Hellenic journal of cardiology : HJC = Hellenike kardiologike epitheorese · 2011
Modulation of hemodynamics, endogenous antioxidant enzymes, and pathophysiological changes by Angiotensin-converting enzyme inhibitors in pressure-overload rats.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Moinuddin Ghulam, Inamdar Mohammed Naseeruddin, Kulkarni Kala S, Kulkarni Chanda
Аннотация
INTRODUCTION: We sought to assess the role of angiotensin-converting enzyme (ACE) inhibitors on systolic blood pressure (BP), endogenous antioxidant enzymes and histopathological changes in pressure-overload rats.
METHODS: Pressure overload was produced in male rats by abdominal aortic banding (AAB) using a blunt 22-gauge needle, as a model of cardiac hypertrophy. After surgery, AAB-induced hypertensive (AABIH) groups were treated with captopril 4 mg and ramipril 10 mg/kg per day p.o. for 16 weeks. At 16 weeks, rats were observed for general characteristics and mortality, non-invasive blood pressure (NIBP) and endogenous antioxidant enzyme catalase and superoxide dismutase (SOD) activity and histological evaluation of target organs.
RESULTS: In the AABIH group a significant increase in systolic BP was observed in week 3 (149.3 ± 0.821) and persisted until week 16, along with lower levels of serum catalase (144.7 ± 2.204) and SOD (12.92 ± 0.4601) activity compared to the control group. Captopril and ramipril treated groups showed a significantly smaller increase in systolic BP (25.47 ± 3.685, 20.21 ± 3.306) and greater serum SOD (27.33 ± 2.338, 28.95 ± 1.143) and catalase (181.7 ± 8.407, 187.9 ± 8.497) activity, respectively, than the hypertensive rats. The histological changes induced in target organs (heart, liver, kidneys and thoracic aorta) in AABIH rats were attenuated in treated rats.
CONCLUSIONS: ACE-inhibition causes an improvement in myocardial antioxidant reserve, reduces oxidative stress, and prevents pathophysiological alterations, while showing a trend for potential target organ protection in hypertensive rats.
METHODS: Pressure overload was produced in male rats by abdominal aortic banding (AAB) using a blunt 22-gauge needle, as a model of cardiac hypertrophy. After surgery, AAB-induced hypertensive (AABIH) groups were treated with captopril 4 mg and ramipril 10 mg/kg per day p.o. for 16 weeks. At 16 weeks, rats were observed for general characteristics and mortality, non-invasive blood pressure (NIBP) and endogenous antioxidant enzyme catalase and superoxide dismutase (SOD) activity and histological evaluation of target organs.
RESULTS: In the AABIH group a significant increase in systolic BP was observed in week 3 (149.3 ± 0.821) and persisted until week 16, along with lower levels of serum catalase (144.7 ± 2.204) and SOD (12.92 ± 0.4601) activity compared to the control group. Captopril and ramipril treated groups showed a significantly smaller increase in systolic BP (25.47 ± 3.685, 20.21 ± 3.306) and greater serum SOD (27.33 ± 2.338, 28.95 ± 1.143) and catalase (181.7 ± 8.407, 187.9 ± 8.497) activity, respectively, than the hypertensive rats. The histological changes induced in target organs (heart, liver, kidneys and thoracic aorta) in AABIH rats were attenuated in treated rats.
CONCLUSIONS: ACE-inhibition causes an improvement in myocardial antioxidant reserve, reduces oxidative stress, and prevents pathophysiological alterations, while showing a trend for potential target organ protection in hypertensive rats.