No description available.

Thesis (M.S. Ed.)--Virginia Polytechnic Institute and State University, 1994. / Vita. Abstract. Includes bibliographical references (leaves 69-71). Also available via the Internet.

There is epidemiological and experimental evidence suggesting that exercise training may reduce the mortality rate from coronary heart disease, in particular the sudden death rate, and that it may improve the peak functional capacity of the heart. This thesis includes experimental work that is relevant to both these questions.

No description available.

No description available.

The Cardiac Profile, a pattern of serum enzyme changes seen within seventy-two hours after an AMI, is diagnostic aid for detecting occurrence of infarcts. The effects of exercise stress on the Cardiac Profile aid clinicians in avoiding diagnostic errors in patients immediately after exercise. Five male volunteers ran from six to ten miles. Serum enzyme levels were monitored serially three days before and five days after stress. Enzyme activity was determined spectrophotometrically and electrophoretically. Significant increases in total CPK and LDH were seen. An LDH 'one-two flip' occurred eight hours after exercise. No MB-CPK was found following the run.

Wang Mei. / "July 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 208-233). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

This thesis describes the development of MRI techniques for identifying disease within cardiac muscle of the rodent heart at 4.7 T. The new methods allow measurement of myocardial T1 and T2* relaxation times and ventricular volumes from cine images. Before in-vivo application, each MRI pulse sequence and imaging protocol was tested using tissue representative phantoms on a cardiac motion simulator. A multi-slice cardiac cine pulse sequence was developed for measuring cardiac volumes that used a modified slice acquisition order compared to standard cine MRI to extend TR and thereby increase the signal without extending the total scan time. This acquisition method was compared to a slower conventional cine pulse sequence by measuring the signal to noise ratio and the left ventricular mass and volumes of the mouse heart. T1 values are known to increase in hearts affected by dilated and hypertrophic cardiomyopathy, so pulse sequences were developed for measuring myocardial relaxation values. In-vivo T1 measurements were made using saturation and inversion recovery pulse sequences. Comparison of the results showed that the inversion recovery pulse sequence gave results that were more consistent with published values from similar studies so it was concluded that this should be used for future cardiomyopathy investigations. A study was carried out on an in-vivo control group to test the effectiveness of the superparamagnetic contrast agent Ferumoxytol in enhancing T2* differences between healthy and pathological tissues. It was found that Ferumoxytol did not affect the T2* of the healthy myocardium and this result was confirmed by histology which revealed very little Ferumoxytol uptake in the heart but plentiful uptake in the liver. The results of this study indicate that future investigations in rats with induced cardiomyopathy can assume that changes in myocardial relaxation times are due to the effects of cardiac disease rather than the contrast agent.

This study sought to examine the exercise-induced ST-segment shifts, J₀ and J₆₀, attributable to ECG lead configuration, specifically to evaluate if ischemic changes are modified as a function of using the Mason-Likar lead system. Males (N=30) referred for diagnostic testing underwent a symptom-limited graded exercise test (SLGXT). ST-segment shifts, J₀ and J₆₀, measured as the difference from baseline to recovery minute one, were not significantly different in responses measured from two simultaneous complexes for lead V₅. In frontal lead II, differences were found in the ST-segment response at baseline vs. recovery minute one. All ST-segment shifts were computed as the difference between J_x obtained at resting baseline vs. the J_x obtained at the exercise measurement in the same posture. ST-segment shifts, J₀ and J₆₀, measured at peak-exercise vs. recovery minute one using the Mason-Likar lead system, revealed a significant difference according to the measurement recorded in both leads V₅ and II (p<.05). Comparisons of frequencies for clinically abnormal ST-segment shifts according to ECG lead configuration at recovery minute one when measured from peak-exercise using Mason-Likar were significant in only lead II (p<.05). Observation of the data suggest that the Mason-Likar lead system may affect the interpretation of ischemic ST-segment shifts in lead II. However, these results do not invalidate the interpretation of ischemic ST-segment shifts in lead V₅ using the Mason-Likar lead system. / Master of Science

