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Rajesh P. Shah - One of the best experts on this subject based on the ideXlab platform.

  • evaluation of tissue kallikrein activity on survival time after acute Coronary Artery Ligation in hypertensive rats
    International Immunopharmacology, 2003
    Co-Authors: Jagdish N. Sharma, Atif S Abbas, Pauzi A M Yusof, Rajesh P. Shah
    Abstract:

    It is known that the tissue kallikrein-kinin system is located in the cardiac tissue, and the lack of this system in the cardiac tissue might induce cardiac dysfunctions. In this study, we investigated the potential role of tissue kallikrein and Trasylol, an inhibitor of tissue kallikrein, on survival time with acute left Coronary Artery Ligation for 15 min in spontaneously hypertensive rats (SHR). Tissue kallikrein (8 and 16 Ag/kg, i.v.) treatment caused significant (P<0.05) increases in the survival time of SHR as compared with the saline-treated control SHR. Trasylol pretreatment abolished (P<0.05) the beneficial effect on tissue kallikrein on survival time. The Ligation of Coronary Artery resulted in significant (P<0.05) reduction in systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) of SHR compared with the saline-treated control SHR. The tissue kallikrein treatment caused greater (P<0.001) reduction in the SBP, DBP and HR of SHR, when the mean values were compared between before Coronary Artery Ligation and after Coronary Artery Ligation. Trasylol (6 Ag/kg) treatment antagonized the effects of tissue kallikrein associated with survival time, SBP, DBP and HR. These findings may suggest that tissue kallikrein is able to act as a cardioprotective agent as demonstrated by the increase in survival time of SHR with acute Coronary Artery Ligation. The significance of these observations is discussed. D 2002 Elsevier Science B.V. All rights reserved.

  • Evaluation of tissue kallikrein activity on survival time after acute Coronary Artery Ligation in hypertensive rats.
    International immunopharmacology, 2003
    Co-Authors: Jagdish N. Sharma, S. Atif Abbas, A.pauzi M. Yusof, Rajesh P. Shah
    Abstract:

    It is known that the tissue kallikrein-kinin system is located in the cardiac tissue, and the lack of this system in the cardiac tissue might induce cardiac dysfunctions. In this study, we investigated the potential role of tissue kallikrein and Trasylol, an inhibitor of tissue kallikrein, on survival time with acute left Coronary Artery Ligation for 15 min in spontaneously hypertensive rats (SHR). Tissue kallikrein (8 and 16 Ag/kg, i.v.) treatment caused significant (P

Jagdish N. Sharma - One of the best experts on this subject based on the ideXlab platform.

  • A bradykinin antagonist abolishes beneficial effect of captopril on duration of survival after acute Coronary Artery Ligation in hypertensive rats
    Pharmacological research, 2005
    Co-Authors: Jagdish N. Sharma, S. Atif Abbas
    Abstract:

    It has been recently suggested that bradykinin (BK) may act as a cardioprotectve agent. In the present investigation, we evaluated the effects of captopril, an angiotensin-converting enzyme inhibitor (ACEI), and kinin B 2 receptor antagonist, d-Arg-[Hyp3-d-Phe7]-BK, on the duration of survival after acute Coronary Artery Ligation for 15 min in spontaneously hypertensive rats (SHR). The captopril treatment (16 and 32 ug/kg, i.v.) resulted in a significant ( p 0.05) the beneficial effect of captopril on survival time as compared to saline-treated control SHR. Both the Ligation of Coronary Artery and captopril treatment resulted in a significant ( p 0.05) in SBP, DBP and HR between saline- and kinin B2 receptor antagonist plus captopril-treated SHR during preLigation. These finding might indicate that captopril possesses a cardioprotective property as demonstrated by increased in survival time of SHR. This beneficial effect of captopril is mediated via the kinin B 2 receptor pathway because kinin B2 receptor antagonist pretreatment blocked the captopril-induced increase in survival time of SHR. © 2005 Elsevier Ltd. All rights reserved.

  • evaluation of tissue kallikrein activity on survival time after acute Coronary Artery Ligation in hypertensive rats
    International Immunopharmacology, 2003
    Co-Authors: Jagdish N. Sharma, Atif S Abbas, Pauzi A M Yusof, Rajesh P. Shah
    Abstract:

    It is known that the tissue kallikrein-kinin system is located in the cardiac tissue, and the lack of this system in the cardiac tissue might induce cardiac dysfunctions. In this study, we investigated the potential role of tissue kallikrein and Trasylol, an inhibitor of tissue kallikrein, on survival time with acute left Coronary Artery Ligation for 15 min in spontaneously hypertensive rats (SHR). Tissue kallikrein (8 and 16 Ag/kg, i.v.) treatment caused significant (P<0.05) increases in the survival time of SHR as compared with the saline-treated control SHR. Trasylol pretreatment abolished (P<0.05) the beneficial effect on tissue kallikrein on survival time. The Ligation of Coronary Artery resulted in significant (P<0.05) reduction in systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) of SHR compared with the saline-treated control SHR. The tissue kallikrein treatment caused greater (P<0.001) reduction in the SBP, DBP and HR of SHR, when the mean values were compared between before Coronary Artery Ligation and after Coronary Artery Ligation. Trasylol (6 Ag/kg) treatment antagonized the effects of tissue kallikrein associated with survival time, SBP, DBP and HR. These findings may suggest that tissue kallikrein is able to act as a cardioprotective agent as demonstrated by the increase in survival time of SHR with acute Coronary Artery Ligation. The significance of these observations is discussed. D 2002 Elsevier Science B.V. All rights reserved.

