) containing estradiol valerate (EV) and norethisterone enanthate (NET-EN) on aorta function and morphology, as well as on redox status, of female Wistar rats. Female rats (9-10 weeks of age) received intramuscular injections of CIC (0.1 mg EV plus 1 mg NET-EN) or castor oil (control group, CTL) for 8 weeks, once a week. Food intake, body weight and systolic blood pressure were measured during the treatment period. Thoracic aortic segments were prepared for isometric tension recording and morphological analysis. Redox status was evaluated by total oxidant status (TOS) and lipid peroxidation (LP) on plasma and reduced glutathione (GSH) on whole blood. CIC group presented lower food intake and lower total weight gain compared to CTL group. There was no change in systolic blood pressure, vascular response of aorta to phenylephrine and acetylcholine and aorta thickness. Plasma TOS and LP values were reduced in CIC group, although GSH was not altered. It was shown that the long-term treatment with the CIC containing EV plus NET-EN does not induce endothelial dysfunction and histomorphometric changes of vascular wall, as well as improves redox status on female Wistar rats.

The aim of this study was to perform the isolation and characterization of vasodilatory flavonoids fromTapirira guianensisAubl. (Annacardiaceae) leaves. In this context, ethyl acetate fraction (EA fraction) was obtained and subjected to fractionation batches by HSCCC affording: myricetin 3-O-alpha-L-rhamnopyranoside (myricitrin,1); quercetin 3-O-(6"-O-galloyl)-beta-D-galactopyranoside (2); quercetin 3-O-alpha-L-arabinofuranoside (avicularin,3); and quercetin 3-O-alpha-L-rhamnopyranoside (quercitrin,4). Myricitrin (1) induced a relaxation of 56.07 +/- 13.04% at 300 mu M (P < 0.05; n = 5), indicating that this flavonoid contributes to the vasodilatory activity of EA fraction. In addition, all EA fraction flavonoids were evaluated for their capacity of inhibiting myeloperoxidase activity and flavonoid (2) (IC(50)1.0 +/- 0.3 mu M) was the strongest peroxidase inhibitor. In conclusion, it was possible to verify that myricitrin together with quercetin are mainly responsible for vasodilatory potential, besides flavonoid2for myeloperoxidase inhibition. Together these flavonoids seem to be responsible forTapirira guianensiscardiovascular effects.

PurposeObesity predisposes to cardiovascular and metabolic diseases. The amino acid, L-taurine (Tau), regulates glucose and lipid homeostasis and vascular function. Here we investigated whether Tau supplementation prevents endothelial dysfunction in the thoracic aortas of monosodium glutamate-induced obese (MSG) rats.MethodsMale rats received subcutaneous injections of MSG (4mg/kg body weight/day) or saline (control group, CTL) during the first five days of life. From 21 to 150days of age, the rats were distributed into the groups: CTL, MSG, and CTL and MSG supplemented with 2.5% Tau in their drinking water (CTAU and MTAU).ResultsAt 150-days old, MSG rats presented massive abdominal fat deposition, hypertriglyceridemia, hyperinsulinemia, glucose intolerance and high plasma levels of malondialdehyde (MDA), a lipid peroxidation marker. Tau supplementation attenuated fat accumulation in perigonadal adipose tissue and prevented the increase in triglycerides and MDA plasma levels. Aortic rings of MSG rats presented reduced vasodilation in response to acetylcholine (ACh). No modifications in insulin-induced vasodilatation, or Akt and eNOS phosphorylation, were observed in MSG aortas; thoracic aortas from MSG rats presented reduced tunica media thickness, with a lower aortic wall thickness/lumen diameter ratio and decreased total collagen content. Tau supplementation restored ACh-induced vasodilation and collagen content.ConclusionsOur study presents the first evidence that Tau prevents disruptions in vascular reactivity and in extracellular matrix composition in thoracic aortas of MSG-obese rats. The vascular protective actions of Tau may be linked to reduced lipid peroxidation and a reduction in cardiovascular risk factors, such as abdominal fat and hypertriglyceridemia.

