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Biomedical subjects

M G Gomes

Publications and source records attributed to M G Gomes.

6 recordsLinked to original sources
PubMed1999

Black-eye patterns: a representation of three-dimensional symmetries in thin domains.

What is believed to be the first experimental evidence for Turing patterns was observed in the CIMA reaction by De Kepper and colleagues. Ouyang and Swinney performed further experiments in a "thin" layer of gel. Patterns observed at onset were basically two-dimensional. However, beyond onset a structure that does not typically occur in two-dimensional domains was observed-the black-eye pattern. In this paper we use the full three-dimensionality of the patterned layer to find a setting where black-eye patterns naturally occur. We propose that black-eye patterns have the symmetry of a body-centered-cubic lattice.

Journal Article↗
PubMed1997

Effects of captopril on interstitial collagen in the myocardium after infarction in rats.

BACKGROUND: Myocardial infarction is an important cause of heart failure because it cause tissue loss and contractility disturbances. In chronically infarcted hearts the increase in the collagen content in the extracellular matrix of the surviving viable myocardium has been considered a major factor contributing to development of heart failure. Postinfarction neuroendocrine activation involving the renin-angiotensin system has been implicated in this cardiac fibrosis. METHODS AND RESULTS: As collagen synthesis and degradation are dynamic processes and postinfarction remodeling is a time-dependent phenomenon, rats submitted to coronary artery ligation to produce myocardial infarction were treated with captopril after infarction (30 mg/kg, intraperitoneally, daily) to investigate whether blockade of the renin-angiotensin system can prevent postinfarction myocardial hypertrophy and reactive fibrosis. Groups of rats with myocardial infarction were treated with captopril throughout the protocol period (6 weeks), or during the first 3 weeks after infarction (early therapy), or only during the last 3 weeks of the protocol (late therapy). Untreated groups of rats with or without myocardial infarction were used as control subjects. All animals were killed 6 weeks after surgery to evaluate hypertrophy of heart chambers and collagen deposition in the right ventricle wall and in surviving left ventricular muscle. Protein and hydroxyproline concentrations were assayed biochemically in these tissue homogenates. Only rats with an infarct covering 20 to 40% of the left ventricular surface were included in the study. In the control uninfarcted group (n = 12), hydroxyproline content was 152 +/- 12 micrograms in the right ventricle and 370 +/- 30 micrograms in the left ventricle. These values increased (P < .05) to 232 +/- 13 and 630 +/- 46 micrograms, respectively, in the group with myocardial infarction (n = 8) without treatment. These values were significantly reduced (P < .05) to 160 +/- 9 micrograms in the right ventricle and 520 +/- 40 micrograms in the left ventricle in the group with myocardial infarction treated with captopril for 6 weeks. The percentage decreases in collagen content and myocardial weight produced by captopril were similar. Thus, hydroxyproline concentration (mg hydroxyproline muscle), which increases significantly in both ventricles after myocardial infarction, was not modified by captopril therapy. Protein concentration in the right and left ventricular muscles decreased after myocardial infarction. This decrease was enhanced in the infarcted groups submitted to captopril treatment, mainly in the group treated for 6 weeks. Lesser effects on hypertrophy and hydroxyproline content were observed in the groups of rats treated with captopril in only the earlier or later phase of infarction. CONCLUSIONS: It is concluded that captopril reduces similarly postinfarction hypertrophy and collagen deposition in surviving myocardium. These effects, although less intense, also occur when the drug is used for a short period immediately after myocardial infarction or when used later, when ventricular remodeling is almost fully developed.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Changes in collagen content in the residual myocardium surviving after infarction in rats. Influence of propranolol or hydralazine therapy.

The changes occurring in the collagen content in the residual myocardium after infarction have been poorly studied. The aim of this study was to determine the changes in the collagen content in the right and left ventricular muscle of chronically infarcted hearts. Male albino rats were submitted to ligature of the left coronary artery to produce infarction (Inf). Controls underwent a sham surgery (Sh). Inf rats were divided into groups designed to receive chronic therapy with propranolol (Prop, 1 g/l, n = 10) or hydralazine (Hydr, 0.125 g/l, n = 10) dissolved in the drinking water. One group of Inf rats (n = 12) and the Sh group (n = 10) received no treatment. The animals were killed 1 month after surgery to obtain the cardiac wet weights and to determine protein and hydroxyproline (OH-Pro) concentrations in the right ventricle (RV) free wall and in the left ventricular remaining muscle (LV), including the interventricular septum. Inf determined a 42% increase of the RV weight to body weight ratio (Sh = 0.57 +/- 0.04 mg/g; Inf = 0.81 +/- 0.06 mg/g; p < 0.05) and a 64% increase of OH-Pro concentration (Sh = 450 +/- 25 micrograms/g; Inf = 738 +/- 32 micrograms/g; p < 0.05). In Inf hearts the LV OH-Pro concentration increased similarly as in the RV. No effect of drug therapy was observed in the LV. In the RV however, propranolol reduced the hypertrophy and the OH-Pro concentration by the same amount (around 30%). Hydr on the other hand reduced OH-Pro and tended to increase hypertrophy. We conclude that a similar collagen deposition occurs in the myocardium of both ventricles after infarction in rats. Prop and Hydr were able to partially reduce this collagen increase in the right but not in the left ventricle.

