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1.
Acta cient. venez ; 57(1): 8-14, 2006. ilus, tab
Article in Spanish | LILACS | ID: lil-537153

ABSTRACT

La proteinuria produce un desbalance importante del metabolismo proteico y lipídico, que favorece la desproteinización del organismo, con grandes repercusiones sistémicas que llegan a afectar hasta el músculo esquelético. En los pacientes con falla renal, usualmente disminuye su masa muscular y se observa debilidad. Los pacientes urémicos terminales, manifiestan atrofia de las fibras musculares tipo II, además de daño miopático primario, causado probablemente por un déficit de la microcirculación. En un afán de dilucidar las posibles alteraciones ultraestructurales precoces presentes en el músculo esquelético de pacientes con glomerulopatías primarias que cursan con proteinuria, se estudiaron 4 pacientes (2 hombres y 2 mujeres) con edades entre 42 y 66 años, pertenecientes al servicio de nefrología del hospital militar ®Dr. Calos Arvelo¼ de Caracas-Venezuela. En todos ellos se realizaron mediciones de enzimas musculares (CK, LDH, AST y ALT), electromiografía de los miembros inferiores y biopsia del músculo cuadriceps femoral. En ninguno de los pacientes se observaron modificaciones en los niveles séricos de las enzimas y a excepción de uno de ellos (caso 4), los registros eletromiográficos fueron normales. A nivel ultraestructural se observó: hinchamiento de los componentes del sistema sarcotubular con presencia de tríadas prominentes, signos de atrofia muscular, núcleos hipercromáticos, glucógeno abundante y glucogenosomas. Algunos capilares intramusculares con la luz parcial o totalmente ocluida, citoplasma endotelial electrón denso, presencia de prolongaciones del citoplasma endotelial hacia la luz del capilar, vesículas pinocíticas y cavéolas. Dichos cambios nos permiten concluir el compromiso estructural del músculo esquelético en pacientes con proteinuria, el cual se hace más evidente a medida que avanza hacia la falla renal y que dicho compromiso tiene una base microvascular que condiciona cambios del metabolismo muscular.


The proteinuria produces an important unbalance of the protein and lipid metabolism that it favors thedesproteinitation of the organism, with big systemic repercussions that end up affecting the skeletal muscle. In the patients with renal failure it usually diminishes their muscular mass and weakness is observed. The terminal uremic patient, manifests atrophy of the fibers muscular type II, besides miopatic primary damage, caused probably for a deficit of the microcirculación. In a desire of elucidating the early ultraestructural alterations present in the skeletal muscle of patient with primary glomerulopaties that curse with proteinuria, four patients were studied (2 men and 2 women) with ages between 42 and 66 years, belonging to the service of nephrology of the military hospital ®Dr. Calos Arvelo¼ of Caracas-Venezuela. In all they were carried out mensurations of muscular enzymes (CK, LDH, AST and ALT), electromiografie of the inferior members and biopsy of the muscle femoral cuadriceps. In none of the patients modifications were observed in the seric levels of the enzymes and to exception of one of them (case 4); the eletromiografic registrations are normal. At ultraestructural level it was observed: swelling of the components of the system sarcotubular with presence of prominent triads, signs of muscular atrophy, hyperchromatic nuclei, abundant glucogen and glucogenosome. Some capillary ones intramuscular with the partial or completely occluded light, electron dense cytoplasm, presence of continuations of the endothelial cytoplasm toward the light of the capillary one, pinocitic vesicles and caveole. This changes allow us to conclude the structural commitment of the skeletal muscle in patient with proteinuria, which becomes more evident as it advances toward the renal failure and that said commitment has a microvascular origin that conditions changes of the muscular metabolism.


Subject(s)
Humans , Male , Adult , Female , Middle Aged , Kidney Diseases , Muscle, Skeletal/abnormalities , Muscle, Skeletal/ultrastructure , Proteinuria , Zona Glomerulosa , Nephrology
2.
Acta odontol. venez ; 39(1): 4-6, 2001. ilus
Article in Spanish | LILACS | ID: lil-315010

ABSTRACT

Se reporta el caso de un paciente masculino de 65 años de edad a quien se le extrajo un tumor en el piso de la boca con el diagnóstico de carcinoma de células fusiformes. Una muestra del tumor fue procesada con técnicas de rutina para microscopía electrónica de transmisión. Dos componentes celulares se encontraron: carcinomatoso y sarcomatoso. El carinomatoso estuvo constituido por células epiteliales y el sarcomatoso por células similares a las musculares lisas. Estos resultados indicaron que este tumor presenta evidencias ultraestructurales de que su elemento sarcomatoso podría no provenir de la diferenciación de su elemento carcinomatoso


Subject(s)
Humans , Male , Middle Aged , Carcinosarcoma , Mouth Neoplasms , Sarcoma , Biopsy, Needle , Carcinosarcoma , Microscopy, Electron/methods , Mouth Floor , Sarcoma , Venezuela
3.
Acta cient. venez ; 44(6): 349-54, 1993. ilus, tab
Article in English | LILACS | ID: lil-137249

