35 resultados para Vasodilator prostanoids


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The most frequent cause of vasodilatory shockis outcome from sepsis, a systemic inflammatory response to infection, characterized by hypotension, hyporeactivity to the catecholamines and disseminated intravascular coagulation. The commonest cause of sepsis has reported to be infection with Gram-negative bacteria, typically E. coli, resulting in the release of lipopolysaccharide (endotoxin) from the bacterial outer membrane during autolysis or death of these microorganisms, with the involvement of many mediators, including nitric oxide. Later it was found that plasma levels of vasopressin in sepsis patients were abnormally low and observed that some patients with advanced septic shock were extremely sensitive to the activity actions of exogenous vasopressin.

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The aim of this study is to report the case of a quick growing brown tumour in the jaw after a parathyroidectomy due to the presence of a rare fifth parathyroid gland. The patient had chronic renal disease and the diagnosis was tertiary hyperparathyroidism. Thirty days after the parathyroidectomy, the patient returned with a significant increase in the tumour size. The suspicion of a supernumerary gland was confirmed by parathyroid scintigraphy. The treatment of brown tumour is dependent on the treatment of the hyperparathyroidism. However, curettage should be considered if a large lesion is disturbing mastication. In conclusion, this case should attract the attention of general practitioner dentists, since they may be the first professionals who have contact with the patient with a brown tumour in the jaws. Likewise, this case emphasises the importance of knowing the type of hyperparathyroidism involved to allow for effective treatment planning. © 2011 European Association for Cranio-Maxillo-Facial Surgery.

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Annona species have been used as a natural remedy for a variety of illnesses with antiparasitic, antispasmodic, antidiarrheal, antiulcer, sedative, analgesic, hypotensive, and vermifugal effects. These properties are due to the presence of a number of bioactive compounds on the leaves, fruit, seeds, and stem. The aim of this review is to show the main species of Annona, their medicinal properties and the chemical constituents that may be related to these effects. In the leaves it is possible to find acetogenins, annopentocins A, B, and C, cis- and trans-annomuricin-D-ones, goniothalamicin, arianacin, and javoricin, related to anticancer properties. Quercetin-3-O-glucoside, also found in the leaves mediates antidiabetic and antioxidative effects. In the fruit are found annonaine, nornuciferine and asimilobine, associated to antidepressive effects. In the seeds are found muricatetrocin A and muricatetrocin B, longifolicin, corossolin, corossolone, uvarigrandin A, bullatacin, squamotatin. These acetogenins are associated with anticancer effects. Cyclosquamosin B, quercetin, and cyclosquamosin from the seeds have respectively vasorelaxant, antithyroidal and, antiinflammatory activity. In the stem parts there are several components as N-trans-feruloyltyramine, N-p-coumaroyltyramine, and N-trans-caffeoyltyramine, lignans, syringaresinol, syringaldehyde, beta-sitosterol and beta-sitosterol-beta-D-glucoside which exhibit antiplatelet aggregation activity. Copaene, patchoulane, 1H-cycloprop (e) azulene and kaur-16-en-19-oic acid found in the barks exhibit significant central as well as peripheral analgesic and antiinflammatory activities. The properties of the biological compounds in Annona species support information that may provide validation for its medicinal uses, but further studies should be performed to establish ideal and safe doses of consumption to ensure the effectiveness of the benefits. © 2012 Bentham Science Publishers.

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Resistant hypertension (RH) is characterized by blood pressure above 140 × 90 mm Hg, despite the use, in appropriate doses, of three antihypertensive drug classes, including a diuretic, or the need of four classes to control blood pressure. Resistant hypertension patients are under a greater risk of presenting secondary causes of hypertension and may be benefited by therapeutical approach for this diagnosis. However, the RH is currently little studied, and more knowledge of this clinical condition is necessary. In addition, few studies had evaluated this issue in emergent countries. Therefore, we proposed the analysis of specific causes of RH by using a standardized protocol in Brazilian patients diagnosed in a center for the evaluation and treatment of hypertension. The management of these patients was conducted with the application of a preformulated protocol which aimed at the identification of the causes of resistant hypertension in each patient through management standardization. The data obtained suggest that among patients with resistant hypertension there is a higher prevalence of secondary hypertension, than that observed in general hypertensive ones and a higher prevalence of sleep apnea as well. But there are a predominance of obesity, noncompliance with diet, and frequent use of hypertensive drugs. These latter factors are likely approachable at primary level health care, since that detailed anamneses directed to the causes of resistant hypertension are applied. © 2012 Livia Beatriz Santos Limonta et al.

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Accumulating evidence demonstrates that chronic inflammation plays an important role in heart hypertrophy and cardiac diseases. However, the fine-tuning of cellular and molecular mechanisms that connect inflammatory process and cardiac diseases is still under investigation. Many reports have demonstrated that the overexpression of the cyclooxygenase-2 (COX-2), a key enzyme in the conversion of arachidonic acid to prostaglandins and other prostanoids, is correlated with inflammatory processes. Increased level of prostaglandin E2 was also found in animal model of left ventricle of hypertrophy. Based on previous observations that demonstrated a regulatory loop between COX-2 and the RNA-binding protein CUGBP2, we studied cellular and molecular mechanisms of a pro-inflammatory stimulus in a cardiac cell to verify if the above two molecules could be correlated with the inflammatory process in the heart. A cellular model of investigation was established and H9c2 was used.We also demonstrated a regulatory connection between COX-2 and CUGBP2 in the cardiac cells. Based on a set of different assays including gene silencing and fluorescence microscopy, we describe a novel function for the RNA-binding protein CUGBP2 in controlling the pro-inflammatory stimulus: subcellular trafficking of messenger molecules to specific cytoplasmic stress granules to maintain homeostasis. © 2013 International Federation for Cell Biology.