The aim of this research was to perform a phytochemical study of the methanol leaves extract of T. guianensis (MET) guided by vasodilatory and antioxidant activities. The chemical profile of MET and the ethyl acetate fraction (EA fraction) was determined by HPLC-UV-MS and EA fraction guided fractionation by reverse-phase chromatography. The vasorelaxant effects of MET, fractions, sub-fractions and constituents were assessed on rat aorta pre-contracted with phenylephrine. Antioxidant activity was evaluated by using a DPPH assay. The results show that MET-induced vasodilation was dependent on NO/cGMP; and that the PI3K/Akt pathway seems to be the main route involved in eNOS activation. The EA fraction showed greater vasodilatory and antioxidant potency and was submitted to further fractionation. This allowed the isolation and characterization of quercetin, quercetin 3-O-(6″-O-galloyl)-β-d-galactopyranoside and 1,4,6-tri-O-galloyl-β-d-glucose. Also, galloyl-HHDP-hexoside and myricetin deoxyhexoside were identified by HPLC-UV-MS. These compounds are being described for the first time for T. guianensis. 1,4,6-tri-O-galloyl-β-d-glucose and quercetin 3-O-(6″-O-galloyl)-β-d-galactopyranoside showed no vasodilatory activity. Quercetin and myricetin glycoside seems to contribute to the MET activity, since they have been reported as vasodilatory flavonoids. MET-induced vasodilation could contribute to the hypotensive effect of T. guianensis previously reported.

Abstract Natural products extracted from plants represent a valuable source of new bioactive substances. Many studies describe the potential of plant products for the treatment of cardiovascular diseases. Species of the Mandevilla genus have been studied for their biological activities, mainly as antioxidant, anti-inflammatory, and vasorelaxant. However, the phytochemical and pharmacological profiles of Mandevilla moricandiana have not been investigated yet. The aim of this study was to evaluate the vasodilator effect of the hydroalcoholic extract of the leaves of M. moricandiana, as well as its chemical profile. Chemical analysis and quantification of major compounds were performed by HPLC analysis. Total flavonoid content was quantified based on rutin equivalents, and major compounds were identified based on HPLC-DAD-MS analysis. M. moricandiana leaf extract-induced vasodilation was investigated in rat aortic rings precontracted with phenylephrine. The total flavonoids were quantified as 3.25 ± 0.11 % w/w of the hydroalcoholic leaf extract, and HPLC-DAD-MS allowed for the identification of luteolin and quercetin glycosides. The maximal relaxant effect of the hydroalcoholic leaf extract was 86.07 ± 1.68 % at a concentration of 30 µg/mL (p < 0.05; n = 6). The concentration of hydroalcoholic extract of the leaves of M. moricandiana necessary to reduce phenylephrine-induced contractions of the endothelium-intact aorta by 50 % was 0.82 ± 0.10 µg/mL. M. moricandiana leaf extract-induced vasodilation was abolished in aortas pretreated with NG-nitro-L-arginine methyl ester and 1H-[1,2,4]oxadiazolo-[4,3-α]quinoxalin-1-one. In addition, diphenhydramine partially inhibited the effect of the hydroalcoholic extract of the leaves of M. moricandiana. Thus, M. moricandiana-induced relaxation depends on the endothelium and on the activation of the nitric oxide/cyclic GMP pathway, with the involvement of endothelial histamine H1 receptors. Luteolin and quercetin glycosides seem to contribute to the extract activity.

