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Made available in DSpace on 2018-03-22T15:51:26Z (GMT). No. of bitstreams: 1 tese_11640_RAPHAEL AMORIM LORENZONI .pdf: 3870633 bytes, checksum: 2160a28463d4da3c8a66dc6eaa497c3c (MD5) Previous issue date: 2017-12-21 A termoeconomia agrega conceitos de economia e termodinâmica para descrever o processo de formação de custos em sistemas térmicos. Possui uma grande aplicabilidade em problemas de alocação de custos, otimização e diagnóstico visando reduzir custos operacionais e provar a viabilidade econômica do sistema. O diagnóstico termoeconômico é aplicado para identificar a fonte do consumo adicional de recursos em caso de falhas ou desvios das condições de projeto e seus respectivos impactos em cada componente do sistema a fim de gerar uma ordem de prioridade de manutenção nas paradas programadas. Neste trabalho, diferentes metodologias termoeconômicas (E, E&S, H&S, UFS e UFS+) são aplicadas no diagnóstico termoeconômico em diferentes sistemas térmicos utilizando a equação do impacto no combustível e visando avaliar o aumento de precisão e qualidade dos resultados por meio do isolamento dos componentes dissipativos na estrutura produtiva e desagregação da exergia física. Os sistemas analisados foram escolhidos em função de seus equipamentos dissipativos: um ciclo Rankine (condensador), uma bomba de calor (válvula) e um sistema de refrigeração (válvula e condensador). Os modelos E e E&S mostraram-se inadequados em todos os casos por não permitirem o isolamento dos equipamentos na estrutura produtiva, sendo que o último também apresenta inconsistências termodinâmicas. Os modelos H&S e UFS apresentaram bons resultados para o ciclo Rankine quantificando as falhas em todos os componentes. Os modelos UFS e UFS+ foram os únicos que permitiram total isolamento dos componentes na bomba de calor e no sistema de refrigeração, entretanto, a influência das unidades fictícias no diagnóstico não permitiu uma análise exata dos impactos das anomalias. Palavras-chave Termoeconomia, Diagnóstico, Equipamentos Dissipativos, Desagregação de Exergia.

Made available in DSpace on 2016-08-29T15:36:28Z (GMT). No. of bitstreams: 1 tese_9007_Rodrigo Monte Lorenzoni.pdf: 954098 bytes, checksum: 5aea780df5fa2ff2c51790957419c8fd (MD5) Previous issue date: 2016-02-18 O biribá (Annona mucosa) é uma espécie que tem como centro de origem a Floresta Amazônica, seu fruto possui grande aceitação para consumo in natura, além de ser uma fonte promissora de compostos bioativos com propriedades farmacológicas. Entretanto, apesar da importância, pouco se sabe sobre a variabilidade e diversidade genética desta espécie. O conhecimento da variabilidade genética de espécies pouco explorado possibilita a utilização das mesmas em programas de melhoramento genético e/ou de conservação, sendo os microssatélites (SSR) uma ferramenta interessante para esse tipo de estudo, contudo para realizar estudos com essa classe de marcadores é necessário o conhecimento da ploidia da espécie. Porém, dados referentes ao conteúdo de DNA nuclear e número cromossômico, ainda não foram descritos para a espécie. Portanto, objetivou-se mensurar o valor 2C nuclear, determinar o número cromossômico, avaliar a transposição de marcadores microssatélites desenvolvidos para Phaseolus vulgaris e Coffea sp. e estimar a diversidade genética entre acessos de A. mucosa. O conteúdo de DNA nuclear foi estimado por meio da citometria de fluxo onde foi verificado que a espécie apresenta valor 2C= 5,42 pg e que não existe variação intraespecífica. A técnica de citogenética clássica gerou metáfases onde foi possível determinar que a espécie possui 42 cromossomos e, portanto, é uma espécie hexaploide. Com base na ploidia encontrada foi possível avaliar a transferibilidade dos marcadores, onde foram transferidos e validados 42,25% dos primers. A partir dos 157 fragmentos gerados com 82% de polimorfismo foi possível estimar a diversidade genética entre os acessos estudados, onde os indivíduos foram separados em três grupos distintos pelo método UPGMA e em dois grupos pela análise bayesiana. Com este estudo foi possível verificar que após o conhecimento da ploidia, onde 2n= 6x= 42 cromossomos, os marcadores puderam ser avaliados e mostraram-se eficientes para amplificação heteróloga de amostras de DNA de A. mucosa e os primers que apresentaram polimorfismo poderão ser utilizados em estudos moleculares desta espécie, sem o gasto de recursos financeiros e tempo no desenvolvimento de novos marcadores.

