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Biomedical subjects

V Sahgal

Publications and source records attributed to V Sahgal.

At least 55 records · Page 3Linked to original sources
PubMed1985

Mitochondrial cytochemistry in experimental myopathies.

In this paper, we have described mitochondrial cytochemistry (NADH oxidase, cytochrome c oxidase), in the light and electron microscopic studies of the experimental mitochondrial myopathies. DNP, oleate and crotoxin were employed to produce mitochondrial changes in the rat skeletal muscle. The DNP and oleic acid lesions showed strong NADH oxidase and cytochrome c oxidase activities in mitochondria--both at the light microscopic as well as at ultrastructural level. However, the crotoxin lesions showed marked reduction of both the enzyme activities in histochemistry and electron microscopy. Muscle necrosis was seen only in the crotoxin lesion. On the basis of these data, we propose that DNP and oleic acid treatment produced mitochondrial myopathies in which the mitochondrial structure was altered but they were enzymatically active, while the crotoxin treatment produced the structural and enzymatic alterations of the mitochondria.

2,4-Dinitrophenol↗
PubMed1984

Uremic myopathy.

Explore the source record for details and available documents.

Atrophy↗
PubMed1983

Ultrastructure of muscle spindle in congenital myotonic dystrophy. A study of preterm infant muscle spindles.

The muscle spindle in the preterm infants with congenital myotonic dystrophy consisted of numerous, unfused intrafusal fibers. These fibers showed immature myofilament arrangement at 27 weeks but had the nuclear arrangement of bag and chain type. The motor endings were very sparse while prominent sensory endings were seen. At 34-37 weeks, even though the muscle fibers were unfused, the nuclear bag and chain fibers could be differentiated by the presence and absence of M line. Immature motor endings were seen at this stage. In conclusion, the muscle spindle in the preterm infants is immature.

Cytoskeleton↗
PubMed1983

Skeletal muscle in preterm infants with congenital myotonic dystrophy. Morphologic and histochemical study.

The skeletal muscle in 3 preterm infants (27, 34, 37 weeks gestation age) born to mothers with myotonic dystrophy showed a syncytial pattern at 27 weeks and a decreasing percentage of satellite cells and central nuclei at 34 and 37 weeks gestation. The fiber type differentiation was observed only at 37 weeks of gestational age. In all 3 cases muscle fibers with multiple acid phosphatase positive were seen. The muscle spindles also had thick capsules and showed lack of morphologic and histochemical differentiation into fiber types. These findings suggest immaturity of skeletal muscle in comparison to the normal. The immaturity of the skeletal muscle correlated well with the prognosis of the patients.

Acid Phosphatase↗
PubMed1983

Morphologic and morphometric studies of muscle in idiopathic scoliosis.

The gluteus maximus and paraspinal muscles in 15 cases of idiopathic scoliosis at the apex of the curve showed myopathic changes and a significant decrease in the type II fibers. Fiber type II atrophy was observed only on the concave side. Ultrastructure of paraspinal and gluteus muscle biopsies showed disruption of myofilaments, Z band streaming and subsarcolemmal accumulation of glycogen, lipid and mitochondria. Quantitative estimation of these subcellular organelles pointed out that a higher glycogen content was significant in both paraspinal as well as the gluteus muscles while a higher mitochondrial content was significant only on the convex side and the gluteus muscle but not the concave side of the apex when compared to normal quadriceps muscle. These findings suggest that idiopathic scoliosis is a diffuse disease process and may be considered a primary muscle disease.

Adolescent↗
PubMed1983

Rehabilitation of craniocerebral trauma.

Rehabilitation of the craniocerebral trauma patient is an increasing challenge worldwide. The return of these individuals to society requires the foresight to begin rehabilitation efforts as soon as the patient receives medical attention. This article reviews the spectrum of medical, physical, and social problems associated with craniocerebral trauma and provides guidelines for the rehabilitation process.

Brain Injuries↗
PubMed1983

Muscle in chronic uremia--a histochemical and morphometric study of human quadriceps muscle biopsies.

This report describes qualitative and quantitative studies performed on ten muscle biopsies from chronic uremic patients on renal dialysis at light and electron microscopic (EM) levels. The muscle biopsies showed myopathic changes (variation in fiber size, central nuclei, and fiber splitting). Histochemical studies showed type II fiber atrophy and lipid deposits. The ultrastructural study showed disruption of myofibrillary architecture and subsarcolemmal deposits of glycogen, mitochondria, and lipids. Quantitative estimations of the subcellular organelles revealed a statistically significant increase in lipid and glycogen contents of the muscle. The myopathic changes, type II atrophy, and lipid and glycogen deposits in chronic uremic patients raise the question of the effects of uremia and/or chronic dialysis on muscle metabolism.

