Resistência à compressão de prismas de blocos de concreto grauteados e não grauteados

Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro Tecnológico.O trabalho teve como objetivo principal estudar as propriedades mecânicas e o modo de ruptura de prismas de blocos de concreto grauteados e não grauteados submetidos à compressão axial. Foram moldados 60 tipos de prismas, com três blocos de diferentes resistências à compressão, dois tipos de argamassas (1:1:6) e (1:0,5:4,5), quatro grautes com diferentes resistências à compressão e dois tipos de assentamento, assentamento total e lateral. Foram realizados vários ensaios nos componentes dos prismas. Dos blocos foram determinadas as dimensões, resistências à compressão, resistências à tração, absorção e o módulo de elasticidade. Nas argamassas e grautes foram determinadas as resistências à compressão, módulo de elasticidade e coeficiente de Poisson. As deformações dos prismas foram monitoradas através de "demec gauges" durante o ensaio de compressão. Posteriormente, foi feita uma análise estatística para a avaliação da influência da resistência à compressão do bloco, argamassa, graute e tipo de assentamento na resistência do prisma. Também foram feitas comparações entre as resistências especificadas pela BS 5628: Part 1 (1992) e os resultados obtidos neste estudo. Os principais resultados foram: Para prismas não grauteados o aumento na resistência do bloco, aumenta a resistência à compressão do prisma, embora de forma não diretamente proporcional. O mesmo não ocorre para prismas grauteados, que a partir de um determinado nível de resistência do bloco, a medida em que se aumenta a resistência do graute, quando se utiliza argamassa de baixa resistência, não se obtém aumento de resistência nos prismas. Não há ganho de resistência na alvenaria usando-se graute com resistência acima da resistência do bloco na área líquida A melhor eficiência da alvenaria foi obtida com grautes e blocos de resistências aproximadamente iguais. Para os diferentes tipos de assentamento utilizados, pode-se concluir que, no caso de assentamento de argamassa apenas nas laterais (AL) com graute, o uso de blocos mais resistentes contribui para o aumento da resistência do prisma de forma mais significativa do que no caso em que o assentamento de argamassa seja feito em todas as faces do bloco (AT). Em relação à resistência à compressão da argamassa de assentamento, de uma maneira geral, pode-se afirmar que, para prismas grauteados, a influência da resistência da argamassa na resistência dos prismas é menos importante do que para os prismas não grauteados

Prevention of experimental carotid and coronary artery thrombosis by the glycoprotein IIb/IIIa receptor antagonist CRL42796

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72568/1/sj.bjp.0704744.pd

Effect of OKY-1581, a thromboxane synthetase inhibitor, on coronary thrombosis in the conscious dog

OKY-1581, a new thromboxane synthetase inhibitor, was studied in a conscious canine model of coronary thrombosis. After thoracotomy with placement of a left circumflex coronary artery flow probe and implantation of an electrode into the circumflex artery, animals were assigned randomly to the following groups: 0.9% NaCl vehicle control or OKY-1581 1 mg/kg every 4 h intravenously for 24 h. During the drug treatment period, a 50 [mu]A anodal current was passed through the circumflex electrode, and venous blood was obtained for platelet aggregation studies. As compared to control animals, the OKY-1581 treated animals developed a greater mean coronary flow at the end of the treatment period, smaller thrombi by wet weight, smaller infarcts, and fewer ventricular arrhythmias. Ex vivo platelet aggregation studies revealed significant inhibition of aggregation to standard aggregating agents for the drug treated group only. OKY-1581 is an effective antitbrombotic agent which maintains coronary flow after a thrombogenic stimulus, presumably via blockade of the synthesis of thromboxane by blood platelets.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24663/1/0000076.pd

The effect of diltiazem on coronary thrombosis in the conscious canine

The effect of diltiazem vs. saline was studied in a conscious canine model of coronary thrombosis. Diltiazem given as a 0.75 mg/kg loading dose intravenously followed by 0.4 mg/kg intravenously every 4 h for 24 h had no significant effect on thrombus wet weight, left ventricular infarct size, frequency of ventricular arrhythmias or ex vivo platelet aggregation. The search for antithrombotic agents using in vitro or ex vivo platelet aggregation studies should include concomitant in vivo thrombosis studies using therapeutic dosages of the drug in question.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24078/1/0000331.pd