ABSTRACT

A light and transmission electron microscopic study was perfomed in skeletal muscles from mice experinmentally infected with Toxoplasma gondii. Parasite cysts were not observed. Capillary endothelial cytoplasm abnormalities included proliferation of organelles, decrease of pynocytic vesicles, degenerative changes and necrosis. In some capillaries the lumen was reduced or absent. Pericytes also were altered. In all animals (n=13), the basement membrane was normal. The cellular infiltrate consisted of macrophages, lymphocytes, mastocytes and eosinophils. The alterations observed in muscle microvasculature in absence of Toxoplasma gondii cysts, could be due to a host-immune response to the parasite


Subject(s)
Rats , Animals , Capillaries/parasitology , Capillaries/ultrastructure , Mice/parasitology , Microscopy, Electron, Scanning , Muscles/ultrastructure , Toxoplasma
4.
Acta cient. venez ; 44(3): 168-74, 1993. ilus
Article in English | LILACS | ID: lil-185509

ABSTRACT

This study reports the ultrastructural alterations observed in muscle biopsies from 4 patients with Turner's syndrome and a mild, non-progressive form of musclular compromise. The abnormalities found were fiber atrophy, mitochondrial changes, swelling of sarcotubular system elents, lysosomal proliferation and presence of filamentous bodies. Fiber necrosis was not evident. Microvascular alterations included thickening and reduplication of basement membranes, vacuolation of endothelial cells and pericytes and a mononuclear cell infiltrate formed mainly by macrophages. These histopathological changes seem to be part of the phenotypic manifestation of this syndrome. These observstions indicate that the presence of muscle problems in patients with Turner's syndrome does not necessarily mean the coexistence of a muscular disease


Subject(s)
Humans , Genetics , Hypogonadism , Microscopy, Electron , Muscles/pathology , Turner Syndrome/diagnosis
5.
Acta cient. venez ; 43(1): 26-33, 1992. ilus, tab
Article in English | LILACS | ID: lil-105921

ABSTRACT

Simultaneous denervation and tenotomy causes atrophy of rat slow twitch soleus muscle. Apparently, the alterations are similar to those seen in denervated or tenotomized slow muscle. However, the extent of disorganization of myofibrils appers lower than that expected after a moderate period of time in only denervated or tenotomized muscle. This study indicates that after an initial proliferation of lysosomes, alterations of sarcotubular system and mitochondria proceed. Nevertheless, 45 days after denervation and tenotomy many mitochondria have a normal aspect


Subject(s)
Animals , Male , Rats , Muscle Denervation , Muscles/innervation , Muscular Atrophy , Muscle Contraction , Muscles/ultrastructure , Rats, Inbred Strains
6.
Acta cient. venez ; 43(4): 229-34, 1992. ilus
Article in English | LILACS | ID: lil-125497

ABSTRACT

This ultrastructural study was undertaken to investigate the morphological changes which occur in the fast twitch gastrocnemius muscle of the reptile Iguana after nerve section. It was found that initial degenerative alterations appeared in muscle fibers two weeks after denervation and prograssed aling the two months of the investigative period. They consisted of disorganization of contractile and sarcotubular elements and the appearance of autophagic vacuoles with mitochondrial debris. However, even two months after nerve section some myofibrils and mitochondria looked normal. Our results suggest that although the general course of denervation atrophy in iguana gastrocnemius is sinilar to that in other twitch muscle of vertebrates, the chonology of the process shows that iguana fast twich skeletal muscle exhibit an intermediary position among the vertebrates in relation to their velocity of response to denervation


Subject(s)
Animals , Muscle Denervation/adverse effects , Iguanas/physiology
7.
Acta cient. venez ; 42(6): 319-25, 1991. ilus
Article in English | LILACS | ID: lil-105915

ABSTRACT

Effects of neurotomy on human skeletal muscle ultrastucture were studied in biopsies from denervated abdominal muscles. After 35 days of denervation the alterations included fiber atrophy which varied from slight to total, swelling and disalignment of sarcotubular system, nuclear changes, mitochondrial abnormalities, and lysosomal proliferation. Capillaries were normal and no cell infiltration was evident. Cases studied several months after neurotomy showed signs of reinnervation with a partial recovery of normal structure. The differences between the histopathological pictures caused by neurotomy and by degenerative diseases which produce neurogenic atrophy are discussed. The restorative capacity of human skeletal muscle after spontaneous reinnervation is also studied. Key words: Neurotomy, Denervation, Reinnervation, Ultrastructure, Muscle pathology, Neurogenic atrophy


Subject(s)
Adult , Middle Aged , Humans , Abdominal Muscles/ultrastructure , Muscle Denervation , Microscopy, Electron , Muscular Atrophy
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