  • Evaluation of tissue kallikrein activity on survival time after acute Coronary Artery Ligation in hypertensive rats.
    International immunopharmacology, 2003
    Co-Authors: Jagdish N. Sharma, S. Atif Abbas, A.pauzi M. Yusof, Rajesh P. Shah
    Abstract:

    It is known that the tissue kallikrein-kinin system is located in the cardiac tissue, and the lack of this system in the cardiac tissue might induce cardiac dysfunctions. In this study, we investigated the potential role of tissue kallikrein and Trasylol, an inhibitor of tissue kallikrein, on survival time with acute left Coronary Artery Ligation for 15 min in spontaneously hypertensive rats (SHR). Tissue kallikrein (8 and 16 Ag/kg, i.v.) treatment caused significant (P

Satoshi Takeo - One of the best experts on this subject based on the ideXlab platform.

  • Effects of angiotensin I-converting enzyme inhibitor and angiotensin II type 1 receptor blocker on the right ventricular sarcoglycans and dystrophin after left Coronary Artery Ligation
    European Journal of Pharmacology, 2005
    Co-Authors: Masaya Takahashi, Kouichi Tanonaka, Hiroyuki Yoshida, Miki Koshimizu, Ryo Oikawa, Takuya Daicho, Satoshi Takeo
    Abstract:

    Abstract We examined the effects of trandolapril and candesartan on changes in the levels of sarcoglycans and dystrophin in the right ventricle of rats with the left Coronary Artery Ligation. Hemodynamic and morphological alterations suggested the development of hypertrophy of the right ventricle and chronic heart failure by the 8th week. By the end of the 8th week, α- and β-sarcoglycans and dystrophin were decreased. Increases in μ- and m-calpains in the hypertrophied right ventricle were associated with an elevation of casein-proteolytic activity in the cytosolic fraction. Oral administration of 3 mg/kg/day trandolapril or 1 mg/kg/day candesartan from the 2nd to 8th week after the left Coronary Artery Ligation attenuated decreases in α-sarcoglycan and dystrophin and reduced the increased proteolytic activity. The results suggest that attenuation of decreases in sarcoglycans and dystrophin is a possible mechanism underlying trandolapril- and candesartan-mediated improvement of structural and functional alterations of the right ventricle in the Coronary Artery-ligated rat.

  • Effects of angiotensin I-converting enzyme inhibitor and angiotensin II type 1 receptor blocker on the right ventricular sarcoglycans and dystrophin after left Coronary Artery Ligation.
    European journal of pharmacology, 2005
    Co-Authors: Masaya Takahashi, Kouichi Tanonaka, Hiroyuki Yoshida, Miki Koshimizu, Ryo Oikawa, Takuya Daicho, Satoshi Takeo
    Abstract:

    We examined the effects of trandolapril and candesartan on changes in the levels of sarcoglycans and dystrophin in the right ventricle of rats with the left Coronary Artery Ligation. Hemodynamic and morphological alterations suggested the development of hypertrophy of the right ventricle and chronic heart failure by the 8th week. By the end of the 8th week, alpha- and beta-sarcoglycans and dystrophin were decreased. Increases in mu- and m-calpains in the hypertrophied right ventricle were associated with an elevation of casein-proteolytic activity in the cytosolic fraction. Oral administration of 3 mg/kg/day trandolapril or 1 mg/kg/day candesartan from the 2nd to 8th week after the left Coronary Artery Ligation attenuated decreases in alpha-sarcoglycan and dystrophin and reduced the increased proteolytic activity. The results suggest that attenuation of decreases in sarcoglycans and dystrophin is a possible mechanism underlying trandolapril- and candesartan-mediated improvement of structural and functional alterations of the right ventricle in the Coronary Artery-ligated rat.