Acute myocardial infarction can produce alterations in the topography of the left ventricle both in the infarcted and remote areas. These changes as a whole, have been termed ventricular remodelling. Attention has been focused on myocyte alterations due to the remodelling process, but the myocardial wall also contains fibroblasts, which produce collagen and elastin fibers, and endothelial and smooth muscle cells which are the main constituents of the vascular wall. In left ventricular hypertrophy, a form of myocardial remodelling, structural changes of myocytes, cardiac interstitium as well as the coronary microcirculation have been found (vascular remodelling). In vivo, the function of coronary microcirculation can be evaluated by measuring myocardial blood flow and coronary reserve. In fact the study of coronary reserve in patients with left ventricular hypertrophy disclosed microcirculatory dysfunction which probably represents the functional counterpart of the structural changes already described. Positron emission tomography (PET) can noninvasively quantitate myocardial blood flow and coronary reserve in humans. Recently studies with PET disclosed microcirculatory alterations also in patients with coronary artery disease (CAD) in the absence of gross myocardial hypertrophy. In particular, after myocardial infarction, coronary vasodilator capacity has been shown to be impaired not only in the infarcted areas but also in the remote ones subtended by angiographically normal vessels. A blunted coronary reserve has been identified with PET also in remote regions from ischemia in patients with stable angina and single vessel CAD.

A sizeable proportion (20-30%) of patients undergoing coronary arteriography for a chest pain syndrome are found to have angiographically normal coronary arteries. Some of these subjects (10-15%) have ischemic-like electrocardiographic changes during stress and no evidence of spasm of the epicardial coronary arteries (syndrome X). The vast majority of these patients are middle aged females. In the present investigation we evaluated the psychological and social characteristics of a group of patients with syndrome X (PX, n = 30). The results obtained in the PX group were compared with those in a sex and age matched group of patients with angiographically proven coronary artery disease (PI, n = 32) and with those in a group of control subjects (C, n = 29). Two original questionnaires were employed to collect the demographic and family data. The psychological data were obtained through the following 4 questionnaires: Symptom Rating Test (SRT); Symptom Questionnaire (SQ); Illness Behaviour Questionnaire (IBQ); Maudsley Personality Inventory (MPI). The results of our study indicated that in most of the patients with syndrome X the psychological and social conditions are similar and they are not compatible with a satisfactory lifestyle. In most cases both family and social difficulties are present, which impose excessive workload and distress on the patients. Very often the beginning of the chest pain history tends to coincide with the periods of greatest stress and with the occurrence of dramatic events in the family. On the other hand, the onset of symptoms often has the effect of releasing some of the environmental pressure on the patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects. At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p < 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS). At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p < 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during pacing and recovery, whereas normal subjects produced alanine throughout the study. Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p < 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p < 0.01). The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.

To assess regional coronary reserve in hypertrophic cardiomyopathy, regional myocardial blood flow was measured in 23 patients with hypertrophic cardiomyopathy and 12 control subjects by means of nitrogen-13 ammonia and dynamic positron emission tomography. In patients with hypertrophic cardiomyopathy at baseline study, regional myocardial blood flow was 1.14 +/- 0.43 ml/min per g in the hypertrophied (20 +/- 3 mm) interventricular septum and 0.90 +/- 0.35 ml/min per g (p < 0.05 versus septal flow) in the nonhypertrophied (10 +/- 2 mm) left ventricular free wall. These were not statistically different from the corresponding values in control subjects (1.04 +/- 0.25 and 0.91 +/- 0.21 ml/min per g, respectively, p = NS). After pharmacologically induced coronary vasodilation (dipyridamole, 0.56 mg/kg intravenously over 4 min), regional myocardial blood flow in patients with hypertrophic cardiomyopathy increased significantly less than in control subjects both in the septum (1.63 +/- 0.58 versus 2.99 +/- 1.06 ml/min per g, p < 0.001) and in the free wall (1.47 +/- 0.58 versus 2.44 +/- 0.82 ml/min per g, p < 0.001). In addition, patients with hypertrophic cardiomyopathy who had a history of chest pain had more pronounced impairment of coronary vasodilator reserve than did those without a history of chest pain. After dipyridamole, coronary resistance in the septum decreased by 38% in patients without a history of chest pain, but decreased by only 14% in those with such a history (p < 0.05). Coronary resistance in the free wall decreased by 45% in patients without and by 27% in those with a history of chest pain (p = 0.06). These results show that, in patients with hypertrophic cardiomyopathy, coronary vasodilator reserve is abnormal not only in the hypertrophied interventricular septum, but also in the nonhypertrophied free wall of the left ventricle. This finding suggests that the reduction in coronary reserve is not necessarily due to myocardial hypertrophy, but may be a primary defect.

