Sistema via internet web Marista system

O Sistema via Internet foi desenvolvido para atender ao Colégio Marista João Paulo II no que diz respeito à renovação de matrículas, emissão de 2ª via de boleto, solicitação de documentos diversos como: declaração escolar, histórico escolar, boletim entre outros. Ele conta também com registro das informações e tramitações das matrículas pelo interior do colégio. O sistema é desenvolvido para intranet da empresa e para Internet, tendo, portanto um alcance e uma interação maior entre o colégio e as famílias. O sistema faz uso de técnicas de Análise Estrutura de Sistemas, utilizando Diagramas de Contexto, Diagrama de fluxo de dados, Depósitos de Dados, elementos de dados, relações normalizadas, documentos de captação de dados e relatórios impressos. Este documento também descreve os problemas diagnosticados, os objetivos específicos bem como os objetivos esperados, utilizam o modelo de entidade x relacionamento (de contexto e de implementação)

Propofol infusion syndrome and Brugada syndrome electrocardiographic phenocopy

This anesthetic drug may cause a rare condition named propofol infusion syndrome, characterized by unexplained lactic acidosis, lipemia, rhabdomyolysis, cardiovascular collapse and Brugada-like electrocardiographic pattern or Brugada electrocardiographic phenocopy changes following high-dose propofol infusion over prolonged periods of time. Several articles have contributed to our understanding of the cause of the syndrome, and the growing number of case reports has made it possible to identify several risk factors. Uncertainty remains as to whether a genetic susceptibility exists. The favorable recovery profile associated with propofol offers advantages over traditional anesthetics in clinical situations in which rapid recovery is important. Propofol is a safe anesthetic agent, but propofol infusion syndrome is a rare lethal complication. (Cardiol J 2010; 17, 2: 130-135

Myocardium tissue changes caused by electrical transthoracic discharges in rats

<p>Abstract</p> <p>Background</p> <p>Cardiomyocytes cytoarchitecture changes caused by transthoracic countershocks have been focused recently. We aimed to evaluate the effects of electrical discharge application in the mitochondria structure in atrial myocardium of rats.</p> <p>Methods</p> <p>An electrical cardioverter was adapted to small rodent animals for our research. Electrical discharges were applied to the precordial region of 30 albino rats: (1) control group - animals that remained on resting period and were afterwards sacrificed; (2) electrical discharge group - animals that remained on resting period, followed by ten electrical discharges of 300 mV and sacrificed, and; (3) electrical post-discharge group - animals that remained on a resting period and received ten electrical discharges like the electrical discharge group, but were sacrificed seven days subsequently. We examined liver, adrenal and left atrium tissue fragments of the three groups.</p> <p>Results</p> <p>It was observed in control and post-discharge groups a normal cellular structure aspect with preserved architecture of cardiomyocytes and continuous sarcoplasmic membrane integrity. On the other hand, cardiac muscle fibers with mitochondrial edema and lysis occurred in the discharge group. Glycogen and adrenal lipids were not depleted in all groups.</p> <p>Conclusion</p> <p>These data suggest that transthoracic electrical discharges induce mitochondrial injuries in atrial cardiac cells of rats.</p

Efeitos da fluoxetina sobre a ultraestrutura mitocondrial no ventrículo direito de ratos expostos ao estresse pelo frio

