123 resultados para heart muscle necrosis


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Inotropic effects of Propafenon were studied in isovolumic isolated guinea pig hearts submitted to infusion of the drug during 10 minutes. The dosages utilized caused: bradycardia, depression of AV nodal conduction and QRS widening. Simultaneously there was: decrease of the developed pressure (DP) and of the rate of rise of pressure (dp/dt), and elongation of the time of peak pressure. Since there was no clear relation between the heart rate and the inotropic indices (PD and dp/dt), it could be supposed that the depressor effect was not due to impairment of the chronotropism only. After the infusion of Propafenon, the chronotropic effect disapeared after 15 min, while the inotropic state presented a less satisfatory recuperation. The coronary output accompanied the myocardial metabolic needs, that is to say, there was a fall during the period of depressed cardiac function and a later tendency to increase during recovery.

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The relationship between coronary sinus blood oxygen tension (CSPO 2) and myocardial oxygen tension (MPO 2) variations during cardiac ischemia and reperfusion was studied in anesthetized open-chest dogs. Oxygen tension was measured by a polarographic method. Ischemia resulted in a slightly decreased CSPO 2 and a more pronounced reduction of MPO 2. After reperfusion the CSPO 2 rose rapidly and transiently before it returned gradually to the control level. By contrast, during the recovery period, the MPO 2 increased slowly, with recovery occurring long after the peak of CSPO 2. These data suggest that during the reperfusion phase, the CSPO 2 variation is probably due to opening of the myocardial arteriovenous shunts instead of an increase of flow through the myocardial capillary bed.

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The rate removal of nickel from the airway was measured in vivo. Removal in vivo was studied by intratracheal injection of nickel chloride solutions. Regardless of time after injection, the lungs and heart retained the greatest concentration of nickel and 40 days after 1.68 mumol administration they were the organs where nickel was still significantly measurable. The slow removal of nickel may indicate the presence of high affinity binding sites in the lung. Nickel can interact with others metals, such as copper and zinc, so that nickel exposure may have public health implications.

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This work was conducted aiming to evaluate the effect of dietary energy level and the previous heat exposure on the respiratory activity of the mitochondria from the cardiac muscle of broiler chickens. It was used broiler chickens (Hubbard) from both sexes and fed with diet containing 2900 kcal ME/kg or 3200 kcal ME/kg. The birds were heat stressed (35°C/4h) in the 1 st, 21 st and 42 nd days of age. The respiratory activity of mitochondria from cardiac muscle was evaluated in a Gilson oxygraph, model 5/6, by using alpha-ceto-glutaric as substrate and the ADP (adenosine-di-phosphate) to stimulate the respiratory activity. There was not effect of dietary energy level and previous heat exposure on the respiratory activity of the mitochondria from cardiac muscle. However, the females presented higher respiratory activity than males. By reason of the low oxidative capability of the heart muscle fiber of the male broiler chickens, these could be more sensitive to cardiac disease than females.

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Silent period was evaluated in 20 adult male patients with chronic renal failure undergoing hemodialysis. Readings were obtained by supramaximal stimulus to the median nerve, during maximum isometric effort of the abductor pollicis brevis muscle against resistance. Two types of abnormalities were observed, motor neuron hypoexcitability with elongated silent period, and motor neuron hyperexcitability with reduction or absence of silent period. Some abnormalities are probably linked with dialysis duration, but show no correlation to presence or absence of peripheral neuropathy. The silent period alterations described in this study could possibly correlate with some other clinical feature frequently seen in patients with chronic renal failure such as hypereflexia of the deep tendon reflexes.

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The aim of this study was to test the hypothesis that protein-calorie undernutrition decreases myocardial contractility jeopardizing ventricular function, and that ventricular dysfunction can be detected noninvasively. Five-month-old male Wistar-Kyoto rats were fed with regular rat chow ad libitum for 90 days (Control group, n = 14). A second group of rats received 50% of the amount of diet consumed by de control group (Food restricted group, n = 14). Global LV systolic function was evaluated in vivo, noninvasively, by transthoracic echocardiogram. After echocardiographic study, myocardial contractility was assessed in vitro in the isovolumetrically beating isolated heart in eight animals from each group (Langendorff preparation). The in vivo LV fractional shortening showed that food restriction depressed LV systolic function (p < 0.05). Myocardial contractility was impaired as assessed by the maximal rate of rise of LV pressure (+dP/dt), and developed pressure at diastolic pressure of 25 mmHg (p < 0.05). Furthermore, food restriction induced eccentric ventricular remodeling, and reduced myocardial elasticity and LV compliance (p < 0.05). In conclusion, food restriction causes systolic dysfunction probably due to myocardial contractility impairment and reduction of myocardial elasticity. © 2002 Elsevier B.V. All rights reserved.

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Purpose: To determine the effect of dietary restriction on metabolic pathways and the relationship of the metabolic shifting on antioxidant enzymes in cardiac tissue. Design: Randomized, controlled study. Male rats at 60 days old were randomly divided into four groups. Materials and Methods: The rats of control groups C30 and C60 were given free access to the diet over 30 and 60 days. The rats of the DR30 group were fed 60% of the chow consumed by the control groups over 30 days. The animals of the DR60 group ate 60% of the amount consumed by the C60 group over 60 days. Serum was used for total protein, lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Protein, glycogen, total lipids, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), LDH, AST and ALT were determined in cardiac tissue. Results: Dietary restriction induced diminished serum and cardiac LDH activities. AST activities were lower in the serum and cardiac muscle of the DR60 animals. Dietary restriction induced elevated total lipid concentrations in cardiac muscle. No significant differences were observed in total protein and glycogen content among the groups. Antioxidant enzyme determinations demonstrated increased cardiac GSH-Px activities in the DR60 animals and increased SOD activities in the cardiac tissue of both feed-restricted groups. Conclusions: Dietary restriction was protective against oxidative stress in the heart by improving cardiac endogenous antioxidant defences and shifting the metabolic pathway for energy production.

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Dietary modification ought to be the first line of strategy in prevention of the development of cardiac disease. The purpose of this study was to investigate whether dietary restriction, dietary-fibre-enriched diet, and their interactions might affect antioxidant capacity and oxidative stress in cardiac tissue. Male Wistar rats (180-200 g; n = 10) were divided into four groups: control ad libitum diet (C), 50% restricted diet (DR), fed with fibre-enriched diet (F), and 50% restricted fibre-enriched diet (DR-F). After 35 days of the treatments, F, DR, and DR-F rats showed low cholesterol, LDL-cholesterol, and triacylglycerol, and high HDL-cholesterol in serum. The DR, DR-F, and F groups had decreased myocardial lipoperoxide and lipid hydroperoxide. The DR-F and F treatments increased superoxide dismutase and glutatione peroxidase (GSH-Px). The DR treatment increased GSH-Px and catalase activities. Dietary fibre beneficial effects were related to metabolic alterations. The F and DR-F groups showed high cardiac glycogen and low lactate dehydrogenase/citrate synthase ratios, indicating diminished anaerobic and elevated aerobic myocardial metabolism in these animals. There was no synergistic effect between dietary restriction and dietary fibre addition, since no differences were observed in markers of oxidative stress in the F and DR-F groups. Dietary fibre supplementation, rather than energy intake and dietary restriction, appears to be the main process retarding oxidative stress in cardiac tissue.