El aumento de la actividad y expresión de la enzima convertidora de angiotensina I homóloga (ECA2) inducido por enalapril se asocia a menor fibrosis e hipertrofia ventricular izquierda post infarto al miocardio en la rata / Enalapril induced increase in Homologous Angiotensin I converting enzyme (ECA2) is associated to decreased fibrosis and decreased left ventricular hypertrophy post myocardial infarction in rats

Recientemente se ha descubierto el gen de una nueva enzima convertidora de angiotensina I- homóloga a ECA y denominada ECA-2 que finalmente lleva a producir angiotensina 1-7. Esta segunda vía del sistema reninaangiotensina (SRA), con la ECA-2 tendría acciones opuestas a la ECA. Objetivo y Métodos: Determinar la actividad y expresión de la ECA2 en el tratamiento de la hipertrofia y fibrosis ventricular izquierda tardía post IAM en la rata. Se usaron ratas Sprague Dawley 200 +/- 10 g sometidas a ligadura de la coronaria izquierda. Como controles se usaron ratas sham (S). 48 hrs. post cirugía, un grupo de ratas IAM recibió enalapril (IAM-ENA; 10 mg/kg, gavage). A las 8 semanas post-operatorias se determinó la presión arterial sistólica (PAS), masa corporal(MC), masa cardíaca relativa (MCR, mg VI/100 g MC, expresión proteica de la cadena pesada de la miosina beta(betaMHC) por Western blot, mRNA por RT-PCR, las actividades enzimáticas de ECA y de ECA-2 por fluorimetría tanto circulante como en ventrículo izquierdo (VI), el contenido de colágeno total por rojo picrosirio y la actividad de metaloproteasa 2 (MMP-2) por zimografía. Conclusión: El aumento de la actividad y expresión de la ECA2 (a nivel circulante y tisular cardíaco) se asocia a menor fibrosis e hipertrofia ventricular izquierda, lo que podría aumentar – en ese periodo - el efecto cardioprotector de Ang-(1-7).

Background. Recently the gene of a new angiotensin-1 converting homologous enzyme (ACE-2) which leads to the production of angiotensin 1-7 (Ang (1-7) has been reported. This new pathway of the renin-angiotensin system(RAS) is supposed to have opposite effects to those of ACE. Aim: To determine the activity and expression of ACE-2 in the development of left ventricular hypertrophy and fibrosis late after induced myocardial infarction (AMI) in rats. Methods: 200 +/- 10g Sprague-Dawley rats were submitted to left coronary artery ligation. Sham operated rats were used as controls. 48 hr after surgery, one group of AMI rats received enalapril (AMI-En), 10mg/Kg. 8 weeks after surgery the systolic blood pressure (SBP), body mass (BM) and relative cardiac mass (RCM, mg/100g BM) were measured. The protein expression of heavy weight chain beta myosin (beta HCM) was determined by Western Blot, mRNA through RT-PCR, circulating and left ventricular ACE and ACE-2 activities through fluorometry, total collagen content by the pycrosirius red method and metaloproteinase-2 (MMP-2) through zymography were determined. Conclusion: The increased activity and expression of ACE-2 both in plasma and the LV is associated to less fibrosis and left ventricular hypertrophy after AMI. This could temporarily boost the cardioproctive effect of Ang (1-7).

Mitochondrial oligomycin-sensitive ATPase during isoproterenol-induced cell injury of myocardium

En el presente trabajo se investigó la actividad enzimática de la ATPasa mitocondrial sensible a la oligomicina durante una lesión celular del miocardio inducida por el isoproterenol, usando homogenados de corazón de rata y una técnica potenciométrica. La actividad enzimática de la ATPasa mitocondrial sensible a la oligomicina, al igual que la acción inhibidora de la oligomicina sobre esta enzima, no muestra alteraciones significativas durante el tratamiento con isoproterenol. Estos resultados no concuerdan con la hipótesis sobre posibles modificaciones en la configuración activa de la ATPasa mitocondrial durante una lesión celular del miocardio inducida por el isoproterenol.

Effect of smoking on myocardial enzymes and some haematological parameters

Effects of cigarette smoking on healthy and cardiac ptients were evaluated by studying myocardial enzyme profiles and some selected haematological parameters. The smokers, whether normal or cardiac patients, had relatively higher values of Hb. conc., [13.90g/dL], ESR [11.05 mm/hr] and TLC [7102 per cu mm]. Similarly, Neutrophil and Eosinophil counts [65% and 2.6% respectively] were found elevated in smokers. Myocardial enzymes, such as, LDH, CK-MB, GOT were found maximally raised [mean as 295.68, 68.21, 21.08, 35.86 and 68.92 U/L respectively] in exclusively the cardiac patients who also smoked. Moreover, cholesterol levels were also highest for cardiac smoker patients. The statistical analysis revealed the evaluation as significant [P<0.01, P < 0.05] Thus, the smoking was identified as a significant risk factor among normal individuals as well as those with myocardial complaints