331 resultados para Atrium
Resumo:
Atrial mechanoreceptors, sensitive to stretch, contribute in regulating heart rate and intravascular volume. The information from those receptors reaches the nucleus tractus solitarius and then the paraventricular nucleus (PVN), known to have a crucial role in the regulation of cardiovascular function. Neurons in the PVN synthesize CRF, AVP, and oxytocin (OT). Stimulation of atrial mechanoreceptors was performed in awake rats implanted with a balloon at the junction of the superior vena cava and right atrium. Plasma ACTH, AVP, and OT concentrations and Fos, CRF, AVP, and OT immunolabeling in the PVN were determined after balloon inflation in hydrated and water-deprived rats. The distension of the balloon increased the plasma ACTH concentrations, which were higher in water-deprived than in hydrated rats (P < 0.05). In addition, the distension in the water-deprived group decreased plasma AVP concentrations (P < 0.05), compared with the respective control group. The distension increased the number of Fos- and double-labeled Fos/CRF neurons in the parvocellular PVN, which was higher in the water-deprived than in the hydrated group (P < 0.01). There was no difference in the Fos expression in magnocellular PVN neurons after distension in hydrated and water-deprived groups, compared with respective controls. In conclusion, parvocellular CRF neurons showed an increase of Fos expression induced by stimulation of right atrial mechanoreceptors, suggesting that CRF participates in the cardiovascular reflex adjustments elicited by volume loading. Activation of CRF neurons in the PVN by cardiovascular reflex is affected by osmotic stimulation.
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The objective of this study was to describe multiple Doppler ultrasound parameters of ductus venosus and inferior vena cava in fetuses at gestational ages ranging from 22 to 38 weeks. In this prospective observational study, Doppler ultrasound exams were performed in 45 healthy fetuses at 22, 26, 34, and 38 weeks. Maximum venous velocity, minimum venous velocity, venous pulsatility index, and venous acceleration time (VAT) (defined as the time between minimum and maximum venous velocity) were evaluated at those gestational periods. Increase in the velocities and decrease in the pulsatility index were observed in these vessels throughout gestational age. The VAT increased with gestational age. The VAT, a Doppler parameter still not described elsewhere, increased during pregnancy could be related to a longer period of time needed to fill the atrium in bigger hearts. In this study, we provide reference values for VAT in healthy fetuses.
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Objectives: Up-regulated matrix metalloproteinases may be involved in the development of cardiomyocyte injury and the degradation of troponin associated with acute pulmonary thromboembolism. We examined whether pretreatment with doxycycline (a nonspecific matrix metalloproteinase inhibitor) protects against cardiomyocyte injury associated with acute pulmonary thromboembolism. Design: Controlled animal study. Setting: University research laboratory. Subjects: Mongrel dogs. Interventions: Anesthetized animals received doxycycline (10 mg/kg intravenously) or saline and acute pulmonary thromboembolism was induced with autologous blood clots injected into the right atrium. Control animals received doxycycline (or saline). Measurements and Main Results: Hemodynamic measurements were performed, and acute pulmonary thromboembolism increased baseline mean pulmonary arterial pressure and pulmonary vascular resistance by approximately 160% and 362%, respectively (both p<.05), 120 mins after acute pulmonary thromboembolism. Pretreatment with doxycycline attenuated these increases (to 125% and 232%, respectively; both p<.05). Although acute pulmonary thromboembolism tended to increase the right ventricle maximum rate of isovolumic pressure development and the maximum rate of isovolumic pressure decay, doxycycline produced no effects on these parameters. Gelatin zymograms of right ventricle showed that acute pulmonary thromboembolism marginally increased matrix metalloproteinase-9 (but not matrix metalloproteinase-2) levels in the right ventricle. A fluorometric assay to assess net matrix metalloproteinase activities showed that acute pulmonary thromboembolism increased matrix metalloproteinase activities in the right ventricle by >100% (p<.05), and this finding was confirmed by in situ zymography of the right ventricle. Doxycycline attenuated acute pulmonary thromboembolism-induced increases in right ventricle matrix metalloproteinase activities. Acute pulmonary thromboembolism induced neutrophil accumulation in the right ventricle, as estimated by myeloperoxidase activity, and doxycycline blunted this effect (p<.05). Serum cardiac troponin I concentrations, which reflect cardiomyocyte injury, increased after acute pulmonary thromboembolism, and this increase was attenuated by pretreatment with doxycycline (p<.05). Conclusions: We found evidence supporting the idea that acute pulmonary thromboembolism is associated with increased matrix metalloproteinase activities in the right ventricle, which may lead to degradation of sarcomeric proteins, including cardiac troponin I. Inhibition of matrix metalloproteinases may be an effective therapeutic intervention in the management of acute pulmonary thromboembolism. (Crit Care Med 2011; 39: 349-356)
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Background: The diagnosis of acute pulmonary thromboembolism (APT) and its severity is challenging. No previous study has examined whether there is a linear relation between plasma DNA concentrations and the severity of APT. We examined this hypothesis in anesthetized dogs. We also examined the changes in plasma DNA concentrations in microspheres lung embolization and whether the therapy of APT with nitrite could modify APT-induced changes in plasma DNA concentrations. In vitro DNA release from blood clots was also studied. Methods: APT was induced with autologous blood clots (saline, 1, 3, or 5 ml/kg) injected into the right atrium. A group of dogs received 300 pm microspheres into the inferior vena cava to produce similar pulmonary hypertension. Another group of dogs received 6.75 mu mol/kg nitrite after APT with blood clots of 5 ml/kg. Hemodynamic evaluations were carried out for 120 min. DNA was extracted from plasma samples using QIAamp DNA Blood Mini Kit and quantified using Quant-iT (TM) PicoGreen (R) dsDNA detection kit at baseline and 120 min after APT. Results: APT produced dose-dependent increases in plasma DNA concentrations. which correlated positively with pulmonary vascular resistance (P=0.002, r=0.897) and with mean pulmonary arterial pressure (P=0.006, r=0.856). Conversely, lung embolization with microspheres produced no significant changes in plasma DNA concentrations. While nitrite attenuated APT-induced pulmonary hypertension, it produced no changes in plasma DNA concentrations. Blood clots released dose-dependent amounts of DNA in vitro. Conclusions: Cell-free DNA concentrations increase in proportion to the severity of APT, probably as a result of increasing amounts of thrombi obstructing the pulmonary vessels. (C) 2009 Elsevier B.V. All rights reserved.