Adult↗
PubMed1982

Morphogenesis of the mitochondrial alterations in muscle diseases.

In this paper we present sequential morphologic changes produced in rat muscle mitochondria. Respiratory toxins such as crotoxin (rattle-snake venom) and 2,4-dinitrophenol (DNP-an uncoupler of oxidative phosphorylation) were injected in rat quadriceps muscle and the mitochondrial alterations were studied at various time intervals. The series of mitochondrial changes consisted of rounding and swelling of mitochondria, unfolding of the cristae as straight lines, formation of the concentric rings, appearance of paracrystalline inclusions, formation of multiple vesicles and finally vacuole formation. These changes were comparable to the range of mitochondrial alterations seen in the human material examined. Similarity of the time-related mitochondrial changes in the rat to the spectrum of changes observed in human muscle biopsies suggests that the mitochondrial alteration in the human muscle disorders is a stepwise process in which respiratory alterations and calcium ion may play a role.

2,4-Dinitrophenol↗
PubMed1981

Morphological and histochemical correlation of recovery after spinal transection in rat.

Previous studies from our laboratory have shown disappearance of aminergic terminals with relative preservation of cholinergic activity below the level of the lesion (Rodriques & Sahgal, 1978). Since then we have extended our study to look at the behaviour of aminergic fibres and neurons at various time intervals following the lesion and attempted to correlate with the functional recovery. Three to 4 weeks after spinal transection (thoracic), the rats started to show spinal-stepping which became stronger and dexterous with the passage of time. Up to 6 months after thoracic transection, maximum recovery was observed. Studies of catecholamine fluorescence revealed proliferation of new aminergic terminals which were observed four or five segments below the transection. These observations demonstrate regeneration of aminergic fibres in rat. The significance of the data in the light of neurophysiologic studies will be discussed.

Acetylcholinesterase↗
PubMed1980

Alterations in intercostal muscle morphology and biochemistry in patients with obstructive lung disease.

Twenty-two patients undergoing thoracotomy for the diagnosis or treatment of a suspected pulmonary neoplasm had separate biopsies taken from their external and internal intercostal muscles at the time of surgery. Pulmonary function abnormalities ranged from none to moderate airway obstruction. Seventeen of the twenty-two patients had morphologic changes (targeting, variation in fiber size, splitting, and atrophy) in both respiratory muscles, but not in the control latissimus dorsi. Fiber atrophy was more marked in the internal intercostal muscle and was significantly related to the degree of airway obstruction, but not to age, malignancy, or weight loss. Biochemical analyses revealed decreased adenosine triphosphate (ATP) and phosphocreatine (PC) in 47 of 52 muscles, including the latissimus dorsi. The data suggested a relation between increasing airway obstruction and decreasing amounts of phosphocreatine in both intercostal muscles. This relationship may have been enhanced by the presence of malignancy or weight loss. There was a selective decrease in muscle glycogen found only in the external intercostal muscle that was not affected by airway obstruction, malignancy, or weight loss. Intercostal muscle abnormalities are common in patients with obstructive lung disease who undergo thoracotomy, and are probably multifactorial in origin. It is possible that these abnormalities affect the natural history of lung disease in some patients.

Adenosine Triphosphate↗
PubMed1980

Neuropathy in thoracic scoliosis.

The erector spinae muscles of 20 normal humans were evaluated at C7, T3, T11, and L5 vertebral body levels bilaterally. At each level, the mean potential duration of the motor unit action potential was calculated. This control group was compared with a group of patients with C7 and L5 radiculopathy and with a group of patients with thoracic scoliosis. The mean potential durations of the radiculopathy group at the C7 and L5 levels were prolonged as were those values at the convex thoracic levels in the scoliotic group. Muscle biopsy of the erector spinae in the scoliotic group revealed grouped atrophy and changes consistent with a neuropathic process. A radiculopathic process was associated with idiopathic thoracic scoliosis and involved the convex side. It was maximal near the apex of the curve.

Action Potentials↗
PubMed1979

On the pathogenesis of mitochondrial myopathies. An experimental study.

The intra-arterial injection of 2-4 dinitrophenol, an uncoupler of oxidative phosphorylation, resulted in the production of ragged red fibers. The ultrastructure of these fibers showed intramitochondrial paracrystalline inclusions, laminar and fingerprint bodies. Antimycin A and oligomycin injection (which inhibit mitochondrial respiration) only caused swelling and disruption of the mitochondria. An increase in muscle lactic acid, decrease in ATP, glycogen and phosphocreatine was observed after the injection of all these agents. This indicates that lactic acidosis has no significant role in the pathogenesis of mitochondrial pathology. It is concluded that mitochondrial changes are a morphological expression of uncoupled but intact mitochondrial respiration.

Animals↗