Obesity predisposes to the development of cardiovascular diseases and type 2 diabetes. Detrimental impacts of maternal obesity on adiposity and cardiovascular function in offspring are well known, whereas the contribution of obese fathers to these processes is poorly described. Taurine (Tau) regulates glucose homeostasis and cardiovascular function. Here, we analyzed whether paternal obesity may influence adiposity, glucose tolerance and vascular reactivity in their offspring. We also determined whether Tau supplementation in fathers modulates these effects. Male rats received subcutaneous injections of MSG [4 g/kg body weight (BW)] or saline [1.25 g/kg BW, control (CTL)] during the first 5 days of life. At 21 days, rats were distributed into four groups: CTL, MSG, and CTL and MSG supplemented with 2.5 % Tau (CTAU and MTAU). At 90 days of age, all groups were mated with female CTL rats to obtain offspring that were designated according to their fathers' treatment. MSG-treated rats were obese, hyperinsulinemic and hypertriglyceridemic. Tau decreased fat stores and plasma triglyceride levels in MTAU. At 5 months of age, female offspring from MSG rats demonstrated higher retroperitoneal and perigonadal fat stores. While male offspring did not exhibit any alteration in adiposity or glucose homeostasis, the aortas of these rats had a lower maximal vasodilatory response to acetylcholine (Ach). In contrast, Ach-induced aorta relaxation was normal in MTAU offspring. In conclusion, data indicate that MSG-hypothalamic obesity in fathers may contribute to obesity, in female offspring, and vascular dysfunction in male offspring, and that supplementation of Tau to founders may preserve only vascular function

BACKGROUND:Tramadol is a centrally acting analgesic, whose mechanism of action involves opioid-receptor activation. Previously, we have shown that tramadol and its enantiomers had a negative inotropic effect on the papillary muscle in which the (+)-enantiomer is more potent than (-)- and (±)-tramadol. OBJECTIVE:In this study, we investigated the effects of tramadol and its enantiomers on L-type calcium current (ICa-L). METHODS:The experiments were carried out in isolated Wistar rat ventricular myocytes by using the whole cell patch clamp technique. RESULTS:Tramadol (200 µM) reduced the peak amplitude of ICa-L at potentials from 0 to +50 mV. At 0 mV, I(Ca-L) was reduced by 33.7 ± 7.2%. (+)- and (-)-tramadol (200 µM) produced a similar inhibition of ICa-L, in which the peak amplitude was reduced by 64.4 ± 2.8% and 68.9 ± 5.8%, respectively at 0 mV (p > 0.05). Tramadol, (+)- and (-)-tramadol shifted the steady-state inactivation of ICa-L to more negative membrane potentials. Also, tramadol and (+)-tramadol markedly shifted the time-dependent recovery curve of I(Ca-L) to the right and slowed down the recovery of I(Ca-L) from inactivation. The time constant was increased from 175.6 ± 18.6 to 305.0 ± 32.9 ms (p < 0.01) for tramadol and from 248.1 ± 28.1 ms to 359.0 ± 23.8 ms (p < 0.05) for (+)-tramadol. The agonist of µ-opioid receptor DAMGO had no effect on the I(Ca-L). CONCLUSION:The inhibition of ICa-L induced by tramadol and its enantiomers was unrelated to the activation of opioid receptors and could explain, at least in part, their negative cardiac inotropic effect.

LASSBio-985 is a sulfonamide compound designed as a simplified structure of a nonselective phosphodiesterase type 4 (PDE-4) inhibitor that promotes vasodilatory activity in vitro. PDE are enzymes responsible for the hydrolysis of cyclic adenosine 3',5'- monophosphate and cyclic guanosine 3',5'-monophosphate. Five different isozymes of PDE are found in vascular smooth muscle (PDE1-PDE5). Aortic rings, with or without endothelium, from male normotensive and spontaneously hypertensive rats (SHR) were prepared for isometric tension recording. Blood pressure was measured in Wistar Kyoto (WKY) rats and SHR during intravenous infusion of LASSBio-985 (10 mg/kg/min) during 15 min. LASSBio-985 induced a concentration-dependent vasodilation in aortic rings from normotensive and SHR, which was almost completely inhibited in endothelium-denuded vessels. Vasodilatory activity was also reduced in endothelium-intact aortic rings that had been pretreated with N(ω)-nitro-L-arginine methyl ester hydrochloride (L-NAME), a nitric oxide synthase inhibitor and 1H-[1,2,4]oxadiazolod[4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor. LASSBio-985-induced vasodilation was also inhibited by sildenafil (100 μm) and SQ 22536, a PDE5 inhibitor and adenylate cyclase inhibitor, respectively. To evaluate the involvement of some endothelial receptors, atropine, diphenhydramine, HOE 140, naloxone, propranolol, indomethacin, and wortmannin were tested, but none inhibited the effects of LASSBio-985. The residual effect observed on endothelium-denuded aortic rings was abolished by nicardipine, a voltage-sensitive-Ca(2+)-channel blocker. Intravenous infusion of LASSBio-985 (10 mg/kg/min) significantly reduced systolic and diastolic pressures in both WKY and SHR. LASSBio-985 is a compound with vasodilatory activity, which could be consequent to PDE1 inhibition and voltage-sensitive-Ca(2+)-channel blockade.