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Pretestis laticaecum is described from the small intestine of the freshwater turtle Emydura krefftil. The new species can be distinguished from its congener P. australianus by the following characters; significantly smaller ovary, main lymph vessels reach anterior to posterior testis, genital atrium in mid-oesophageal region, small vitelline follicles clumped around the ovary and significantly larger caeca overlapping. The, position of this species and related genera in fish, the life cycle of P. australianus and the presence of P. laticaecum in turtles suggest that it is a relatively recent host capture.
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A new acanthocolpid, Tormopsolus attenuatus n. sp., is described from the carangid Seriola hippos from waters off the coast of SW Australia. A cladistic analysis of the genus using 31 morphological and metrical characters indicates that the closest species is T. asiatica Parukhin, 1976 status amend. (previously T. orientalis asiatica). T. attenuatus differs from T. asiatica in its smaller overall dimensions, more attenuated outline, relatively shorter post-testicular region, vitelline interruption at the level of the ovary, papillae on the oral sucker and, possibly, much longer genital atrium. Other similar species, T. orientalis Yamaguti, 1934 and T. medius Reimer, 1983, differ in having interruptions of the vitelline fields at the level of both testes and at the level of the ovary.
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The effects of the recently identified human peptide urotensin-II (hU-II) were investigated on human cardiac muscle contractility and coronary artery tone. In right atrial trabeculae from non-failing hearts, hU-II caused a concentration-dependent increase in contractile force (pEC(50)=9.5+/-0.1; E-max= 31.3+/-4.8% compared to 9.25 mM Ca2+; n = 9) with no change in contraction duration. In right ventricular trabeculae from explanted hearts, 20 nM hU-II caused a small increase in contractile force (7.8+/-1.4% compared to 9.25 mM Ca2+; n= 3/6 tissues from 2 out of 4 patients). The peptide caused arrhythmic contractions in 3/26 right atrial trabeculae from 3/9 patients in an experimental model of arrhythmia and therefore has less potential to cause arrhythmias than ET-1. hU-II (20 nM) increased tone (17.9% of the response to 90 mM KCI) in 7/7 tissues from 1 patient, with no response detected in 8/8 tissues from 2 patients. hU-II is a potent cardiac stimulant with low efficacy.
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The aim was to test whether dofetilide has some potential for use in the treatment of heart failure. Dofetilide at less than or equal to 3 x 10(-5) m had no effect on the quiescent Wistar Kyoto (WKY) rat aorta, mesenteric and intralobar arteries, or the spontaneous contractions of the WKY rat portal vein. Dofetilide at 10(-6) to 3 x 10(-5) m relaxed the KCl-contracted aorta. Dofetilide at 10(-9)-10(-7) m augmented the force of contraction of left ventricle strips from 12- and 18-month-old WKY rats at 2 Hz. Spontaneously hypertensive rats (SHRs) at 12 and 17-21 months of age are models of cardiac hypertrophy and failure, respectively. The augmentation of force at 2 Hz with dofetilide was similar on 12- and 18-month-old WKY rats and 12-month-old SHRs but reduced on the 18-month-old SHR left ventricle. At a higher more physiological frequency, 4 Hz, the threshold concentration of dofetilide required to augment the force responses of 21-month-old SHR left ventricles was markedly increased and the maximum augmenting effect was decreased. Dofetilide at 10(-7)-10(-5) m reduced the rate of the 17-month-old WKY rat right atrium, and had a similar effect on age-matched SHR right atrium. In summary, dofetilide is a positive inotrope and negative chronotrope in the rat. However, as the positive inotropic effect is not observed with clinically relevant concentrations at a physiological rate in heart failure, dofetilide is unlikely to be useful as a positive inotrope in the treatment of heart failure.