OBJECTIVE: To assess fluoxetine effects on mitochondrial structure of the right ventricle in rats exposed to cold stress. METHODS: The experimental study procedures were performed in 250-300g male EPM-Wistar rats. Rats (n=40) were divided into four groups: 1) Control group (CON); 2) Fluoxetine (FLU); 3) Induced hypothermia (IH) and; 4) Induced hypothermia treated with fluoxetine (IHF). Animals of FLU group were treated by the administration of gavages containing 0.75 mg/kg/day fluoxetine during 40 days. The induced hypothermia was obtained by maintaining the groups 3 and 4 in a freezer at -8ºC for 4 hours. The animals were sacrificed and fragments of the right ventricle (RV) were removed and processed prior to performing electron microscopic analysis. RESULTS: The ultrastructural changes in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristolysis). The CON (3.85%), FLU (4.47%) and IHF (8.4%) groups showed a normal cellular structure aspect with preserved cardiomyocytes cytoarchitecture and continuous sarcoplasmic membrane integrity. On the other hand, the IH (34.4%) group showed mitochondrial edema and lysis in cristae. CONCLUSION: The ultrastructural analysis revealed that fluoxetine strongly prevents mitochondrial cristolysis in rat heart, suggesting a protector effect under cold stress condition.OBJETIVO: Analisar os efeitos da fluoxetina sobre a estrutura mitocondrial do ventrículo direito de ratos expostos ao estresse pelo frio. MÉTODOS: Os procedimentos do estudo foram realizados em ratos Wistar-EPM (250-300g) machos. Os ratos (n=40) foram divididos em quatro grupos: 1) Controle (CON); 2) Fluoxetina (FLU); 3) Induzidos à hipotermia (IH) e; 4) Induzidos à hipotermia tratados com fluoxetina (IHF). O grupo FLU foi tratado com gavagem contendo 0,75 mg/kg/dia de fluoxetina durante 40 dias. O estresse induzido pelo frio foi realizado mantendo os grupos 3 e 4 em um freezer (-8ºC) por quatro horas. Os animais foram sacrificados e fragmentos do ventrículo direito (VD) foram removidos e processados antes de serem conduzidos para a microscopia eletrônica. RESULTADOS: As alterações ultraestruturais dos cardiomiócitos foram quantificadas pelo número padrão de cristas mitocondriais (cristólises). Os grupos CON (3,85%), FLU (4,47%) e IHF (8,4%) mostraram aspecto normal de suas estruturas celulares com a citoarquitetura dos cardiomiócitos preservada com integridade sarcoplasmática contínua. Por outro lado, o grupo IH (34,4%) apresentou edema mitocondrial e lise nas cristas. CONCLUSÃO: A análise ultraestrutural revelou que a fluoxetina previne fortemente cristólises mitocondriais em miocárdio de ratos, sugerindo possível efeito protetor na condição de estresse induzido pelo frio.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo (UNIFESP)Faculdade de Medicina do ABCFaculdade de Medicina do ABC Departamento de Morfologia e FisiologiaUniversidade Federal de São Paulo (UNIFESP) Departamento de MedicinaUNIFESP, Depto. de MedicinaSciEL

Early repolarization variant: Epidemiological aspects, mechanism, and differential diagnosis

Early repolarization variant (ERV or ERPV) is a enigmatic electrocardiographic phenomenon, characterized by prominent J wave and ST-segment elevation in multiple leads. Recently, there has been renewed interest in ERV because of similarities to the arrhythmogenic Brugada syndrome (BrS). Not much is known about the epidemiology of ERV and several studies have reported that this condition is associated with a good prognosis. Both syndromes exhibit some similarities including the ionic underlying mechanism, the analogous responses to changes in heart rate and autonomic tone, sympathicomimetics (isoproterenol test) as well as in sodium channel and beta-blockers. These observations raise the hypothesis that ERV may be not as benign as traditionally believed. Additionally, there are documents showing that ST-segment height in the man is greatly influenced by central sympathetic nervous activity, both at baseline and during physiologic and pharmacological stress. Central sympathetic dysfunction regularly results in multilead ST-segment elevation or J wave that decreases or below isoelectric baseline during low dose isoproterenol infusion. In this review, we describe the characteristics of ERV and the main differences with acute pericarditis, acute myocardial infraction/injury and Brugada syndrome. (Cardiol J 2008; 15: 4-16

Memantine Prevents Cardiomyocytes Nuclear Size Reduction in the Left Ventricle of Rats Exposed to Cold Stress

