Browsing by Subject "Cardiac remodeling"

Now showing 1 - 5 of 5
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    Allopurinol attenuates L-NAME induced cardiomyopathy comparable to blockade of angiotensin receptor
    (Murcia : F. Hernández, 2008) Kasal, Daniel Arthur B.; Fritsch Neves, Mario; Oigman, Wille; Mandarim-de-Lacerda, Carlos A.
    It is widely recognized that L-NAME exposed rats develop myocardial fibrosis and hypertrophy. The aim of this study was to evaluate the contribution of xanthine oxidase (XO) to these phenomena using allopurinol, isolated or associated with olmesartan. Thirty adult male Wistar rats were divided into 5 groups (n=6) and studied for 5 weeks: L group (LNAME, 40mg/kg/day); L+A group (L-NAME and allopurinol, 40 mg/kg/day); L+O group (L-NAME and olmesartan, 15mg/kg/day); L+A+O group (L-NAME, allopurinol, and olmesartan); and control group. LNAME caused arterial hypertension and cardiomyocyte hypertrophy. Hypertension was prevented by olmesartan, but not by allopurinol. There was an increase of left ventricular mass index in the L-NAME group that was prevented by allopurinol, olmesartan and by the combination of both. The increase in mean cardiomyocyte transversal area caused by L-NAME was prevented by the allopurinol and olmesartan combination, or by olmesartan used as monotherapy, but not by allopurinol alone. There was a reduction in the myocardial vascularization index caused by L-NAME which was abolished by allopurinol or by olmesartan, but not by the association. L-NAME caused a reduction in the total number of cardiomyocyte nuclei. This was prevented by olmesartan alone or associated with allopurinol, but not by allopurinol alone. We conclude that XO has an important contribution to adverse cardiac remodeling in L-NAME exposed animals. Moreover, allopurinol acts without interfering with L-NAME induced hypertension. The protective action of this drug is comparable to the results obtained with olmesartan. Antioxidative mechanisms are proposed to account for the pressure independent effects of allopurinol.
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    Experimental study design: gene silencing model using siRNAs in mice with cardiotoxicity.
    Lax Pérez, Antonio Manuel; Asensio López, Maria del Carmen; Medicina
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    Galectin-3 expression in cardiac remodeling after myocardial infarction
    (2014-03) Sanchez Mas, Jesus; Lax Pérez, Antonio Manuel; Asensio Lopez, Maria del Carmen; Fernandez del Palacio, Maria J; Caballero, Luis; Garrido, Iris P; Pastor, Francisco; Januzzi, James L; Pascual Figal, Domingo A.; Medicina
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    Soluble sST2 isoform is related to cardiotoxicity
    (2023-07-19) Lax Pérez, Antonio Manuel; Asensio López, Maria del Carmen; Medicina
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    The TBX1 Transcription Factor in Cardiac Remodeling After Myocardial Infarction
    (2016-11) Sanchez Mas, Jesus; Lax Pérez, Antonio Manuel; Asensio Lopez, Maria del Carmen; Fernandez del Palacio, Maria J; Caballero, Luis; Navarro-Peñalver, Marina; Perez Martinez, Maria T; Gimeno Blanes, Juan R; Pascual Figal, Domingo A.; Medicina
    Introduction and objectives: The transcription factor TBX1 plays an important role in the embryonic development of the heart. Nothing is known about its involvement in myocardial remodeling after acute myocardial infarction (AMI) and whether its expression can be modulated by a treatment with proven benefit such as mineralocorticoid receptor blockade. Methods: Acute myocardial infarction was induced in 60 rats via left coronary artery ligation: 50 animals were randomized to be euthanized after 1, 2, 4, 12, or 24 weeks; 10 animals were treated with eplerenone (100 mg/kg/days) 7 days before the AMI until their euthanasia (4 weeks later); 8 additional animals underwent surgery without ligation (control). We analyzed the cardiac expression of TBX1, fetal genes, and fibrosis markers. Results: The gene and protein expression of TBX1 was increased in the infarcted myocardium, peaking 1 week after AMI (P < .01), without changes in the noninfarcted myocardium. Levels of the fetal genes and fibrosis markers also increased, peaking 4 weeks (P < .001) and 1 week (P < .01) after AMI, respectively. The TBX1 expression was correlated with that of the fibrosis markers (P < .01) but not the fetal genes. Eplerenone reduced the TBX1 increase and fibrosis induced by AMI, with an association improvement in ventricular function and remodeling in echocardiography. Conclusions: These results show the reactivated expression of TBX1 and indicate its involvement in cardiac fibrosis and remodeling after AMI and its participation in the benefit from mineralocorticoid receptor blockade.