No description available.

This thesis is concerned with the influence of acute and long-term beta-adrenergic blockade on myocardial infarction in man. An original statistical evaluation of all published and some available unpublished clinical trials is presented in Chapter I. Chapter III and TV concern the measurement and evolution of infarct size in man. In Chapter III, praecordial ECG mapping and the standard 12 lead ECG have been correlated with cumulative release of the MB isomer of creatine kinase. Using these techniques, I have found that approximately 50% of eventual infarction is complete in 6 hours; implying that interventions designed to salvage ischaemic myocardium may be feasable (Chapter IV). In Chapter V, I have demonstrated delayed beta-adrenergic blockade after oral administration of atenolol and that an initial intravenous dose is essential to achieve early and effective beta-blockade. In a randomised control trial of 215 patients, atenolol administered intravenously within 12 hours of pain, prevented infarction in treated patients with initial threatened infarcts and reduced infarct size and morbidity in those with initial definite infarcts (Chapter VI). Patients with anterior myocardial infarction, randomised to receive atenolol for a year, showed significantly greater R wave recovery and Q wave disappearance on serial praecordial maps compared to placebo patients. In a further study, this was demonstrated to be due to lowering the heart rate. This phenomenon of improved EGG recovery with atenolol was reproduced in experimental infarction and was shown to be due to improved scar shrinkage (Chapter VII). The implications of these studies are discussed. It is likely that both early and long-term beta-blockade will be beneficial to patients with myocardial infarction.

Thesis (M. Phil.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 107-121) Also available in print.

Thesis (M.S.)--University of Toledo, 2009. / Typescript. "Submitted as partial fulfillment of the requirements for the Master of Science Degree in Medicinal Chemistry." "A thesis entitled"--at head of title. Bibliography: leaves 45-48.

Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references (leaves [64]-71).

Thesis (M.D.)--University of Hong Kong, 1982. / Also available in print.

No description available.

Beta adrenergic antagonists and antianginal drugs are used with the aim to ultimately decrease mortality and enable patients to lead an improved quality of life by avoidance of anginal episodes. Each class of medications used for this purpose has a variety of actual or potential side effects associated with their use. Side effects and drug interactions involving these medications are discussed in the following chapter. Evidence presented should be used in the context of the patient populations described and may aid clinical decision making through avoidance or identification of actual or potential side effects. This review includes literature published from January 2019 to January 2020 written in English.

published_or_final_version / Anaesthesiology / Master / Master of Philosophy

Orientador: André Sampaio Pupo / Banca: Wilma de Grava Kempinas / Banca: Edson Antunes / Resumo: A ejaculação precoce é a disfunção sexual masculina com maiores taxas de incidência e prevalência. De etiologia complexa, as principais abordagens farmacológicas desta condição têm sido a utilização de anestésicos locais, inibidores seletivos da recaptura de serotonina e mais recentemente, inibidores da fosfodiesterase tipo 5. O reflexo ejaculatório é um processo altamente organizado com a interação de áreas centrais encefálicas e espinhais, centros autonômicos simpáticos e parasimpáticos além de reflexos somáticos. O sistema nervoso autônomo simpático, através da ativação de adrenoceptores 1 ( 1-ARs), particularmente o subtipo 1A, desempenha papel fundamental na fase de emissão do reflexo ejaculatório através da modulação da contratilidade de órgãos como o ducto deferente, vesícula seminal e próstata. Além disso, a participação do influxo de cálcio extracelular via canais de cálcio dependentes de voltagem tipo L (canais de cálcio tipo L) na atividade contrátil destes órgãos é bem caracterizada. Devido à importância dos 1-ARs e canais tipo L no reflexo ejaculatório, este trabalho avaliou a eficácia do antagonista de 1-ARs Tamsulosin e das diidropiridinas bloqueadoras de canais de cálcio Nifedipina e (S)-(+)-Niguldipina no retardo da ejaculação em ratos. Os resultados obtidos demonstram que a atividade contrátil do ducto deferente e vesícula seminal ao estímulo adrenérgico via ativação de 1-ARs in vitro é fortemente inibida pelo antagonista de 1-ARs Tamsulosin e pelas bloqueadoras de canais de cálcio Nifedipina e (S)-(+)-Niguldipina. Entretanto, embora a contração destes órgãos e, portanto, a fase de emissão do reflexo ejaculatório tenha sido afetada, a latência ejaculatória dos animais não foi alterada. Estes resultados indicam que o bloqueio de canais de cálcio tipo L ou o antagonismo de 1-ARs no ducto deferente... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Premature ejaculation is one of the most common male sexual dysfunctions. With complex aetiology, the main pharmacological approaches involve local anesthetics, selective serotonin reuptake inhibitors and, more recently, phosphodiesterase 5 inhibitors. The sympathetic nervous system plays a crucial role in the ejaculation, controlling vasa deferentia, seminal vesicles and prostate contraction through 1- adrenoceptor ( 1-AR) activation. In addition, the contractions of these organs are dependent on influx of extracellular calcium through L-type voltage-dependent calcium channels (L-type calcium channels). Due to the involvement of 1-ARs and L-type calcium channels in the ejaculatory reflex, this dissertation evaluated the efficacy of the 1-AR antagonist Tamsulosin and of dihydropyridine calcium channel blockers Nifedipine and (S)-(+)-Niguldipine in the delay of ejaculation in rats. The results showed that the vas deferens and seminal vesicle contraction in response to 1-AR activation is potently inhibited by Tamsulosin, Nifedipine and (S)-(+)- Niguldipine. However, although vas deferens and seminal vesicles contractions have been inhibited, the ejaculatory latency in vivo was not affected. These results show that although L-type calcium channel blockade and 1-ARs antagonism in the vas deferens and seminal vesicle are effective in the inhibition of events related to the seminal emission phase of ejaculation, they are not able to delay the ejaculation. The present results indicate that modulation of contractions of organs involved in seminal emission is not a suitable strategy to retard of ejaculation / Mestre