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Two forms of the activated beta(1)-adrenoceptor exist, one that is stabilized by (-)-noradrenaline and is sensitive to blockade by (-)-propranolol and another which is stabilized by partial agonists such as (-)-pindolol and (-)-CGP 12177 but is relatively insensitive to (-)-propranolol. We investigated the effects of stimulation of the propranolol-resistant PI-adrenoceptor in the human heart. Myocardium from non-failing and failing human hearts were set up to contract at 1 Hz. In right atrium from non-ailing hearts in the presence of 200 nM (-)-propranolol, (-)-CGP 12177 caused concentration-dependent increases in contractile force (-logEC(50)[M] 7.3+/-0.1, E-max 23+/-1% relative to maximal (-)-isoprenaline stimulation of beta(1)- and beta(2)-adrenoceptors, n=86 patients), shortening of the time to reach peak force (-logEC(50)[M] 7.4+/-0.1, E-max 37+/-5%, n=61 patients) and shortening of the time to reach 50% relaxation (t(50%), -logEC(50)[M] 7.3+/-0.1, E-max 33+/-2%, n=61 patients). The potency and maxima of the positive inotropic effects were independent of Ser49Gly- and Gly389Arg-beta(1)-adrenoceptor polymorphisms but were potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (-logEC(50)[M] 7.7+/-0.1, E-max 68+/-6%, n=6 patients, P
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Este relatório de estágio, que se realizou no Edifício Atrium Saldanha em Lisboa, tem por finalidade demonstrar as aptidões adquiridas no decorrer do Mestrado e que tornaram possíveis a participação num estágio que envolveu várias áreas da Engenharia Mecânica. Nos últimos anos, tem-se assistido a um crescente aumento do consumo e do custo da energia eléctrica. De acordo com análises realizadas pela União Europeia, uma percentagem significativa deste aumento de consumo está relacionado com edifícios e habitações. A manutenção preventiva das instalações técnicas é, entre outros aspectos, uma das ferramentas essenciais na redução desta factura energética. A questão que se coloca relaciona-se com a metodologia a aplicar para esse efeito. De que forma podem ou devem os planos de manutenção ser elaborados, qual a periodicidade das intervenções a considerar de modo a aumentar a eficiência energética dos edifícios, reduzir as emissões de dióxido de carbono e garantir uma maior protecção do utilizador? Numa fase inicial do estágio foi feita uma caracterização geral das principais instalações técnicas do edifício de modo a se analisarem, posteriormente, os procedimentos de manutenção adoptados pelas equipas de manutenção. Foram ainda sugeridas algumas periodicidades para os procedimentos de manutenção já existentes e algumas intervenções que não estavam incluídas no plano de manutenção do edifício e que podem contribuir para aumentar a fiabilidade dos equipamentos e consequentemente a eficiência energética e a qualidade do ar interior dos edifícios.
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Mestrado em Tecnologia de Diagnóstico e Intervenção Cardiovascular - Área de especialização: Ultrassonografia Cardiovascular.
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Mestrado em Tecnologia de Diagnóstico e Intervenção Cardiovascular - Ramo de especialização: Intervenção Cardiovascular
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Mestrado em Tecnologia de Diagnóstico e Intervenção Cardiovascular - Ramo de especialização: Ultrassonografia Cardiovascular
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A case of human rabies with cardiac involvement and viral inclusion bodies in the heart is presented. The Negri bodies were found in the Schwann cells of the right epicardial atrium, with secondary mononuclear cells inflammation. In the myocardium, an interstitial edema, proliferation of Anitschkov and rare mononuclear inflammatory cells were seen. There was no relevant cardiovascular signs or symptoms. The rarity of histological descriptions of Negri bodies in the heart is stressed, as well as the importance of cardiac involvement as a potential complication for cases with life prolonged by intensive care units, or in the end-stages of the disease.
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Lesions observed in chronic chagasic cardiopathy frequently produce electrocardiographic alterations and affect cardiac function. Through a computerized morphometrical analysis we quantified the areas occupied by cardiac muscle, connective and adipose tissues in the right atrium of dogs experimentally infected with Trypanosoma cruzi. All of the infected dogs showed chronic myocarditis with variable reduction levels of cardiac muscle, fibrosis and adipose tissue replacement. In the atrial myocardium of dogs infected with Be78 and Be62 cardiac muscle represented 34 and 50%, fibrosis 28 and 32% and adipose tissue 38 and 18%, respectively. The fibrosis observed was both diffuse and focal and mostly intrafascicular, either partially or completely interrupting the path of muscle bundles. Such histological alterations probably contributed to the appearance of electrocardiographic disturbances verified in 10 out 11 dogs which are also common in human chronic chagasic cardiopathy. Fibrosis was the most important microscopic occurrence found since it produces rearrangements of collagen fibers in relation to myocardiocytes which causes changes in anatomical physiognomy and mechanical behavior of the myocardium. These abnormalities can contribute to the appearance of cardiac malfunction, arrythmias and congestive cardiac insufficiency as observed in two of the analyzed dogs. Strain Be78 caused destruction of atrial cardiac muscle higher than that induced by strain Be62.