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Background: The peptide Paulistine was isolated from the venom of wasp Polybia paulista. This peptide exists under a natural equilibrium between the forms: oxidised - with an intra-molecular disulphide bridge; and reduced - in which the thiol groups of the cysteine residues do not form the disulphide bridge. The biological activities of both forms of the peptide are unknown up to now. Methods: Both forms of Paulistine were synthesised and the thiol groups of the reduced form were protected with the acetamidemethyl group [Acm-Paulistine] to prevent re-oxidation. The structure/activity relationships of the two forms were investigated, taking into account the importance of the disulphide bridge. Results: Paulistine has a more compact structure, while Acm-Paulistine has a more expanded conformation. Bioassays reported that Paulistine caused hyperalgesia by interacting with the receptors of lipid mediators involved in the cyclooxygenase type II pathway, while Acm-Paullistine also caused hyperalgesia, but mediated by receptors involved in the participation of prostanoids in the cyclooxygenase type II pathway. Conclusion: The acetamidemethylation of the thiol groups of cysteine residues caused small structural changes, which in turn may have affected some physicochemical properties of the Paulistine. Thus, the dissociation of the hyperalgesy from the edematogenic effect when the actions of Paulistine and Acm-Paulistine are compared to each other may be resulting from the influence of the introduction of Acm-group in the structure of Paulistine. General significance: The peptides Paulistine and Acm-Paulistine may be used as interesting tools to investigate the mechanisms of pain and inflammation in future studies. © 2013 Elsevier B.V.

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Fundamento: Estresse e etanol são ambos, independentemente, importantes fatores de risco cardiovascular. Objetivo: avaliar o risco cardiovascular do consumo de etanol e exposição ao estresse, isolados e em associação, em ratos machos adultos. Métodos: Os ratos foram separados em quatro grupos: controle, etanol (20% na água de beber durante seis semanas), estresse (imobilização 1h dia/5 dias por semana/ 6 semanas) e estresse/etanol. As curvas de concentração-resposta à noradrenalina - na ausência e na presença de ioimbina, L-NAME ou indometacina - ou fenilefrina foram determinadas em aortas torácicas com e sem endotélio. EC50 e resposta máxima (n = 8-12) foram comparadas através de ANOVA de dois fatores (two-way) / método de Bonferroni. Resultados: Estresse ou estresse em associação com o consumo de etanol aumentaram as respostas máximas de noradrenalina em aortas intactas. Essa hiper-reatividade foi eliminada pela remoção do endotélio, ou pela presença da indometacina ou ioimbina, mas não foi alterada pela presença de L-NAME. Enquanto isso, o consumo de etanol não alterou a reatividade à noradrenalina. As respostas da fenilefrina em aortas com e sem endotélio também permaneceram inalteradas independentemente do protocolo. Conclusão: O estresse crônico aumentou as respostas aórticas dos ratos à noradrenalina. Esse efeito é dependente do endotélio vascular e envolve a liberação de prostanóides vasoconstritores através da estimulação de α-2 adrenoceptores endoteliais. Além disso, o consumo crônico de etanol pareceu não influenciar as respostas de noradrenalina em aorta de rato, nem modificar o aumento de tais respostas observadas em consequência da exposição ao estresse.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Pós-graduação em Cirurgia Veterinária - FCAV

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Objective: This study investigated the physiological and somatic changes evoked by daily exposure to the same type of stressor (homotypic) or different aversive stressor stimuli (heterotypic) in adolescent and adult rats, with a focus on cardiovascular function. The long-term effects of stress exposure during adolescence were also investigated longitudinally. Methods: Male Wistar rats were exposed to repeated restraint stress (RRS, homotypic) or chronic variable stress (CVS, heterotypic). Results: Adrenal hypertrophy, thymus involution, and elevated plasma glucocorticoid were observed only in adolescent animals, whereas reduction in body weight was caused by both stress regimens in adults. CVS increased mean arterial pressure (adolescent: p = .001; adult: p = .005) and heart rate (HR; adolescent: p = .020; adult: p = .011) regardless of the age, whereas RRS increased blood pressure selectively in adults (p = .001). Rest tachycardia evoked by CVS was associated with increased cardiac sympathetic activity in adults, whereas a decreased cardiac parasympathetic activity was observed in adolescent animals. Changes in cardiovascular function and cardiac autonomic activity evoked by both CVS and RRS were followed by alterations in baroreflex activity and vascular reactivity to vasoconstrictor and vasodilator agents in adolescent adult animals. Except for the circulating glucocorticoid change, all alterations observed during adolescence were reversed in adulthood. Conclusions: These findings suggest a stress vulnerability of adolescents to somatic and neuroendocrine effects regardless of stress regimen. Our results indicated an age-stress type-specific influence in stress-evoked cardiovascular/autonomic changes. Data suggest minimal consequences in adulthood of stress during adolescence.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)