Browsing by Author "Diaz Araya, G"
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- ItemEffects of carvedilol on oxidative stress and chronotropic response to exercise in patients with chronic heart failure(WILEY, 2005) Castro, P; Vukasovic, JL; Chiong, M; Diaz Araya, G; Alcaino, H; Copaja, M; Valenzuela, R; Greig, D; Perez, O; Corbalan, R; Lavandero, SBackground: Our previous studies suggest that the increase in heart rate from rest to peak exercise is reduced in patients with chronic heart failure (CHF) and this is associated with increased oxidative stress, as determined by malondialdehyde (MDA) plasma levels.
- ItemEffects of Carvedilol upon intra- and interventricular synchrony in patients with chronic heart failure(EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC, 2005) Castro, PF; Mc Nab, P; Quintana, JC; Bittner, A; Greig, D; Vergara, I; Vukasovic, JL; Corbalan, R; Copaja, M; Diaz Araya, G; Chiong, M; Troncoso, R; Alcaino, H; Lavandero, SRadionuclide isotopic ventriculography with phase analysis was performed in 30 patients with stable heart failure (HF), determining left ventricular (LV) and interventricular contraction synchrony at baseline and after 6 months of treatment with maximal tolerated doses of carvedilol. Patients with HF had significant ventricular dyssynchrony compared with a normal population. The 50th percentile of patients with the greatest dyssynchrony at baseline showed significant improvement in ventricular synchrony after receiving carvedilol, and this was correlated positively with a reduction in end-diastolic LV volumes. (c) 2005 Elsevier Inc. All rights reserved.
- ItemEffects of early decrease in oxidative stress after medical therapy in patients with class IV congestive heart failure(EXCERPTA MEDICA INC, 2002) Castro, PF; Diaz Araya, G; Nettle, D; Corbalan, R; Perez, O; Nazzal, C; Larrain, G; Lavandero, SIt has been reported that patients with congestive heart failure (CHF) have increased breath pentane content, conjugated diene levels, and plasma malondialdehyde (MDA) levels, an indirect marker of lipid peroxidation.(1-3) Ghatak et al(4) found that patients with chronic CHF had increased MDA and superoxide levels, which correlated with the severity of the CHF. Low glutathione levels and superoxide dismutase (SOD) activity have also been reported.(5,6) There have been no studies in human refractory CHF to evaluate the impact of acute intensive medical therapy on oxidative stress status and antioxidant enzyme activity. We determined the plasma levels of MDA, SOD, catalase (CAT), and glutathione peroxidase (GSH-Px) activities before and after therapeutic intervention in patients with chronic advanced CHF and refractory symptoms (New York Heart Association functional class IV).
- ItemPerindopril regulates beta-agonist-induced cardiac apoptosis(LIPPINCOTT WILLIAMS & WILKINS, 2005) Galvez, AS; Fiedler, JL; Ocaranza, MP; Jalil, JE; Lavandero, S; Diaz Araya, GAdministration of the P-adrenergic agonist isoproterenol results in cardiac apoptosis. The effect of short-term P-adrenergic stimulation by isoproterenol on the activity of plasma, lung, and left ventricular (LV) angiotensin 1-converting enzyme (ACE) activity and its association with the development of cardiac apoptosis was investigated. P-Adrenergic stimulation for 24 hours produced an early increase only in the proapoptotic proteins bax and bcl-XS without changes in the levels of the antiapoptotic protein bcl-XL. The ratio between these bcl family proteins was indicative of apoptosis and correlated with an early and significant increase (300%) in DNA laddering. However, after 5 days of the P-adrenergic stimulation, the ratio changed in favor of antiapoptotic proteins and correlated with the absence of DNA fragmentation. In addition, LV and plasma ACE activities increased markedly with isoproterenol over the study period up to 5 days. ACE activity also regulated expression of the antiapoptotic gene bcl-XL. The administration of perindopril (an ACE inhibitor) prevented the observed increase in bax and bcl-XS levels and attenuated (50% decrease, P < 0.05) the effect of isoproterenol on DNA fragmentation. Thus, early and transient cardiac apoptosis triggered by the beta-adrenergic agonist isoproterenol is reversed in the presence of perindopril.
- ItemPolymorphism in gene coding for ACE determines different development of myocardial fibrosis in rats(AMER PHYSIOLOGICAL SOC, 2004) Ocaranza, MP; Diaz Araya, G; Carreno, JE; Munoz, D; Riveros, JP; Jalil, JE; Lavandero, SIn humans, the effect of angiotensin-converting enzyme (ACE) gene polymorphisms in cardiovascular disease is still controversial. In the rat, a microsatellite marker in the ACE gene allows differentiation of the ACE gene polymorphism among strains with different ACE levels. We tested the hypothesis that this ACE gene polymorphism determines the extent of cardiac fibrosis induced by isoproterenol (Iso) in the rat. We used a male F-2 generation (homozygous LL and BB ACE genotypes determined by polymerase chain reaction) derived from two rat strains [Brown-Norway (BB) and Lewis (LL)] that differ with respect to their plasma ACE activities. For induction of left ventricular (LV) hypertrophy (LVH) and cardiac fibrosis, rats were infused with Iso (5 mg.kg(-1).day(-1)) or saline (control) for 10 days and euthanized at day 1 after the last injection. The interstitial collagen volumetric fraction (ICVF), collagen I, and fibronectin content, but not collagen III content, were significantly higher in the homozygous BB rats than in homozygous LL rats. Differences in metalloprotease (MMP)-9, but not in MMP-2 activities as well as in cardiac cell proliferation, were also detected between LL and BB rats treated with Iso. LV ACE activity was higher in BB rats than LL rats and correlated with ICVF (r=0.61, P<0.002). No changes were observed in plasma ACE activities, ANG II plasma or LV levels, plasma renin activity, and ACE and ANG II type 1 receptor (AT1R) mRNA levels in the LV of rats with the two different ACE polymorphisms. Iso induced a similar degree of LVH [assessed by an increase in LV weight 100 per body weight, LV-to-right ventricle (RV) ratio, and LV protein content] in LL and BB rats. We concluded that rats in the F-2 generation with high plasma ACE activity developed more fibrosis but to a similar degree of LVH compared with rats with low plasma ACE activity.