The effects of enalapril on p53 expression in left ventricular cardiomyocytes after aortic stenosis.

ACE-inhibitors prevent the development of left ventricular hypertrophy (LVH). The tumor suppressor gene p53 up-regulates the cellular renin-angiotensin system, resulting in ANG II synthesis, which activates p53 creating a positive feedback loop. One hundred and fourteen rabbits were separated into groups A (control), B (sham-operated), C and D.

Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy.

Background: Left atrial systolic dysfunction, unexplained by altered loading conditions, has been reported in idiopathic dilated cardiomyopathy suggesting left atrial involvement in the myopathic process.

Materials And Methods: Seventeen patients with idiopathic dilated cardiomyopathy, 16 with ischemic dilated cardiomyopathy and 18 normal controls were studied with transthoracic echocardiography and cardiac catheterization. Transmitral diastolic flow was evaluated with pulsed Doppler.

Antioxidant agent nimesulid and beta-blocker metoprolol do not exert protective effects against rat mitochondrial DNA alterations in adriamycin-induced cardiotoxicity.

Possible protective effects of two therapeutical agents (nimesulid and metoprolol) in adriamycin-induced cardiotoxicity were examined in rat cardiomyocytes at the mitochondrial DNA (mt DNA) level. Analysis by PCR revealed the presence of multiple deletions in a large region of the long arc of mt DNA which codes for several important genes involved in oxidative phosphorylation, in all animals under drug administration. No differences were found in the frequency of defective mt DNA between the animals that received only adriamycin (83%, 10/12), nimesulid and adriamycin (92%, 13/14), or metoprolol and adriamycin (80, 12/15) (p = 0.

Atrial natriuretic peptide levels during and after acute cardiac tamponade in dogs.

The ability of the atrial wall to secrete atrial natriuretic peptide was studied in eight dogs during 2 h of cardiac tamponade and for 2 h after decompression of the pericardium. Cardiac tamponade was induced by instillation of 5% dextrose in water into the pericardial cavity until aortic systolic pressure was reduced by 30% to 35%. Heart rate, cardiac output and atrial, pericardial and aortic pressures were measured at 60 and 120 min of tamponade and at 5, 30, 60, 90 and 120 min after decompression.