David T. Kelly – författare
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2 produkter
2 produkter
Häftad, Engelska, 1989
1 125 kr
Skickas inom 10-15 vardagar
These are the proceedings of the third Asian Pacific Adalat Symposium. The first was held in Tokyo in 1982 and the second in Sydney in 1985. We were honoured that the late Dr. Sukaman and his colleagues were able to host this third symposium in Jakarta. This meeting was designed to contribute to and to promote international collaboration in cardiovascular research, and to help promote further knowledge and understanding about the treatment of vascular disease in the Asian Pacific area. Nifedipine was originally investigated in the mid-1960s by Prof. Fleckenstein. His first results showed this drug was a powerful calcium antagonist which altered excitation contraction. At this time, there was a rapid development of knowledge about the pathophysiology of ischaemic heart disease, and thus the important pharmacological work on calcium antagonists such as nifedipine paralleled and complimented the newer understanding of coronary physiology in man. In a short time most therapy was designed to reduce myocardial oxygen consumption and demand.
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These are the proceedings of the third Asian Pacific Adalat Symposium. The first was held in Tokyo in 1982 and the second in Sydney in 1985. We were honoured that the late Dr. Sukaman and his colleagues were able to host this third symposium in Jakarta. This meeting was designed to contribute to and to promote international collaboration in cardiovascular research, and to help promote further knowledge and understanding about the treatment of vascular disease in the Asian Pacific area. Nifedipine was originally investigated in the mid-1960s by Prof. Fleckenstein. His first results showed this drug was a powerful calcium antagonist which altered excitation contraction. At this time, there was a rapid development of knowledge about the pathophysiology of ischaemic heart disease, and thus the important pharmacological work on calcium antagonists such as nifedipine paralleled and complimented the newer understanding of coronary physiology in man. In a short time most therapy was designed to reduce myocardial oxygen consumption and demand.