  • Myocardial heat shock protein changes in the failing heart following Coronary Artery Ligation.
    Heart lung & circulation, 2003
    Co-Authors: Kouichi Tanonaka, Wakako Toga, Hiroyuki Yoshida, Satoshi Takeo
    Abstract:

    Abstract Background: Production of several heat shock proteins (Hsp) is enhanced after exposure to stress. There is little information concerning changes in myocardial Hsp under pathophysiological conditions. The aim of this study was to determine alterations in Hsp content in the viable left ventricular myocardium during the development of heart failure following Coronary Artery Ligation (CAL). Methods: Myocardial infarction was produced by CAL of Wistar rats. One and eight weeks after the operation, haemodynamic parameters of rats with CAL were determined and then expression of Hsp27, Hsp60 and Hsp72 was measured by western blotting. Results: Animals showed a decrease in cardiac output and an increase in left ventricular end-diastolic pressure, symptoms of chronic heart failure (CHF), 8 weeks after CAL. Myocardial Hsp27 and Hsp72 at 1 week after CAL significantly increased, whereas expression of both proteins at 8 weeks was similar to that in rats which underwent a sham operation (without Coronary Artery Ligation). In contrast, Hsp60 at 8 weeks, but not at 1 week, significantly increased in the sham rats. Conclusions: Diverse changes in myocardial Hsp occurred during the development of CHF.

Juan Guo - One of the best experts on this subject based on the ideXlab platform.

  • Cardioprotective effect of polydatin on ventricular remodeling after myocardial infarction in Coronary Artery Ligation rats.
    Planta medica, 2015
    Co-Authors: Yan Gao, Jian-ping Gao, Chang-xun Chen, Hui-lin Wang, Juan Guo
    Abstract:

    The purpose of this study was to explore the effect of polydatin on ventricular remodeling after myocardial infarction in Coronary Artery Ligation rats and to elucidate the underlying mechanisms. A rat model of ventricular remodeling after myocardial infarction was established by left Coronary Artery Ligation. Rats with Coronary Artery Ligation were randomly divided into five groups: control, plus 40 mg/kg captopril, plus 25 mg/kg polydatin, plus 50 mg/kg polydatin, and plus 100 mg/kg polydatin. The sham-operated group was used as a negative control. Rats were administered intragastrically with the corresponding drugs or drinking water for seven weeks. At the end of the treatment, the left ventricular weight index and heart weight index were assessed. The cross-sectional size of cardiomyocytes was measured by staining myocardium tissue with hematoxylin and eosin. Collagen content was counted by Sirius red in aqueous saturated picric acid. The concentrations of angiotensin I, angiotensin II, aldosterone, and endothelin 1 in myocardium or serum were determined by radioimmunoassay. Hydroxyproline and nitric oxide concentrations and glutathione peroxidase and catalase activities in serum were measured by ultraviolet spectrophotometry. Our results showed that seven weeks of polydatin treatment resulted in a significantly reduced left ventricular weight index, heart weight index, serum concentrations of hydroxyproline and aldosterone, an increased concentration of nitric oxide as well as enhanced activities of glutathione peroxidase and catalase. Myocardial angiotensin I, angiotensin II, and endothelin 1 levels were also reduced. The cardiomyocyte cross-sectional area and collagen deposition diminished. This study suggests that polydatin may attenuate ventricular remodeling after myocardial infarction in Coronary Artery Ligation rats through restricting the excessive activation of the renin-angiotensin-aldosterone system and inhibiting peroxidation.

  • Beneficial effects of houttuynin on ventricular remodeling induced by Coronary Artery Ligation in rats.
    European journal of pharmacology, 2014
    Co-Authors: Yan Gao, Chang-xun Chen, Jian‑ping Gao, Hui‑lin Wang, Juan Guo
    Abstract:

    To examine the effects of houttuynin on ventricular remodeling induced by Coronary Artery Ligation in rats and the underlying mechanisms. A rat model of ventricular remodeling was established by left Coronary Artery Ligation (CAL). Rats were randomly divided into four groups: CAL control, CAL plus 40 mg/kg captopril, CAL plus 100 mg/kg houttuynin and sham-operated control. The rats were administered intragastrically with the corresponding drugs or distilled water for 7 weeks. At the end of the experiment, the left ventricular weight index (LVWI) and heart weight index (HWI) were determined. Myocardium tissue was stained with hematoxylin and eosin or picric acid/Sirius red for cardiomyocyte cross-section area or collagen content measurements respectively. The concentrations of angiotensin I (Ang I), angiotensin II (Ang II), aldosterone (ALD) and endothelin-1 (ET-1) in myocardium or serum were detected by radioimmunoassay. The hydroxyproline (Hyp) concentration was measured by alkali hydrolysis. Ultraviolet spectrophotometry was used to determine glutathione peroxidase (GSH-Px) and catalase (CAT) activities in serum. Houttuynin significantly diminished LVWI and HWI, decreased Ang I, Ang II, ALD, ET-1 and Hyp concentrations in myocardium or serum, increased NO concentration and GSH-Px, CAT activities after 7 weeks of treatment. Houttuynin could also reduce cardiomyocyte cross-section area and collagen deposition. Houttuynin attenuates ventricular remodeling in Coronary Artery Ligation rats by restricting the excessive activation of rennin-angiotensin-aldosterone system (RAAS) and the peroxidation.

S. Atif Abbas - One of the best experts on this subject based on the ideXlab platform.