Ibuprofen-mediated infarct size reduction: Effects on regional myocardial function in canine myocardial infarction

Normal, marginal, and central ischemic regional myocardial function were evaluated in a canine model of myocardial infarction during 90 minute left circumflex coronary artery occlusion in 25 anesthetized dogs randomly assigned to intravenous ibuprofen infusion (n = 13, 5.36 mg/kg/h beginning 1 hour before occlusion) or vehicle solution as control (n = 12) and in 15 conscious, unsedated dogs 48 and 72 hours after 90 minute circumflex artery occlusion followed by reperfusion (ibuprofen, 5.36 mg/kg/h by intravenous infusion over 7 hours beginning 1 hour before occlusion, n = 7; or vehicle solution infusion as control, n = 8).Miniature subendocardial sonomicrometer crystal pairs were used to calculate left ventricular regional end-diastolic segment length, end-systolic segment length, and regional percent systolic shortening. Infarct size was estimated in 72 hour animals by a postmortem dual perfusion technique using triphenyltetrazolium histochemical dye and Evan's blue dye for determination of infarct area, risk area, and area not at risk. Ibuprofen treatment significantly reduced infarct size expressed as percent of risk area (mean +/- standard deviation of 44.6 +/- 18 versus 64.4 +/- 16% for control dogs, p Thus, ibuprofen does not improve normal, marginal, or ischemic zone regional myocardial function during acute ischemia or 48 or 72 hours after myocardial reperfusion despite a significant reduction of infarct size.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/23860/1/0000099.pd

The Inflammatory Response and Cardiac Repair After Myocardial Infarction

One of the most important therapeutic targets of current cardiology practice is to determine optimal strategies for the minimization of myocardial necrosis and optimization of cardiac repair following an acute myocardial infarction. Myocardial necrosis after acute myocardial infarction induces complement activation and free radical generation, triggering a cytokine cascade initiated by tumor necrosis factor-alpha (TNF-α) release. When reperfusion of the infarcted area is initiated, intense inflammation follows. Chemokines, cytokines and the complement system play an important role in recruiting neutrophils in the ischemic and reperfused myocardium. Cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. The recruited neutrophils have potent cytotoxic effects through the release of proteolytic enzymes, and they interact with adhesion molecules on cardiomyocytes. In spite of the potential injury, reperfusion enhances cardiac repair; this may be related to the inflammatory response. Monocyte chemoattractant protein (MCP)-1 is upregulated in reperfused myocardium and can induce monocyte recruitment in the infarcted area. Monocyte subsets play a role in phagocytosis of dead cardiomyocytes and in granulation tissue formation. In addition, the transforming growth factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation. Resolution of inflammatory infiltration, containment of inflammation and the reparative response affecting the infarcted area are essential for optimal infarct healing. Here, we review the current literature on the inflammatory response and cardiac repair after myocardial infarction

Ibuprofen improves survival and neurologic outcome after resuscitation from cardiac arrest

Post-ischemic inflammatory changes in the central nervous system (CNS) following cardiac arrest and resuscitation are potentially responsible for ultimate survival and much of the neurologic damage, producing greater morbidity and mortality in successfully resuscitated patients. This study was undertaken to assess the non-steroidal anti-inflammatory agent, ibuprofen, in a controlled and monitored experimental model of canine cardiac arrest and resuscitation. With the investigator blinded as to the intervention, eight of 21 dogs were randomly assigned to receive ibuprofen as an i.v. bolus (10 mg/kg) and a 6-h i.v. infusion (5 mg/kg per h). The other 13 dogs received an equivalent volume of 0.9% NaCl to serve as controls. No statistically significant differences between the two groups were detected in any pre-arrest variables. All 21 dogs were successfully resuscitated. At 24 h, dogs receiving ibuprofen exhibited 100% survival, while control dogs exhibited only 54% survival (P = 0.03). The majority of deaths for the control group occurred within the first 6 h. Neurologic deficit scores were assigned at 1, 2, 6 and 24 h after resuscitation. A general trend occurred such that dogs treated with ibuprofen improved over time, while the control dogs remained severely impaired. A significant difference in neurologic deficit score was detected at 6 h (P = 0.01). At 24 h the ibuprofen group exhibited minimal neurologic deficit (5.9 +/- 3.2), and the control group exhibited significantly more severe neurologic impairment (52.2 +/- 13.0, P = 0.01). These results suggest that ibuprofen may be helpful in the pharmacologic management of cardiac arrest as a means of increasing survival and decreasing neurologic impairment.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25949/1/0000015.pd

