PubMed Health⌕ Search

Biomedical subjects

J Milei

Publications and source records attributed to J Milei.

At least 73 records · Page 4Linked to original sources
PubMed1985

Comparison of lipid peroxidation and myocardial damage induced by adriamycin and 4'-epiadriamycin in mice.

Adriamycin (ADM) and 4'-epiadriamycin (4'-ADM) were given to mice in a single dose of 15 mg/kg body weight (i.p.). Twenty-five mice were alloted to 3 groups. One group (Group I; n = 8) was given ADM; another group (Group II; n = 9) was similarly treated with 4'-ADM, and a control group (n = 8) received an equivalent volume of 0.9% NaCl solution. Mice were sacrificed 4 days after the described treatment. A complete autopsy was carried out in each animal. Hydroperoxide-initiated chemiluminescence and malonaldehyde formation were measured in mouse heart homogenates. Control mice showed a maximal photoemission of 52 +/- 2 (X 10(-3)) (mean values +/- S.E.M.) cpm/mg protein and a formation of 20 +/- 4 nmol malonaldehyde/g organ after a 2 hr-incubation. The ADM-treated mice showed a 24% enhanced hydroperoxide-initiated photoemission and a 370% increased malonaldehyde formation. The 4'-ADM-treated mice showed a 15% increased hydroperoxide-stimulated chemiluminescence and an 85% increased malonaldehyde formation. Vitamin A (5000 IU), vitamin E (85 IU) and vitamins A and E (same doses as before) given as a single dose i.p. 1 day before doxorubicin administration were able to decrease the hydroperoxide-initiated chemiluminescence by 24%, 26% and 44%, respectively. Microscopically, only scarce isolated microvacuolated subendocardial fibers were found in the ADM-treated animals. Our data showing that 4'-ADM lacks a statistically significant effect in increasing heart peroxidation as compared to ADM may explain its lower myocardial toxicity.

Animals↗
PubMed1985

Muscle fiber disarray in patients without hypertrophic cardiomyopathy.

Muscle fiber disarray (MFD) has been described as the histologic feature of hypertrophic cardiomyopathy (HC), but it was also found in normal and other abnormal conditions. Its distribution related to the topography of the myocardium has not been described. In this paper, the incidence of MFD in hearts free from HC, the frequency of the histologic disorganization and the affected muscles involved were studied at autopsy. 29 hearts with acute myocardial infarction and 1 with suppurated myocarditis were employed. Macroslides containing the point of maximum septal enlargement were selected for histological examination. The areas of MFD were measured by a polar planimeter and correlated with the involved wall, the total slice area, parietal widths and involved muscles. 27 patients (90%) presented with MFD; hypertrophic ventricular walls were observed in 10, 8 of which had MFD. The remaining 20 patients with nonhypertrophic ventricular walls had MFD in 19 instances. There was septal posterior involvement in 26 cases (p less than 0.0005). 12 patients (44.4%) had only one wall involved. Only 1 patient presented more than 5% of MFD in regard to the total area. The septal wall was the most affected (p less than 0.0005). The most commonly affected muscle was the deep-sinospiral, either alone or combined with other muscles (p less than 0.01). Greater MFD was found (23/30) in patients with septum/posterior wall ratio less than 1.3 cm. It is concluded that MFD may affect up to 10% of the septum in patients free from HC, and that secondary hypertrophy is not a prerequisite for MFD.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Prenylamine inhibition of adriamycin-induced myocardiopathy.