Acute myocardial infarction occurs when there is reduced blood supply to the myocardium promoting decrease of oxygen uptake (O2). It is a major cause of morbidity and mortality worldwide. Tissue injury occurs, for the most part, paradoxically, during reperfusion of the organ. In reoxygenation, there are exacerbated production of reactive oxygen species (ROS) and intracellular calcium overload, which trigger cell death. There are few pharmacological intervention strategies for the prevention and limitation of these lesions. And besides, the available forms of action are not entirely effective. Recently, it has directed attention to the effects of natural products in limiting the damage caused by ischemia and reperfusion (I/R). In this context, thymol, a phenolic monoterpene, has, among its biological activities, anti-inflammatory and antioxidant. In this sense, the objective of the study was to evaluate the potential cardioprotective effect of thymol in preventing reperfusion injury after ischemia in rats. First it performed the test clearance of radical DPPH by thymol. To study its potential cardioprotective, rats Wistar rats (200-300 g) pretreated with thymol (7.5 mg/kg, v.o.) or vehicle for 7 days and subjected to global ischemia of the heart in the Langendorff system. We evaluated parameters of cardiac function as left ventricle developed pressure (LVDP), maximum time derivative (+ dP/dt) and minimum (-dp/dt) and arrhythmia severity index (ASI), size of the infarcted area, and enzymatic activity assays catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and reductase (GR), tissue sulfhydryl quantification. Moreover, the concentration of thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides evaluated too. The DPPH assay showed antioxidant property of thymol. Furthermore, it was observed that pretreatment with thymol preserved LVDP, ASI decreased, reduced infarct area, the TBARS and, similarly, was observed lower concentration of hydroperoxides as compared to vehicle. Pretreatment with thymol prevented to reduce the concentration of sulfhydryl groups when compared to vehicle. The activities of SOD, CAT, GPx and GR were reduced significantly in the hearts of animals pretreated with thymol when compared to vehicle. Pretreatment with thymol preserved contractile heart function, reduced damage to cellular components and limited the infarct area. Demonstrating significant cardioprotective effects against I/R. / O infarto agudo do miocárdio ocorre quando há diminuição do suprimento sanguíneo no miocárdio promovendo queda do aporte de Oxigênio (O2). É uma das principais causas de morbidade e mortalidade em todo o mundo. A lesão tecidual ocorre, em sua maior parte, paradoxalmente, durante a reperfusão do órgão. Na reoxigenação, há exacerbada produção de espécies reativas de oxigênio (EROs) e sobrecarga de cálcio intracelular, que desencadeiam a morte celular. Poucas são as estratégias de intervenção farmacológica para a prevenção e limitação destas lesões. E, além disso, as formas disponíveis de intervenção não são totalmente eficazes. Recentemente, tem-se direcionado as atenções para os efeitos de produtos naturais na limitação dos danos provocados pela lesão de isquemia e reperfusão (I/R). Neste contexto, o timol, um monoterpeno fenólico, possui, dentre as suas atividades biológicas, ação antiinflamatória e antioxidante. Neste sentido, o objetivo do estudo foi avaliar o potencial efeito cardioprotetor do timol na prevenção da lesão de reperfusão pós-isquemia em ratos. Primeiramente foi realizado o ensaio de sequestros de radicais DPPH pelo timol. Para estudar seu potencial cardioprotetor, foram utilizados ratos Wistar machos (200-300 g) pré-tratados com timol (7,5 mg/kg, v.o.) ou veículo por 7 dias e submetidos a isquemia global do coração em sistema Langendorff. Foram avaliados parâmetros da função cardíaca como pressão desenvolvida pelo ventrículo esquerdo (PVDE), derivada temporal máxima (+Dp/dt) e mínima (-dp/dt) e índice de severidade da arritmia (ISA), tamanho da área de infarto, além de ensaios de atividade enzimática da catalase (CAT), Superóxido Dismutase (SOD), glutationas peroxidase (GPx) e redutase (GR), quantificação tecidual de sulfidrilas, bem como a concentração de substâncias reativas ao ácido tiobarbitúrico (TBARS) e hidroperóxidos de lipídeos. O ensaio de DPPH demonstrou propriedade antioxidante do timol. Além disso, foi observado que o pré-tratamento com timol preservou a PDVE, diminuiu o ISA, reduziu a área de infarto, TBARS e, de modo similar, foi observada menor concentração de hidroperóxidos quando comparado ao veículo. O pré-tratamento com timol preveniu a redução da concentração de grupamentos sulfidrila quando comparado ao veículo. As atividades das enzimas SOD, CAT, GPx e GR foram reduzidas de maneira significativa em corações de animais pré-tratados com timol quando comparados ao veículo. O pré-tratamento com timol preservou a função contrátil e cardíaca, reduziu danos aos componentes celulares e limitou a área de infarto. Demonstrando significativos efeitos cardioprotetores contra I/R.