Biomedical subjects

J A Duarte

Publications and source records attributed to J A Duarte.

10 recordsLinked to original sources

PubMed1994

Do invading leucocytes contribute to the decrease in glutathione concentrations indicating oxidative stress in exercised muscle, or are they important for its recovery?

Mice were subjected to one session of strenuous running exercise and their soleus muscles were examined in respect of changes in ultrastructure and to their concentration of reduced glutathione [GSH] which are indicators of oxidative stress. It was hypothesized that invading leucocytes contributed to oxidative stress and they were functionally inhibited in one experimental group by the administration of colchicine. Exercise led to an immediate decrease in [GSH] of about 60%, which slowly recovered during 96 h after exercise. With the administration of colchicine after exercise, [GSH] was higher than in the untreated exercise group 48 h after exercise, indicating an inhibition of the ability of leucocytes to produce oxidative stress. However, at 96 h after exercise, [GSH] was lower in the treated exercise group than in the untreated group. The morphological evaluation of the percentage of affected fibres showed that the invasion of leucocytes increased muscle fibre damage. The results suggested that invading leucocytes enhanced production of reactive species of oxygen that may have participated in inducing muscle damage. However, inhibition of leucocyte invasion did not permit their scavenger action of removing cell debris, which appeared to produce even more oxidative stress in the muscle.

Animals↗

PubMed1994

A comparison of pentamorphone and fentanyl in balanced anaesthesia during general surgery.

The purpose of our randomized, double-blind study of 64 unpremedicated healthy patients undergoing surgical procedures with a duration of at least 60 min was to compare 0.75 micrograms.kg-1 and 1 microgram.kg-1 pentamorphone with 5 micrograms.kg-1 and 7.5 micrograms.kg-1 fentanyl to determine which dose of opioid would reduce the requirement for isoflurane supplementation needed to maintain haemodynamic stability. At 21 points during the procedure, the haemodynamic variables of heart rate and systolic, diastolic, and mean arterial pressures were recorded. The use of isoflurane was quantified; the number of patients requiring inhaled anaesthetic, concentration peaks, MAC minutes, and duration of isoflurane use were noted. The number of equal-volume supplemental opioid analgesic doses, postoperative analgesics, occurrence of postoperative nausea, emesis, and antiemetic doses were compared. The four groups exhibited similar patient demographics, total dose of muscle relaxants, types of surgical procedures, and duration of surgery or anaesthesia. Haemodynamic variables were stable with no difference among the four study groups. The patients given pentamorphone demonstrated both delayed requirement (P < 0.05) and shorter duration (P < 0.05) of isoflurane supplementation. Patients given either 5 micrograms.kg-1 or 7.5 micrograms.kg-1 fentanyl needed isoflurane supplementation within 12 +/- 16 min and 12 +/- 17 min from induction respectively; while patients given either 0.75 micrograms.kg-1 or 1 microgram.kg-1 pentamorphone did not require isoflurane supplementation for 37 +/- 10 min and 43 +/- 26 min respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

[Coronary disease and noncardiac surgery. An evaluation of the surgical risk].

Coronary artery disease is one of the leading causes of death in developed countries and one of the factors contributing to high mortality associated with noncardiac surgical procedures. This is the reason why is so important to correctly assess surgical risk in patients with ischemic heart disease. These patients can be evaluated by a simple clinic examination, electrocardiogram and chest X-ray. In asymptomatic patients or in patients with angina (Class I-II), normal electrocardiogram and chest X-ray, the operative risk is low. On the other hand, patients with severe heart failure (Class IV NYHA), unstable angina or acute myocardial infarction have a high surgical risk. The exercise stress testing must be performed in some cases in order to identify preoperative factors (electrocardiographic ischemic changes, low functional capacity) that might affect the development of cardiac events after noncardiac surgery. When not possible a thallium-dipyridamole scintigraphy should be considered. We discuss preoperative indications for coronary angiography and coronary revascularization. Coronary artery bypass surgery must be thought based on clinic severity, therapeutic results, left ventricular function and patient age, among other factors.