Adriamycin (ADM) is an effective antineoplastic drug. However, ADM induces alterations in cardiac function which limit the safe dose which can be administered. As it was suggested that ADM-induced cardiomyopathy is related to a calcium mediated necrosis and/or an increase in lipid peroxidation, the cardioprotective potential of prenylamine (PNL) (a well known calcium antagonistic drug) was evaluated in rabbits given chronically large doses of ADM. Twenty five rabbits were allotted to 4 groups. Group I (PNL-ADM) was given 334 +/- 82 mg of PNL and 12.2 +/- 3.8 mg of ADM, group II (water-ADM) 14.4 +/- 4.6 of ADM, group III (PNL-saline) 280 +/- 91 mg of PNL and group IV (water-saline), same doses as ADM and PNL. Rabbits were sacrificed between 38 and 65 days after the beginning of the trial. In group I weight increased only 13% and in group II, 39% (p less than 0.01). Correlation coefficients were significant for variations of weight and ADM-doses (r = 0.875). In group II 8/10 rabbits showed post-treatment electrocardiographic changes, while group I changes were found in a lesser extent (5/10). Heart homogenates from ADM-treated rabbits showed an increased lipoperoxidation (74 +/- 5 cpm/mg protein X 10(-3) as compared with the control animals (58 +/- 6 cpm/mg protein X 10(-3) (p less than 0.05), while PNL treatment did not alter myocardial lipoperoxidation. Microscopically, myocardial fibers had from mild to severe hydropic vacuolization of sarcoplasm which led to progressive myocytolysis. Myocardial damage was lower in group I (ADM-PNL), 41.7 +/- 7.6 than in group II (water-ADM), 104 +/- 10.8 (p less than 0.05). It is suggested that ADM-peroxidation effects lead to lipoperoxidation with membrane damage and increase in Ca++ permeability, the latter being counteracted by PNL.

Animals↗
PubMed1984

Chronic Chagas' myocardiopathy. Demonstration of in vivo bound immunoglobulins in heart structures by the immunoperoxidase technique.

Chagas' disease (CHDis) has been described as the commonest form of chronic myocarditis. Although autoimmune phenomena involving the myocardium have been suggested in both human and experimental CHDis, no immunoperoxidase techniques have been used for the detection of immunological deposits in chronic Chagas' myocardiopathy (ChrCHM). The goal of this paper was to show that there is a coincidence between the immunoperoxidase and the immunofluorescence techniques in evidencing autologous deposits in ChrCHM. 4 patients suffering from ChrCHM were selected; their ages ranged from 39 to 52 years (means: 48.5 years). The Shültze and Caves endocavitary bioptome via the right internal jugular vein was used to obtain 3 to 4 right endomyocardial specimens measuring 1-2 mm each. Direct immunofluorescence examination, immunoperoxidase technique (PAP), and routine histological procedure were performed in all cases. Agreement between immunofluorescence and immunoperoxidase techniques was present in all chagasic specimens studied. Patients suffering from ChrCHM showed deposits of IgG, IgA, IgM, and C3 at the interstitial area, capillaries and endocardium and/or myocardial fiber surfaces when serum EVI antibody was positive. Serum EVI antibody was found to be positive in 3 out of 4 patients. The presence of the complement together with immunoglobulin may suggest an immune reaction (in vivo bound immunoglobulins in heart structures) and not just a passive deposition secondary to myocardial damage. As EVI antibody is present to a significant extent in CHDis, a reliable and simple technique like immunoperoxidase may be helpful to clarify the role of these antibodies in the pathogenesis of CHDis.

Adult↗
PubMed1984

Effects of lorcainide and amiodarone on stress-induced myocardial damage in the rat.

This paper is concerned with the effects of Lorcainide (LCN) and Amiodarone (AMD) on stress-induced myocardial lesions in rats. Forty rats were used. The first group (G-1) was used as a control (n = 10) and animals were injected with saline. Animals in group 2 (G-2) (n = 15) received AMD 10 mg per kilogram, and animals in group 3 (G-3) (n = 15) received LCN 3 mg per kilogram. During five minutes before the injections, the rats were submitted to a stress, consisting of intermittent cold water jets (6 degrees C). Animals were sacrificed one hour after injection, and the hearts were histologically studied. The relative areas of necrotic myocardium were assessed by Bertazzoli's modified method. In G-1, myocytolysis in the subendocardium of left ventricle (score: 2.2 +/- 0.79), contraction bands (1.2 +/- 1.03) and subendocardial myocardial damage (0.8) were common findings. In groups G-2 and G-3, the lesions described were found, but to a lesser degree; subendocardial myocytolysis: 1.6 +/- 0.63 and 1.07 +/- 0.4; contraction bands: 0.67 +/- 0.82 and 0.07 +/- 0.26; and subendocardial damage: 0.77 and 0.40. LCN and AMD markedly decreased stress-induced myocytolysis (p less than 0.01) (graph 1), but LCN was more effective than AMD (p less than 0.05). Comparison of severity and extension of contraction bands showed that only LCN had a significant effect (p less than 0.01) (graph 2); the same was observed as regards the decrease of damaged zones (p less than 0.05). From our data, LCN and AMD appears to have the capacity of reversing some of the stress-induced myocardial damage in rats.