The human heart in the fasting state extracts free fatty acids (FFA), glucose, lactate, pyruvate, and ketones from circulating blood. The utilization of FFA accounts for most of the oxygen consumed and energy produced at rest. Patients with angiographically demonstrable coronary artery disease and stable angina pectoris have a resting myocardial metabolism similar to that of normal individuals. During atrial pacing in normal persons, there is a significant enhancement of glucose uptake but that of FFA is unchanged, and the oxidation of carbohydrates accounts for more than 60% of the energy produced. In patients with stable angina, myocardial perfusion becomes regionally inadequate during stress. Despite the increase of myocardial glucose utilization, carbohydrate oxidation is negligible. Pyruvate will not be oxidized but in the presence of increased amounts of reduced coenzymes will be reduced to lactate. In addition, a greater amount of alanine will be released by the myocardium through the transamination of pyruvate, with a concomitantly greater uptake of glutamate that serves as the NH2 donor. In addition, glutamate may be used as an anaerobic fuel through conversion to succinate coupled with GTP formation. Although coronary hemodynamics, including myocardial perfusion, return to baseline within a few minutes after stress, a longer time course is needed for myocardial metabolism to become normal. In particular, myocardial utilization of exogenous glucose remains higher well after the normalization of hemodynamic parameters. This is more pronounced in postischemic myocardium, but it also occurs in nonischemic muscle, and glucose is presumably used for rebuilding glycogen stores that were depleted during ischemia.

Background: Microvascular dysfunction, reflected by an inadequate increase in myocardial blood flow in response to dipyridamole infusion, is a recognized feature of hypertrophic cardiomyopathy. Its long-term effect on the prognosis is unknown. We prospectively evaluated a cohort of patients with hypertrophic cardiomyopathy after they had undergone quantitative assessment of myocardial blood flow by positron-emission tomography (PET). Methods: Fifty-one patients (New York Heart Association class I or II) were followed for a mean (+/-SD) of 8.1+/-2.1 years after PET. Twelve subjects with atypical chest pain served as controls. Measurement of flow was performed at base line and after the infusion of the coronary vasodilator dipyridamole, with the use of nitrogen-13-labeled ammonia. Patients were then divided into three equal groups with increasing values of myocardial blood flow. Results: The response of myocardial blood flow to dipyridamole was severely blunted in the patients, as compared with the controls (1.50+/-0.69 vs. 2.71+/-0.94 ml per minute per gram of tissue, P

We sought to test the response of the coronary microcirculation to alpha-adrenoceptor blockade in patients with syndrome X (angina, ischemia-like stress electrocardiogram, and a normal coronary arteriogram). The response of the microcirculation was assessed by quantification of coronary vasodilator reserve (the ratio of hyperemic to resting myocardial blood flow). We investigated 28 patients with syndrome X [18 women, age 54.4 (7.6) years]. Myocardial blood flow was measured at rest and after dipyridamole by using positron emission tomography with H(2)15O. The measurements were made before and after treatment for 10 days with doxazosin (1 mg o.d. for 3 days, followed by 2 mg o.d. for 7 days) or a matched placebo, similarly administered. Patients were randomized to alpha1-blockade or to placebo in double-blind fashion. No significant differences were demonstrable between syndrome X patients treated with doxazosin and those receiving placebo, with respect to resting myocardial blood flow, myocardial blood flow after dipyridamole, or coronary vasodilator reserve (the ratio of the latter two). In addition, no relations were demonstrable among myocardial blood flow, coronary vasodilator reserve, development of chest pain after dipyridamole, or development of ischemia-like ECG changes. Doxazosin had no effect on the perception of chest pain after dipyridamole. No differences were found between the effects of alpha1-blockade with doxazosin or those of placebo with respect to myocardial blood flow in syndrome X. The values obtained for myocardial blood flow and coronary vasodilator reserve for the patients were within the normal range. The data do not support the case for alpha1-mediated vasoconstriction having an etiologic role in the chest pain of syndrome X.

Non-sustained ventricular tachycardia on Holter and syncope have been considered risk factors for sudden death in hypertrophic cardiomyopathy. Aims In these patients the coronary vasodilator reserve is impaired despite normal coronaries, so we evaluated the correlation between the severity of coronary vasodilator reserve impairment and the occurrence of syncope and non-sustained ventricular tachycardia. Methods and Results Eighty-four patients with hypertrophic cardiomyopathy (62 males, age 43 +/- 12 years) had a two-dimensional echocardiographic study and a 48-h Holter. Myocardial blood flow was measured by positron emission tomography, at baseline and after dipyridamole, and the coronary vasodilator reserve was computed as dipyridamole myocardial blood flow/baseline myocardial blood flow. In 27 patients, subendocardial and subepicardial myocardial blood flow was measured in the septum and the subendocardial/subepicardial ratio was computed. Twenty of 84 patients had at least one syncopal episode, and 26 had at least one run of non-sustained ventricular tachycardia on Holter. Baseline and dipyridamole myocardial blood flow, coronary vasodilator reserve, and baseline and dipyridamole subendocardial/subepicardial myocardial blood flow ratio were similar in patients with and without syncope and with and without non-sustained ventricular tachycardia on Holter. However, patients with nonsustained- ventricular tachycardia had larger left ventricular end-diastolic (47+/-6 vs 44+/-5 mm, P