| Project/Area Number |
13660329
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied veterinary science
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| Research Institution | Azabu University |
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Principal Investigator |
WAKAO Yoshito Azabu University, Vet. Med., Professor, 獣医学部, 教授 (20063969)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Youko Azabu University, Vet. Med., Assistant, 獣医学部, 助手 (10318884)
KANAI Takao Azabu University, Medicine, Lecturer, 医学部, 講師 (60104642)
MUTO Makoto Azabu University, Vet. Med., Associate Professor, 獣医学部, 助教授 (90130898)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Ventricular remodeling / ACEI / PA Banding / Dog |
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| Research Abstract |
In this study, we prepared a PS model that is commonly found in dogs, and examined the inhibitory effect of ACEI on myocardial remodeling. The effect was examined following administration of ACEI by monitoring clinical conditions and various laboratory test parameters, as well as by measuring enzyme activity in cardiac muscle, fibrous tissue and cardiomyocyte diameter.
In this 60-day experiment, laboratory tests revealed a time-dependent decrease in flow rate in the pulmonary artery in the ACEI group. However, exacerbation of the clinical conditions caused by administration of ACEI was not observed. The cause of the decrease in flow rate in the pulmonary artery in the ACEI group is unknown, and it is therefore considered necessary to determine the influence of this decrease by carrying out long-term observation. Although ACEI inhibited ACE activity in circulating blood, no significant inhibition of ACE activity was observed in the right ventricular muscle. In addition, histological examinations revealed an increase in the thickness of the right ventricular wall, an increase in fibrous tissue and an increase in cardiomyocyte diameter in both the PS and ACEI groups. As such, inhibition of myocardial remodeling by ACEI was not observed. It was suggested that this is because more ANG II is produced by chymase than by ACE in dogs. In fact, in the Sham group, chymase activity was greater than ACE activity in the right ventricle. It is considered necessary in the future to examine the usefulness of ANG II receptor blockers against PS, which can control ANG II formation that involves chymase.
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