Amiodarone↗
PubMed1984

Hemodynamic changes produced by molsidomine in patients with congestive myocardiopathy.

The hemodynamic effects of a new drug: molsidomine (M) were evaluated in 9 patients with congestive myocardiopathy. To that end, with a 4-channel Swan-Ganz catheter and cardiac output computer, the following hemodynamic parameters were measured in the control condition (CC) and 5, 15 and 30 minutes after sublingual administration of 4 mg of M: heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and the stroke work index (SWI). Comparing the data in CC and at the end of the study, we found a decrease of 80 +/- 5 to 76 +/- 5 b/m (p less than 0.01) in HR, of 91 +/- 4 to 84 +/- 4 mmHg (p less than 0.01) in MAP and of 3087 +/- 151 to 2758 +/- 131 d/c/s-5 in SVR (p less than 0.02); a drop in PWP of 27 +/- 3 to 20 +/- 3 mmHg (p less than 0.001) and in PVR of 1367 +/- 293 to 1115 +/- 256 d/c/s-5 (p less than 0.001); an increase in SVI of 31 +/- 3 to 34 +/- 2 ml/b/m2 (p less than 0.05) and non-significant changes in CI of 2380 +/- 96 to 2459 +/- 82 ml/m2 (p less than 0.03) and in the SWI of 34 +/- 4 to 37 +/- 4 gm/m2 (p less than 0.1). We conclude that in patients with severe heart failure, the fundamental effects of M appears to be vasodilation in both pulmonary and systemic circulations demonstrated by a fall in PWP, PVR, MAP and SVR together with a mild increase in SVI without significant changes in CI and SWI.

Adolescent↗
PubMed1983

A routine method for diagnosis of early myocardial infarction.

We compared Barbeito-Lopez Trichrome stain with H-E, the basic fuchsin picric acid and Nitro Blue of Tetrazolium stains. The Barbeito-Lopez Trichrome stain was much more sensitive than the other stains for the diagnosis of early myocardial coagulation necrosis.

Animals↗
PubMed1983

Long term-treatment of ventricular tachycardia in ambulatory patients with amiodarone.

The antiarrhythmic effects of amiodarone hydrochloride 200 to 600 mg/daily were studied in 25 patients with ventricular tachycardia (VT). The arrhythmia was registered on a 24 hours two channel Holter recording. This study was performed before and after one month treatment with the drug. The adequate suppression of the VT was observed in 25 patients. The drug showed a total suppression of ventricular ectopic activity in 10 patients (40%) (4 at a dose of 200 mg/daily, 5 at 400 mg/daily and 1 at 600 mg/daily) and a satisfactory reduction (total suppression of couplets and VT and more than 85% reduction of premature ventricular beat frequency) in 12 patients (48%) (6 at a dose of 200 mg/daily, 5 at a dose of 400 mg/daily and 1 at a dose of 600 mg/daily). After a mean follow up of 15.9 months on continuous amiodarone therapy there have been no recurrences of arrhythmia on Holter recordings. No patient died during the study. Side effects were minimal and limited to corneal microdeposits at slit lamp examination without impairment of visual acuity. According to our results amiodarone is an excellent and safe agent for the treatment of complex ventricular arrhythmias.

Adult↗