Coronary Disease↗

PubMed1993

Skeletal muscle damage during tourniquet-induced ischaemia. The initial step towards atrophy after orthopaedic surgery?

Muscle biopsies from the vastus lateralis muscle of patients who had undergone anterior cruciate ligament surgery under conditions of tourniquet-induced ischaemia were examined under the electron microscope at different periods of time up to 90 min of ischaemia. The severity of the alterations in ultrastructure appeared to depend on the period of ischaemia. The pathological changes consisted of accumulation of lysosomes, persistent intrafibre oedema, and some extracellular oedema. Signs of fibre necrosis were found after 90 min of ischaemia. Capillary ultrastructure was only altered with regard to some swelling of the endothelium and marked thickening of the basement membrane. It was concluded that skeletal muscle could be severely affected even during relatively short periods of ischaemia, which might facilitate the development of muscle atrophy during immobilization after orthopaedic surgery.

Adult↗

PubMed1993

The possible role of intracellular Ca2+ accumulation for the development of immobilization atrophy.

Little is known about the cellular mechanisms which induce the development of skeletal muscle immobilization atrophy. Initial disturbances in cellular homeostasis seem to occur very early during immobilization. The aim of the study was to investigate whether loss of calcium homeostasis might be of etiological importance for atrophy. Therefore a calcium channel blocker (nifedipine) was administered to mice immobilized for four days, and their soleus muscle was investigated comparatively to immobilized animals without nifedipine. The immobilized muscles showed an atrophy of about 15% which was not the case in nifedipine-treated immobilized muscles. Ultrastructural alterations (lysosomes, mitochondrial damage) were found predominantly in the immobilized muscles, but rarely with nifedipine. It was concluded that nifedipine protected the muscle fibers probably against calcium overload, thereby avoiding an autophagic response and an impairment of mitochondrial respiratory function.

Animals↗

PubMed1993

Endothelium-derived oxidative stress may contribute to exercise-induced muscle damage.

In exercise-induced muscle damage, oxidative stress derived from the liberation of reactive oxygen species (ROS) is assumed to be of etiological importance. Xanthine oxidase (XO) located in capillary endothelium is one of the possible sources for ROS, mainly investigated so far under conditions of ischemia/reperfusion. XO can be inhibited by allopurinol. To investigate the contribution of XO for the oxidative stress-induced development of muscle damage, mice were subjected to a single bout of exhaustive running exercise. Another exercised group received allopurinol. The reduced form of glutathione (GSH) was measured to estimate the amount of oxidative stress in soleus muscle, and the same muscle was examined in the light and electron microscope at different periods of time (0, 48, 96 h) after exercise. While exercise alone resulted in a marked reduction of GSH indicative for oxidative stress, which only recovered at 96 h, the administration of allopurinal to exercised animals induced a complete recovery already at 48 h after exercise. Muscle damage was more pronounced in the exercised animals which had not been treated with allopurinol. It is concluded that endothelium-derived ROS contribute reasonably to oxidative stress to exercised muscle and to fiber and capillary damage.

Allopurinol↗

PubMed1992

Nifedipine diminishes exercise-induced muscle damage in mouse.

The purpose of this study was to evaluate the effects of a calcium channel blocker (nifedipine) on the severity of muscle damage induced by intensive exercise. Male Charles River mice were assigned to four groups (8 mice/group): normal control (C), nifedipine (N), nifedipine and exercise (N + E) and exercise (E). The animals of the C group were not submitted to any exercise nor to drug administration. The animals of the N group received 1 mg.kg-1 per day of nifedipine (Adalat 10 mg, Bayer AG), per os, during 3 days. The mice of the N + E group were submitted to a treadmill run (0 degree slope) at 1000 m.h-1 (80% of their maximal speed) for 1 hour. In this group, the administration of the drug was under the same conditions as for the N group. The administration started 24 h before the run. The E group was submitted to the same exercise protocol as the animals of N + E group. The soleus muscle was excised for light and electron microscopic evaluation using routine histological techniques. In the C and N groups no morphological alterations were detected. In the E group the number of alterations of striated pattern was twice that in the N + E group. The number of fibres with central nuclei was 35% in the E group but only 8% in the N + E group. The total number of damaged fibres was significantly higher in the E group. The results suggest that nifedipine may give protection to exercise-induced skeletal muscle damage in mouse, probably because the blocking of channels impaired Ca2+ influx; and the results of this study therefore confirm earlier contentions about the possible role of calcium ions in producing muscle damage after work.