OBJECTIVES: Memantine is an N-methyl-d-aspartate (NMDA) glutamate receptor antagonist used to treat Alzheimer's disease. Previous studies have suggested that receptor blockers act as neuroprotective agents; however, no study has specifically investigated the impact that these drugs have on the heart. We sought to evaluate the effects of memantine on nuclear size reduction in cardiac cells exposed to cold stress. METHOD: We used male EPM-Wistar rats (n=40) divided into 4 groups: 1) Matched control (CON); 2) Memantine-treated rats (MEM); 3) Rats undergoing induced hypothermia (IH) and 4) Rats undergoing induced hypothermia that were also treated with memantine (IHM). Animals in the MEM and IHM groups were treated by oral gavage administration of 20 mg/kg/day memantine over an eight-day period. Animals in the IH and IHM groups were submitted to 4 hours of hypothermia in a controlled environment with a temperature of - 8ºC on the last day of the study. RESULTS: The MEM group had the largest cardiomyocyte nuclear size (151 ± 3.5 &#956;m³ vs. CON: 142 ± 2.3 &#956;m³; p<0.05), while the IH group had the smallest mean value of nuclear size. The nuclear size of the IHM group was preserved (125 ± 2.9 &#956;m³) compared to the IH group (108 ± 1.7 &#956;m³; p<0.05). CONCLUSION: Memantine prevented the nuclear size reduction of cardiomyocytes in rats exposed to cold stress

The enigmatic sixth wave of the electrocardiogram: The U wave

The U wave is the last, inconstant, smallest, rounded and upward deflection of the electrocardiogram. Controversial in origin, it is sometimes seen following the T wave with the TU junction along the baseline or fused with it and before P of the following cycle on the TP segment. In this review we will study its temporal location related to monophasic action potential, cardiac cycle and heart sounds, polarity, voltage or amplitude, frequency and shapecontour. We will analyze the clinical significance of negative, alternant, prominent U wave, and the difference between T wave with two peaks (T1&#8211;T2) and true U wave. Finally we will analyze the four main hypotheses about the source of U wave: repolarization of the intraventricular conducting system or Purkinje fibers system, delayed repolarization of the papillary muscles, afterpotentials caused by mechanoelectrical hypothesis or mechanoelectrical feedback, and the prolonged repolarization in the cells of the mid-myocardium (&#8220;M-cells&#8221;)

Idiopathic intrafascicular reentrant left ventricular tachycardia in an elite cyclist athlete

A 32 year-old Caucasian male, an elite athlete, was admitted to the emergency department because of a sudden onset of palpitations which had lasted more than 12 hours and were associated with chest discomfort. He had a two-year history of recurrent stress-induced palpitations. He denied either episodes of syncope or any family history of sudden death. Physical examination was normal. He had no evidence of structural heart disease. The electrocardiography (ECG) documented during the event supported the diagnosis of idiopathic reentrant left ventricular tachycardia. Ventricular tachycardia ablation was successful. This case demonstrates that a careful physical examination and correct ECG diagnosis can lead to an appropriate arrhythmia management

Evaluación de la función barorrefleja en ratas jóvenes espontáneamente hipertensas