BACKGROUND: Dyslipidemia results from consumption of a diet rich in saturated fatty acids and is usually associated with cardiovascular disease. A diet rich in unsaturated fatty acids is usually associated with improved cardiovascular condition.OBJECTIVE: To investigate whether a high-fat diet rich in unsaturated fatty acids (U-HFD)-in which fatty acid represents approximately 45% of the total calories-impairs the cardiovascular system.METHODS: Male, 30-day-old Wistar rats were fed a standard (control) diet or a U-HFD containing 83% unsaturated fatty acid for 19 weeks. The in vivo electrocardiogram, the spectral analysis of heart rate variability, and the vascular reactivity responses to phenylephrine, acetylcholine, noradrenaline and prazosin in aortic ring preparations were analyzed to assess the cardiovascular parameters.RESULTS: After 19 weeks, the U-HFD rats had increased total body fat, baseline glucose levels and feed efficiency compared with control rats. However, the final body weight, systolic blood pressure, area under the curve for glucose, calorie intake and heart weight/final body weight ratio were similar between the groups. In addition, both groups demonstrated no alteration in the electrocardiogram or cardiac sympathetic parameters. There was no difference in the responses to acetylcholine or the maximal contractile response of the thoracic aorta to phenylephrine between groups, but the concentration necessary to produce 50% of maximal response showed a decrease in the sensitivity to phenylephrine in U-HFD rats. The cumulative concentration-effect curve for noradrenaline in the presence of prazosin was shifted similarly in both groups.CONCLUSIONS: The present work shows that U-HFD did not impair the cardiovascular parameters analyzed.

In Brazilian folk medicine, extracts from Piper species are used to reduce blood pressure. Previously, we demonstrated the vasodilatory activity of crude extracts from leaves of Piper truncatum explaining their possible use in the treatment of hypertension in traditional medicine. In the present Study, we investigated the effects of eudesmin, a lignan isolated from hexane extract of leaves from Piper truncation. on the contractility of rat aortas and the possible mechanisms involved in its vascular action. Eudesmin induced an intense concentration-dependent relaxation of aortic rings precontracted with phenylephrine. The concentration of eudesmin necessary to reduce phenylephrine-induced aortic contraction by 50% (IC50) was 10.69 +/- 0.67 mu g/ml. Eudesmin-induced vasodilation required an intact endothelium since vascular relaxation was inhibited by mechanic removal of endothelium, and by pretreatment with nitric oxide synthase inhibitor and soluble guanylate cyclase inhibitor. Relaxation induced by eudesmin was also impaired in the presence of indomethacin and diphenhydramine, a cyclooxygenase inhibitor and an antagonist of type 1 histamine receptor (H-1), respectively. IC50) was increased to 18.1 +/- 1.8 and 18.1 +/- 2.6 mu g/ml (P<0.05; n=6) after exposure to indomethacin and diphenhydramine, respectively. Atropine (muscarinic receptor antagonist), propranolol (beta-adrenoceptor antagonist) and glibenclamide (ATP-sensitive K+ channel blocker) did not alter the effect of eudesmin. These results indicate that eudesmin-induced vascular relaxation in rat aorta is mediated by release of nitric oxide and prostanoid through the involvement of histamine receptor Present in the endothelial cells. (C) 2009 Elsevier B.V. All rights reserved.

