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Biomedical subjects

M Soza

Publications and source records attributed to M Soza.

9 recordsLinked to original sources
PubMed1993

[Efficacy and secondary effects of chronic treatment with amiodarone].

Long-term therapy with amiodarone has been associated with a high incidence of adverse side effects, that precludes its indication for common cardiac arrhythmias. We have prospectively studied 218 patients (pts), aged 32-87 years, under chronic amiodarone therapy that were followed for 2 years and evaluated for efficacy and adverse side effects. Previous amiodarone treatment ranged from 1 to 135 months. Cardiac arrhythmias were paroxysmal AF (PAF) in 120 pts, sustained VT (SVT) in 36 pts, paroxysmal supraventricular tachycardia (PSVT) in 21 pts, unsustained VT (UVT) in 18 pts and miscellaneous in 23 pts. Amiodarone doses ranged from 500 to 4200 mg per week. Amiodarone was effective in 65% of all patients. No difference was observed between efficacy and type of arrhythmia. Dermatologic toxicity was found in 36%, neurologic toxicity in 23%, thyroid toxicity in 13.4% and pulmonary fibrosis en 2.5% of pts. Amiodarone was discontinued routinely when pulmonary toxicity was present. We conclude that amiodarone therapy is effective in a wide spectrum of arrhythmias. Although drug therapy was associated with a high incidence of adverse side effects, these did not preclude continuation of treatment.

Adult↗
PubMed1987

Glucocorticoid excess induces preferential depletion of myosin in denervated skeletal muscle fibers.

The combined effects of dexamethasone treatment (1 mg/Kg/day) plus denervation (DEX-DEN), were studied at 7, 13, and 28 days by microscopic, biochemical, and physiological techniques in plantaris and soleus muscles of adult rats. The results were compared with corresponding dexamethasone-treated (DEX) and denervated (DEN) muscles and appropriate controls. There was a significantly more marked atrophy of all fiber types in the DEX-DEN plantares at 7 and 13 days than in either DEX or DEN muscles. The degree of atrophy was greatest in type 2B fibers in DEX-DEN plantares. Electron microscopy revealed a severe preferential depletion of thick myofilaments in DEX-DEN plantares and solei but not in DEX or DEN muscles. The thick myofilament depletion in DEX-DEN muscles occurred in addition to a severe overall reduction of myofibrillar caliber. Gel electrophoresis showed a marked preferential decrease of myosin heavy chain in DEX-DEN plantares and solei, but not in either DEX or DEN muscles. Myosin light chains were also markedly reduced in DEX-DEN plantares and solei. In vitro physiological studies showed a marked reduction of the denervation-induced twitch potentiation in DEX-DEN solei. Maximal tetanic tension (20 Hz stimulation) per gram weight of muscle as well as the twitch-tetanus ratio was significantly reduced only in DEX-DEN solei in relation to controls. Myosin depletion in DEX-DEN muscles may be due to a severe preferential inhibition of its synthesis coupled with an accelerated catabolism.

Actins↗
PubMed1986

Calcium-induced damage of skeletal muscle fibers is markedly reduced by calcium channel blockers.

Vascular perfusion of rat hind limbs with a Ca2+-free physiological solution containing ethylenediaminetetraacetate, when followed by a physiological solution with normal concentration of Ca2+, caused a marked rise of creatine kinase (CK) in the venous effluent. When calcium channel blockers were present in the perfusing solutions, no rise of CK occurred. On histological sampling of perfused muscles, CK rise was roughly correlated with muscle fiber damage of the appropriate muscles. Removal of calcium from the plasmalemma of muscle fibers appears to prevent closure of calcium channels, making the muscle fibers susceptible to a deleterious influx of extracellular calcium. This influx can be prevented by the presence of calcium channel blockers in the perfusates.

Animals↗
PubMed1986

Skeletal muscle endurance: the effect of increased availability of endogenous long-chain fatty acid fuel.

A possible role of intramuscularly derived fatty acid fuel on muscle endurance was investigated in curarized diaphragms of fasted rats. These showed significantly improved endurance during 60 min of intermittent stimulation at 20 Hz in vitro compared with diaphragms of fed control animals. The improved endurance appeared to be related to an increased availability and utilization of fatty acid fuel derived from greatly increased numbers of lipid globules in muscle fibers of fasted animals. The pH of muscles with improved endurance (fasted rats) was not different from that of muscles from fed controls at rest. After 60 min of intermittent stimulation, the muscle pH diminished to the same extent in both groups. Diaphragms of fasted rats that were refed 12 h before testing did not show improved endurance. Epinephrine in the bath abolished the improved endurance of diaphragms of fasted rats. Diaphragms of fasted guinea pigs did not show significantly improved endurance (despite abundant intracellular lipid globules), possibly because of a reduced intracellular carnitine.

Animals↗
PubMedDate not supplied

Calcium paradox in skeletal muscles: physiologic and microscopic observations.

Immersion of rat hemidiaphragms in Ca2+-free Krebs solution (KS) containing Ca2+ chelator in vitro leads to separation of basal lamina from the plasma membrane, as well as transient contracture and rapid loss of twitch response [calcium paradox (CP) phase 1]. Subsequent immersion in regular KS results in necrosis of muscle fibers accompanied by slowly increasing contracture (CP phase 2). This contracture could be prevented or reduced by using either Ca2+-free KS or calcium channel blockers, but not by dantrolene sodium, implying that after drastic reduction of extracellular and sarcolemmal Ca2+ during CP phase 1, the sarcolemma has lost its ability to control normal Ca2+ fluxes. Contracture did not develop at 21 degrees C. CP is a convenient model to study calcium-induced muscle cell death and the role of Ca2+ in maintaining sarcolemmal integrity.

Animals↗
PubMedDate not supplied

[Mitochondrial encephalomyopathy, lactic acidosis and features of cerebrovascular disorders].

A 12 year old girl with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS) is reported. After a normal childhood, at 9 years of age she developed generalized and hemilateralized seizures. Posteriorly, these episodes became more frequent and were accompanied by headache, homonimous hemianopsia, ataxia, vomiting, photophobia, left hemiparesis, slurred speech and even convulsive status. Laboratory tests evidenced lactic acidosis, brain lucencies at CT Scan and ragged skeletal muscle fibers at muscle biopsy.

Acidosis, Lactic↗