BACKGROUND: The literature describes contradictory data regarding the onset of the baroreflex reduction in spontaneously hypertensive rats. OBJECTIVE:This investigation was undertaken to evaluate the baroreflex function in 13-week-old spontaneously hypertensive rats. METHODS:Male Wistar Kyoto (n=15) and spontaneously hypertensive rats (n=15) aged 13 weeks were studied. Cannulas were inserted in the abdominal aortic artery through the right femoral artery to measure mean arterial pressure and heart rate. Baroreflex function was calculated as the derivative of the variation of HR in function of the MAP variation (Δheart rate/Δmean arterial pressure) tested with a depressor dose of sodium nitroprusside (50µg/kg) and with a pressor dose of phenylephrine (8µg/kg) in the right femoral venous approach through an inserted cannula in awake spontaneously hypertensive rats and Wistar-Kyoto. Differences with p values < 0.05 were considered statistically significant. RESULTS:Spontaneously hypertensive rats: Δmean arterial pressure=43.5mmHg±5.2, Δheart rate=-59.7ppm±17.9 and Δheart rate/Δmean arterial pressure=1.3ppm/mmHg±0.1 tested with phenylephrine; Wistar Kyoto: Δmean arterial pressure=&56mmHg±3, Δheart rate=*-114.9ppm±11.3 and Δheart rate/Δmean arterial pressure=#1.9ppm/mmHg±0.3 tested with phenylephrine; spontaneously hypertensive rats: Δmean arterial pressure=-45.6mmHg±8.1, Δheart rate=40.1ppm±11.6 and Δheart rate/Δmean arterial pressure=0.9ppm/mmHg±0.5 tested with sodium nitroprusside; Wistar Kyoto: Δmean arterial pressure=-39.8mmHg±6.2, Δheart rate=51.9ppm±21.8 and Δheart rate/Δmean arterial pressure=1.4ppm/mmHg±0.7 tested with sodium nitroprusside (*p<0.05; #p<0.01; &p<0.001). CONCLUSION: Our results showed that 13-week-old spontaneously hypertensive rats presented reduced baroreflex function when tested with phenylephrine.FUNDAMENTO: La literatura ha descrito datos contradictorios con relación al inicio de la disminución de la función barorrefleja en ratas espontáneamente hipertensas. OBJETIVO: Se realizó este estudio con el objetivo de evaluar la función barorrefleja en ratas jóvenes de 13 semanas, espontáneamente hipertensas. MÉTODOS: Se estudiaron ratas machos Wistar Kyoto (WKY) (n=15) y ratas espontáneamente hipertensas (REH) de 13 semanas de edad (n=15). Se insertaron cánulas en la arteria aorta abdominal -a través de la arteria femoral derecha- para medir la presión arterial media (PAM) y la frecuencia cardiaca (FC). Se calculó la función barorrefleja como la derivada de la variación de la FC en función de la variación de la PAM (ΔFC/ΔPAM). Dicho cálculo se efectuó tras prueba con una dosificación depresora de nitroprusiato de sodio (50µg/kg) y también con una dosificación para presión arterial de fenilefrina (8µg/kg) a través de una cánula insertada en la vena femoral derecha tanto de ratas espontáneamente hipertensas como de WKY. Se consideraron estadísticamente significantes diferencias con un valor de p < 0.05. RESULTADOS: Ratas espontáneamente hipertensas sometidas a prueba con fenilefrina: ΔPAM=43,5 mmHg±5,2, ΔFC=-59,7 ppm±17,9 y ΔFC/ΔPAM=1,3 ppm/mmHg±0,1; Wistar Kyoto probadas con fenilefrina: ΔPAM=&56mmHg±3, ΔFC=*-114,9ppm±11,3 y ΔFC /ΔPAM =#1,9ppm/mmHg±0,3. Ratas espontáneamente hipertensas probadas con nitroprusiato de sodio: ΔPAM=-45,6mmHg±8,1, ΔFC=40,1ppm±11,6 y ΔFC/ΔPAM=0,9ppm/mmHg±0,5; Wistar Kyoto sometidas a prueba con nitroprusiato de sodio: ΔPAM =-39,8mmHg±6,2, ΔFC=51,9ppm±21,8 y ΔFC /ΔPAM =1,4ppm/mmHg±0,7 (*p<0,05; #p<0,01; &p<0,001). CONCLUSIÓN: Nuestros resultados muestran que ratas espontáneamente hipertensas de 13 semanas de edad presentaron reducción de la función barorrefleja cuando probadas con fenilefrina.FUNDAMENTO: A literatura tem descrito dados contraditórios em relação ao início da diminuição da função barorreflexa em ratos espontaneamente hipertensos. OBJETIVO:Este estudo foi realizado para avaliar a função barorreflexa em ratos jovens de 13 semanas espontaneamente hipertensos. MÉTODOS:Foram estudados ratos machos Wistar Kyoto (WKY) (n=15) e ratos espontaneamente hipertensos (REH) de 13 semanas (n=15). Cânulas foram inseridas na artéria aorta abdominal através da artéria femoral direita para medir a pressão arterial média (PAM) e a freqüência cardíaca (FC). A função barorreflexa foi calculada como a derivada da variação da FC em função da variação da PAM (ΔFC/ΔPAM), quando submetida a teste com uma dose depressora de nitroprussiato de sódio (50µg/kg) e com uma dose pressora de fenilefrina (8µg/kg) através de cânula inserida na veia femoral direita em ratos espontaneamente hipertensos e WKY. Diferenças com um valor de p < 0.05 foram consideradas estatisticamente significantes. RESULTADOS:Ratos espontaneamente hipertensos: ΔPAM=43,5 mmHg±5,2, ΔFC=-59,7 ppm±17,9 e ΔFC/ΔPAM=1,3 ppm/mmHg±0,1 testados com fenilefrina; Wistar Kyoto: ΔPAM=&56mmHg±3, ΔFC=*-114,9ppm±11,3 e ΔFC /ΔPAM =#1,9ppm/mmHg±0,3 testados com fenilefrina; ratos espontaneamente hipertensos: ΔPAM=-45,6mmHg±8,1, ΔFC=40,1ppm±11,6 e ΔFC/ΔPAM=0,9ppm/mmHg±0,5 testados com nitroprussiato de sódio; Wistar Kyoto: ΔPAM=-39,8mmHg±6,2, ΔFC=51,9ppm±21,8 e ΔFC/ΔPAM=1,4ppm/mmHg±0,7 testados com nitroprussiato de sódio (*p<0,05; #p<0,01; &p<0,001). CONCLUSÃO: Nossos resultados mostram que ratos espontaneamente hipertensos de 13 semanas apresentaram redução da função barorreflexa quando testados com fenilefrina.Universidade Federal de São Paulo (UNIFESP)Faculdade de Medicina do ABCUNIFESPSciEL