New substances designed for the treatment of anxiety have previously been synthesized, which resulted in the identification of four new pyrazolo[3,4-b]pyrrolo[3,4-d]pyridine derivatives structurally designed by using zolpidem as lead compound. Among them, LASSBio-873 was the most potent to produce analgesic, sedative and hypnotic effects. Thus, we investigated the possible mechanisms involved in LASSBio-873-induced sedation, as well as its effects on different models of inflammatory pain. LASSBio-873 (4mg/kg) reduced locomotor activity of mice in the open field test from 205.2±25.6 to 87.6±16.2movements/min. Atropine, a non-selective muscarinic antagonist, prevented the LASSBio-873-induced sedation and increased locomotor activity to 192.9±30.2movements/min. In the formalin test, LASSBio-873 (4mg/kg) significantly reduced the duration of nociceptive behavior during the inflammatory phase, reducing the control reactivity from 197.6±14.5s to 84.4±10.3s. Carrageenan reduced the latency for the animal reaction from 5.1±0.2s (control) to 2.1±0.3s which was completely reverted by LASSBio-873 (6mg/kg) to 5.6±0.6s. Atropine prevented the LASSBio-873-induced antinociceptive and antihyperalgesic activities, indicating the interference of the cholinergic system. LASSBio-873 is a novel prototype of drug that modulates muscarinic activity and could be used for neuropsychiatric and cognitive disorders and other conditions associated to acute and chronic pain.

BACKGROUND:Several new bioactive compounds of the N-acylhydrazone class were developed from the safrole, a Brazilian natural product obtained from sassafras oil (Ocotea pretiosa). This work investigated the effects on cardiovascular system of LASSBio-897, a new analogue of the lead compound 3,4-methylenedioxybenzoyl-2-thienylhydrazone named LASSBio-294. METHODS:Thoracic aorta from Wistar-Kyoto (WKY) rats was prepared for isometric tension recording and for cGMP content determination. Blood pressure (BP) was measured in WKY rats and spontaneously hypertensive rats (SHR) after treatment with 1 mg/kg intravenously of LASSBio-897 and during 14 days' treatment of SHR with 1 mg/kg/day perorally. RESULTS:LASSBio-897 (0.05-1 micromol/l) exhibited a potent vasodilatory activity in phenylephrine (Phe)-contracted aortic rings from WKY rats. This effect was abolished in endothelium-denuded aortic rings and after treatment with the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) or the guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Also, LASSBio 897 (1 micromol/l) increased about 15 times the intracellular content of cGMP. LASSBio-897-induced vasodilation was totally inhibited by the muscarinic antagonist atropine and by the M(3) subtype selective antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), indicating the involvement of M(3) receptors. Intravenous administration of LASSBio-897 (1 mg/kg) produced significant hypotensive response in both WKY and SHR. The hypotensive effect of LASSBio-897 was also observed during the 14 days of oral administration. CONCLUSIONS:The novel N-acylhydrazone derivative LASSBio-897 exhibited a potent vasodilatory activity in aortic rings mediated by the NO/cGMP pathway via activation of endothelial M(3) receptors and was orally effective in reducing BP on SHR.

European Journal of PainVolume 13, Issue S1 p. S170-S170 580 TREATMENT OF NEUROPATHIC PAIN WITH A NEW PIRAZOL[3,4-B]PIRROL[3,4-D]PIRIDINE DERIVATIVE R. Sudo, R. Sudo Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorT. Mendes, T. Mendes Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorJ. Raimundo, J. Raimundo Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorN. Nascimento-Junior, N. Nascimento-Junior Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorD. Leal, D. Leal Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorC. Fraga, C. Fraga Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorE. Barreiro, E. Barreiro Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorG. Zapata-Sudo, G. Zapata-Sudo Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this author R. Sudo, R. Sudo Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorT. Mendes, T. Mendes Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorJ. Raimundo, J. Raimundo Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorN. Nascimento-Junior, N. Nascimento-Junior Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorD. Leal, D. Leal Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorC. Fraga, C. Fraga Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorE. Barreiro, E. Barreiro Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this authorG. Zapata-Sudo, G. Zapata-Sudo Universidade Federal do Rio de Janeiro, Rio de Janeiro, BrazilSearch for more papers by this author First published: 12 January 2012 https://doi.org/10.1016/S1090-3801(09)60583-8Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume13, IssueS1September 2009Pages S170-S170 RelatedInformation