Animals↗
PubMed1994

Effects of aluminum on the mechanical and electrical activity of the Langendorff-perfused rat heart.

The effect of aluminum (Al3+) chloride (1, 5, 10, 50 and 100 microM) on myocardial electromechanical activity was studied in 10 Langendorff-perfused hearts from adult female Wistar rats. Al3+ decreased the development of isovolumic systolic pressure from 34.3 +/- 2.95 mmHg under control conditions to 11.8 +/- 1.53 mmHg at 100 microM AlCl3 (P < 0.01) (diastolic pressure = 0 mmHg). The atrial and ventricular rates also decreased, but only with AlCl3 concentrations greater than 1 microM (from 180 +/- 5 to 94 +/- 11 bpm for atrial rate and from 180 +/- 5 to 78 +/- 7 bpm for ventricular rate). Reduction of coronary flow was also observed, reaching 60% at 100 microM Al3+. A delay in atrioventricular conduction occurred at 10 microM Al3+, increasing progressively up to 100 microM (62.3 +/- 4 ms in the Al(3+)-free solution to 143 +/- 34 ms in the presence of 100 microM Al3+, P < 0.01, ANOVA). QRS duration did not change as a function of increasing Al3+ concentrations (37.1 +/- 1.7 ms in the Al(3+)-free solution vs 32.1 +/- 1.6 ms in the presence of 100 microM Al3+). No qualitative changes in ECG were observed. These data show that the toxic effects of Al3+ on the myocardium are reflected in reduced systolic pressure development and coronary flow and increased PR interval. These effects are discussed in terms of the inhibition of nucleotide hydrolysis by Al3+.

Aluminum↗
PubMedDate not supplied

Influence of chronic captopril therapy on the mechanical performance of the infarcted rat heart.

The influence of angiotensin converting enzyme inhibition of hemodynamic changes, development of postinfarction myocardial hypertrophy and left ventricular performance was studied in rats. Infarction was produced under ether anaesthesia by ligature of the descending anterior branches of the left coronary artery. Control rats were submitted to a sham surgery. Groups of infarcted (Inf) and sham-operated control (SO) animals were daily treated with intraperitoneal injections of captopril (Cap, 30 mg kg-1) or saline (Sal) for 4-5 weeks. This Cap dose produced a similar decrease in arterial blood pressure in Inf and SO animals. The intraventricular pressures measured in anaesthetized rats showed a marked elevation in the right ventricular systolic (38 +/- 4 mmHg) and end diastolic (4 +/- 1 mmHg) pressures in the Inf group compared with the SO group (24 +/- 1 mmHg and 1 +/- 0.4 mmHg, respectively). Cap did not change the pressure overload in the right ventricle. In the left ventricle, however, the end diastolic pressure of the Inf group under Cap was significantly reduced in relation to Sal (12 +/- 3 mmHg and 19 +/- 2 mmHg, respectively, P < 0.05). The post infarction myocardial hypertrophy was depressed by Cap only in the right heart chambers. Thus the right ventricular weight to body weight ratio (mg/g) increased from 0.56 +/- 0.03 in the SO-Sal group to 0.96 +/- 0.07 (P < 0.05) in the Inf-Sal group and decreased to 0.73 +/- 0.04 (P < 0.05) in the Inf group under Cap. The infarction-induced hypertrophy of the left heart chambers was unaffected by Cap. Left ventricular function was assessed in the hearts perfused in vitro according to the Langendorff technique. The peak isovolumic systolic pressure (ISP) developed at different diastolic pressures (0-30 mmHg) and Ca2+ concentrations (0.62 and 1.25 mM) was measured. The ISP and the positive inotropic response to Ca2+ was similarly depressed in both groups of infarcted hearts. Thus the chronic administration of Cap to Inf rats reduces the left ventricular filling pressure but does not reduce the postinfarction pulmonary hypertension. Despite this latter finding, Cap therapy was able to significantly reduce the post-infarction hypertrophy in both right heart chambers. Cap therapy did not change significantly left ventricular systolic function and Ca2+ responsiveness of the myocardium surviving to infarction.

Animals↗