Enterocyte Shedding and Epithelial Lining Repair Following Ischemia of the Human Small Intestine Attenuate Inflammation

BACKGROUND: Recently, we observed that small-intestinal ischemia and reperfusion was found to entail a rapid loss of apoptotic and necrotic cells. This study was conducted to investigate whether the observed shedding of ischemically damaged epithelial cells affects IR induced inflammation in the human small gut. METHODS AND FINDINGS: Using a newly developed IR model of the human small intestine, the inflammatory response was studied on cellular, protein and mRNA level. Thirty patients were consecutively included. Part of the jejunum was subjected to 30 minutes of ischemia and variable reperfusion periods (mean reperfusion time 120 (+/-11) minutes). Ethical approval and informed consent were obtained. Increased plasma intestinal fatty acid binding protein (I-FABP) levels indicated loss in epithelial cell integrity in response to ischemia and reperfusion (p<0.001 vs healthy). HIF-1alpha gene expression doubled (p = 0.02) and C3 gene expression increased 4-fold (p = 0.01) over the course of IR. Gut barrier failure, assessed as LPS concentration in small bowel venous effluent blood, was not observed (p = 0.18). Additionally, mRNA expression of HO-1, IL-6, IL-8 did not alter. No increased expression of endothelial adhesion molecules, TNFalpha release, increased numbers of inflammatory cells (p = 0.71) or complement activation, assessed as activated C3 (p = 0.14), were detected in the reperfused tissue. CONCLUSIONS: In the human small intestine, thirty minutes of ischemia followed by up to 4 hours of reperfusion, does not seem to lead to an explicit inflammatory response. This may be explained by a unique mechanism of shedding of damaged enterocytes, reported for the first time by our group

Myocardial ischemia and reperfusion: The role of oxygen radicals in tissue injury

Thrombolytic therapy has gained widespread acceplance as a means of treating coronary artery thrombosis in patients with acute myocardial infarction. Although experimental data have demonstrated that timely reperfusion limits the extent of infarction caused by regional ischemia, there is growing evidence that reperfusion is associated with an inflammatory response to ischemia that exacerbates the tissue injury. Ischemic myocardium releases archidonate and complement-derived chemotactic factors, e.g., leukotriene B 4 and C 5a , which attract and activate neutrophils. Reperfusion of ischemic myocardium accelerates the influx of neutrophils, which release reactive oxygen products, such as superoxide anion and hydrogen peroxide, resulting in the formation of a hydroxyl radical and hypochlorous acid. The latter two species may damage viable endothelial cells and myocytes via the peroxidation of lipids and oxidation of protein sulfhydryl groups, leading to perturbations of membrane permeability and enzyme function. Neutrophil depletion by antiserum and inhibition of neutrophil function by drugs, e.g., ibuprofen, prostaglandins (prostacyclin and PGE 1 ), or a monoclonal antibody, to the adherence-promoting glycoprotein Mo-1 receptor, have been shown to limit the extent of canine myocardial injury due to coronary artery occlusion/reperfusion. Recent studies have challenged the hypothesis that xanthine-oxidase-derived oxygen radicals are a cause of reperfusion injury. Treatment with allopurinol or oxypurinol may exert beneficial effects on ischemic myocardium that are unrelated to the inhibition of xanthine oxidase. Furthermore, the human heart may lack xanthine oxidase activity. Further basic research is needed, therefore, to clarify the importance of xanthine oxidase in the pathophysiology of reperfusion injury. Current data are highly suggestive of a deleterious role of the neutrophil in organ reperfusion and justify consideration of the clinical investigation of neutrophil inhibitors in patients receiving thrombolytic agents during the evolution of an acute myocardial infarction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44595/1/10557_2004_Article_BF00133206.pd