OBJECTIVE: To evaluate the potential relationship of mast cells with myocardial fibrosis in the cardiac ventricles of spontaneously hypertensive rats (SHR). DESIGN: Experiments were performed on hearts from 36-week-old SHR with established left ventricular hypertrophy (n = 12) and from 36-week-old normotensive Wistar-Kyoto (WKY) rats (n = 12). Furthermore, to evaluate whether antihypertensive treatment with the angiotensin converting enzyme inhibitor quinapril interferes with the potential relationship between mast cells and fibrosis in SHR, we treated 16-week-old SHR (n = 12) with oral quinapril (10 mg/kg body weight per day) for 20 weeks. METHODS: Mast cells were counted in 25 high-power fields. Toluidine blue-stained sections and avidin staining were used to detect mast cells. The extent of myocardial fibrosis was analysed in samples stained with Masson's trichrome. The amount of collagen was evaluated morphometrically, using an automatic image analyser, and biochemically, using myocardial hydroxyproline concentration. RESULTS: In the left ventricle of untreated SHR compared with age- and sex-matched normotensive WKY rats we found more extensive interstitial and perivascular fibrosis, an increased collagen volume fraction, an increased hydroxyproline concentration and an increased number of mast cells. Similar but less intense abnormalities were observed in the right ventricles of untreated SHR compared with the left ventricles of the same rats. In the left ventricles of quinapril-treated SHR compared with those of untreated SHR we found a marked decrease in fibrosis, a lower collagen volume fraction, a lower hydroxyproline concentration and fewer mast cells. Treatment with quinapril was also accompanied by normalization in the myocardial structure of the right ventricles of SHR. A positive correlation was found between the density of mast cells and the collagen volume fraction in the left ventricles of all of the rats. CONCLUSIONS: The present findings suggest that mast cells can play a part in the development of the myocardial fibrosis that occurs in the cardiac ventricles with hypertensive cardiac hypertrophy. In addition, the present results suggest that the ability of quinapril to interfere with mast cells might be involved in its cardioreparative properties.
OBJECTIVE: To evaluate the potential relationship of mast cells with myocardial fibrosis in the cardiac ventricles of spontaneously hypertensiverats (SHR). DESIGN: Experiments were performed on hearts from 36-week-old SHR with established left ventricular hypertrophy (n = 12) and from 36-week-old normotensive Wistar-Kyoto (WKY) rats (n = 12). Furthermore, to evaluate whether antihypertensive treatment with the angiotensin converting enzyme inhibitor quinapril interferes with the potential relationship between mast cells and fibrosis in SHR, we treated 16-week-old SHR (n = 12) with oral quinapril (10 mg/kg body weight per day) for 20 weeks. METHODS: Mast cells were counted in 25 high-power fields. Toluidine blue-stained sections and avidin staining were used to detect mast cells. The extent of myocardial fibrosis was analysed in samples stained with Masson's trichrome. The amount of collagen was evaluated morphometrically, using an automatic image analyser, and biochemically, using myocardial hydroxyproline concentration. RESULTS: In the left ventricle of untreated SHR compared with age- and sex-matched normotensive WKY rats we found more extensive interstitial and perivascular fibrosis, an increased collagen volume fraction, an increased hydroxyproline concentration and an increased number of mast cells. Similar but less intense abnormalities were observed in the right ventricles of untreated SHR compared with the left ventricles of the same rats. In the left ventricles of quinapril-treated SHR compared with those of untreated SHR we found a marked decrease in fibrosis, a lower collagen volume fraction, a lower hydroxyproline concentration and fewer mast cells. Treatment with quinapril was also accompanied by normalization in the myocardial structure of the right ventricles of SHR. A positive correlation was found between the density of mast cells and the collagen volume fraction in the left ventricles of all of the rats. CONCLUSIONS: The present findings suggest that mast cells can play a part in the development of the myocardial fibrosis that occurs in the cardiac ventricles with hypertensivecardiac hypertrophy. In addition, the present results suggest that the ability of quinapril to interfere with mast cells might be involved in its cardioreparative properties.
Authors: Scott P Levick; Giselle C Meléndez; Eric Plante; Jennifer L McLarty; Gregory L Brower; Joseph S Janicki Journal: Cardiovasc Res Date: 2010-08-24 Impact factor: 10.787
Authors: Saman Rasoul; Oscar A Carretero; Hongmei Peng; Maria A Cavasin; Jialong Zhuo; Alicia Sanchez-Mendoza; David R Brigstock; Nour-Eddine Rhaleb Journal: J Hypertens Date: 2004-03 Impact factor: 4.844
Authors: Jianping Li; Hong Lu; Eric Plante; Giselle C Meléndez; Scott P Levick; Joseph S Janicki Journal: J Mol Cell Cardiol Date: 2012-07-29 Impact factor: 5.000