Relationship among amiodarone, new class III antiarrhythmics, miscellaneous agents and acquired long QT syndrome

Class III drugs prolong the QT interval by blocking mainly the delayed rectifier rapid potassium outward current (IKr), with little effect on depolarization. This K+ channel in encoded by the human ether-a-go-go-related gene (hERG). Inhibition of hERG potassium currents by class III antiarrhythmic drugs causes lengthening of cardiac action potential, which produces a beneficial antiarrhythmic effect. Excessive prolongation of the action potential may lead to acquired long QT syndrome, which is associated with a risk of &#8220;torsade de pointes&#8221;. Class III agents can block all types of potassium channels: IKs, IKr, IKur and IK1. The main representing class III agent is amiodarone. It is the gold standard in the prevention of recurrence of atrial fibrillation. Although it is highly effective in treating many arrhythmias, large number of adverse effects limits its clinical use. Dronedarone is a synthetic amiodarone analogue, iodinefree compound, with fewer adverse effects, and shares amiodarone&#8217;s multichannel blocking effects, inhibiting transmembrane Na+, IKs, IKur, IK1, and slow Ca++L-type calcium currents. The main new generation class III drugs are: dofetilide, dronedarone, azimilide, and ibutilide. Oral dofetilide did not increase mortality in patients with a recent myocardial infarction or congestive heart failure. It is an alternative for the pharmacological conversion of atrial fibrillation and flutter. Azimilide blocks both rapid and slow potassium channels components. Azimilide is not a methanesulfonanilide compound. Trecitilide, tedisamil, ersentilide, ambasilide, chromanol and sematilide are class III miscellaneous agents. Old mixed agents are sotalol and bretylium. The present article reviews the main trials accomplished with these drugs. (Cardiol J. 2008; 14: 209&#8211;219