Animals↗

PubMed1992

Exercise, muscle damage and fatigue.

Fatigue as a functional sign and muscle damage as a structural sign can be observed after prolonged exercise like marathon running or after strenuous exercise, especially with the involvement of eccentric contractions. For fatigue due to prolonged exercise, hypoxic conditions and the formation of free oxygen radicals seem to be of aetiological importance, resulting in an elevated lysosomal activity. Eccentric exercise of high intensity rather results in a mechanical stress to the fibres. Although these different mechanisms can be discerned experimentally, both result in similar impairments of muscle function. A good training status may attenuate the clinical signs of fatigue and muscle damage. The symptoms and events occurring during delayed onset of muscle soreness (DOMS) can be explained by a cascade of events following structural damage to muscle proteins.

Animals↗

PubMed1991

Quantitation of readthrough of termination codons in yeast using a novel gene fusion assay.

A simple quantitative in vivo assay has been developed for measuring the efficiency of translation of one or other of the three termination codons. UAA, UAG and UGA in Saccharomyces cerevisiae. The assay employs a 3-phosphoglycerate kinase-beta-galactosidase gene fusion, carried on a multicopy plasmid, in which the otherwise retained reading frame is disrupted by one or other of the three termination codons. Termination readthrough is thus quantitated by measuring beta-galactosidase in transformed strains. Using these plasmids to quantitate the endogenous levels of termination readthrough we show that readthrough of all three codons can be detected in a non-suppressor (sup+) strain of S. cerevisiae. The efficiency of this endogenous readthrough is much higher in a [psi+] strain than in a [psi-] strain with the UGA codon being the leakiest in the nucleotide context used. The utility of the assay plasmids for studying genetic modifiers of nonsense suppressors is also shown by their use to demonstrate that the cytoplasmic genetic determinant [psi+] broadens the decoding properties of a serine-inserting UAA suppressor tRNA (SUQ5) to allow it to translate the other two termination codons in the order of efficiency UAA greater than UAG greater than UGA.

Antisense Elements (Genetics)↗

PubMed1991

Effects of training and an anabolic steroid on murine red skeletal muscle. A stereological analysis.

The purpose of this study was the evaluation of changes induced by training (swimming 1 h/day, 5 days/week, 6 weeks) and an anabolic hormone (nandrolone decanoate, intramuscular injections of 15 mg.kg-1 per week) on fiber size, capillarization and mitochondrial fraction of murine soleus muscle. The animals (n = 32) were divided into 4 groups: a control group (C), that received the arachis oil carrier; a steroid group (S), that received the hormone; a training group (T), and a group that was submitted to training and to the administration of hormone (S + T). The soleus muscle was selected for quantitative light- and electron-microscopic evaluation. The muscle fiber size was increased in group T and decreased in groups S and S + T. The axial length of capillaries per unit volume of muscle decreased significantly in groups S and T. The number of capillaries per number of fibers showed a significant decrease in groups S and S + T and an increase in group T. The mitochondrial content decreased in group S, which suggested that anabolic steroids can be harmful for these organelles. This hypothesis was confirmed by histological evaluation at the electron-microscopic level. Many swollen and disrupted mitochondria were found in groups S and S + T. The results suggest that administration of nandrolone decanoate may have some deleterious effects on the muscle respiratory system (capillaries and mitochondria).

Animals↗