Akira Nonoyama
Kansai Medical University
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Publication
Featured researches published by Akira Nonoyama.
Journal of Surgical Research | 1986
Hajime Otani; Masao Umemoto; Kiyoshi Kagawa; Yusaku Nakamura; Kazuo Omoto; Kazuho Tanaka; Tadashi Sato; Akira Nonoyama; Terumasa Kagawa
While oxygen-derived free radicals have been implicated in the pathogenesis of myocardial injury, the exact nature of this injury is still unclear. To test the hypothesis that oxygen-induced injury may influence the recovery of cardiac function from ischemic damage, we used an oxygen free radical scavenger, superoxide dismutase (SOD), together with catalase, during the reperfusion of isolated canine heart which had been subjected to 15 min of normothermic ischemic arrest followed by 2 hr of hypothermic cardioplegic preservation using a modified Collins solution. Determinations of thiobarbituric acid reactive substances and coenzyme Q10 within the myocardium showed that the treatment with SOD and catalase was capable of inhibiting lipid peroxidation induced by reperfusion. This inhibition was apparently associated with the improvement of myocardial energy metabolism and cardiac performance. Coronary flow was significantly higher in the heart treated with SOD and catalase during the working stage with a corresponding increase in oxygen consumption. Myocardial adenosine triphosphate (ATP) was partially, but significantly restored during reperfusion in these hearts whereas no restoration was observed in the heart without the enzymes. The treatment with SOD and catalase also improved left ventricular stroke work index and left ventricular maximum dp/dt at an early stage of the working mode. These results suggest that the use of SOD and catalase during reperfusion can protect the ischemic heart against reperfusion injury by scavenging oxygen-derived free radicals.
The Annals of Thoracic Surgery | 1976
Akira Nonoyama; Atoh Masuda; Kenji Kasahara; Toshitake Mogi; Terumasa Kagawa
A patient who sustained a traumatic rupture of the left main bronchus that was successfully repaired nine years later is presented, and reference is made to reports of similar instances in which operation has been performed more than five years after injury. Pulmonary function following operation improved progressively and proved the delayed repair to have been a reasonable decision.
Journal of Molecular and Cellular Cardiology | 1985
Hajime Otani; Kazuo Omoto; Kazuho Tanaka; Tadashi Sato; Masao Umemoto; Akitoshi Tatsumi; Yukihito Saito; Tsutomu Osako; Michio Fukunaka; Kenji Kasahara; Atoh Masuda; Akira Nonoyama; Terumasa Kagawa
This study was designed to investigate the relationship between myocardial oxygen consumption and oxygen-induced myocardial injury. Dog hearts were exposed to 40 min normothermic ischemia and then reperfused for 10 min with three oxygenated perfusates containing different hemoglobin concentrations and with moderate hemodilution. The experimental groups consist of a moderate hemodilution group (Group M) receiving 8 g/dl of hemoglobin, an extreme hemodilution group (Group E) given 4 g/dl of hemoglobin, and a hemoglobin-free autologous plasma group (Group F). Hearts in the non-ischemic control group (Group C) were also perfused with moderate hemodilution throughout. In Group C, Group M and Group E, the O2 tension of perfusates was maintained at about 100 mmHg and in Group F, at over 300 mmHg. Oxygen extraction at 5 min after reperfusion in Group C was 14%, in Group M and Group E less than 10%, but in Group F 70%. Oxygen consumption in Group F was more than twice that in Group E and surpassed that in Group C. Group M also showed a significant increase in oxygen consumption compared with Group E at 5 min after reperfusion. Among the ischemic groups, Group E showed improvement of left ventricular function almost comparable to Group C accompanied by a rapid decrease in myocardial lactate, improved preservation of myocardial adenine nucleotides and prevention of myocardial lipid peroxidation. In contrast, Group F showed persistently higher values of lipid peroxides and lactate, the poorest recovery of adenine nucleotides, and impairment of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
Surgery Today | 1986
Akira Nonoyama; Kazuho Tanaka; Tsutomu Osako; Yukihito Saito; Masao Umemoto; Atoh Masuda; Terumasa Kagawa
A long-term follow-up study on pulmonary function in twelve lobectomized children under ten years of age at the time of surgery was performed to determine the patterns of compensation. In the patients over ten years old at the time of the test performed over two years postoperatively, there was neither compensatory regeneration nor compensatory overdistension of the remaining lung tissue. However, there appeared to be an increase in the vital capacity, probably due to the growth of surrounding tissue such as thorax, respiratory muscles, and diaphragm. In contrast, the children tested under the age of eight years showed evidence of mild overdistension during the early postoperative period, but not at two years. There was no sign of overdistension in the patients over ten years of age at the time of testing.A long-term follow-up study on pulmonary function in twelve lobectomized children under ten years of age at the time of surgery was performed to determine the patterns of compensation. In the patients over ten years old at the time of the test performed over two years postoperatively, there was neither compensatory regeneration nor compensatory overdistension of the remaining lung tissue. However, there appeared to be an increase in the vital capacity, probably due to the growth of surrounding tissue such as thorax, respiratory muscles, and diaphragm. In contrast, the children tested under the age of eight years showed evidence of mild overdistension during the early postoperative period, but not at two years. There was no sign of overdistension in the patients over ten years of age at the time of testing.
Chest | 1984
Akira Nonoyama; Kazuho Tanaka; Tsutomu Osako; Sumio Kotani; Terumasa Kagawa
Japanese Circulation Journal-english Edition | 1970
Akira Nonoyama; Sumio Kotani; Isamu Miyamoto; Hiroshige Katsuda; Terumasa Kagawa
Japanese Circulation Journal-english Edition | 1970
Akira Nonoyama; Hiroshige Katsuda; Masaaki Nakahashi; Susumu Uchiyama; Shinji Kubo; Terumasa Kagawa
The Japanese journal of thoracic diseases | 1978
Kazuho Tanaka; Michio Fukunaka; Tsutom Osako; Akira Fujio; Tadashi Sato; Kenji Kasahara; Atoh Masuda; Akira Nonoyama; Tastumistu Itano; Terumasa Kagawa
Japanese Circulation Journal-english Edition | 1972
Atoh Masuda; Akira Nonoyama; Sumio Kotani; Masaaki Nakahashi; Tetsuhide Ishii; Terumasa Kagawa
Japanese Circulation Journal-english Edition | 1968
Terumasa Kagawa; Akira Nonoyama; Akitoshi Kobayashi