[Carnitine deficiency and severe nausea-induced thiamine deficiency causing a metabolic crisis].
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Biomedical subjects
V Salonen
Publications and source records attributed to V Salonen.
Transient stress lymphocytosis during crisis of sickle cell anemia.
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Adult↗
Diabetes induces the formation of large diameter collagen fibrils in the sciatic nerves of BB rats.
Diabetes mellitus (DM) is known to be associated with widespread connective tissue changes. However, the connective tissue of peripheral nerves in diabetes has gained little attention. Thickening of the basement membranes of Schwann, perineurial and endothelial cells suggests a perturbation in the metabolism of type IV collagen. We studied the ultrastructure of endoneurial collagen fibrils in the sciatic nerves of spontaneously diabetic BB rats and found that the fibrils in the diabetic rats were significantly thicker than in the age and sex matched non-diabetic BB rats, both in the proximal (52.6 vs. 46.1 nm) and the distal part (52.4 vs. 45.5 nm) of the nerve, respectively. The mechanism for the thickening of endoneurial collagen fibrils remains unknown, but conceivably involves changes in the biochemical composition of the nerve connective tissue matrix: e.g. altered metabolism of type I and/or type III collagen, increased glycosylation of the collagen molecules, or changes in the glycosaminoglycan content of the ground substance.
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Long-term endoneurial changes after nerve transection.
Long-term endoneurial changes in the distal stump of transected rat sciatic nerve were examined from 8 to 50 weeks after nerve transection. The morphological alterations were followed both in nerves which were allowed to regenerate and in nerves in which regeneration was prevented by suturing. The nerves prevented from regenerating showed markedly atrophied Schwann cell columns after 20 weeks and a disappearance of some Schwann cell columns after 30 weeks. The surrounding endoneurial fibroblast-like cells gradually lost their delicate cytoplasmic extensions and formed rough fascicles around numerous shrunken Schwann cell columns or around areas from which Schwann cells had apparently disappeared. Inside the fascicles, the Schwann cell loss was replaced by collagen fibrils or occasionally, by a dense accumulation of microfibrils. The loss of endoneurial cytoplasmic processes continued up to 50 weeks, leaving behind patches of thin fibrils around numerous shrunken Schwann cell columns or around collagenous areas where Schwann cells were lost. The endoneurial matrix showed presence of thin 25- to 30-nm collagen fibrils close to shrunken Schwann cell columns up to 50 weeks but in areas with advanced degeneration a shift towards regular 50- to 60-nm collagen fibrils occurred. The degenerated areas resembled those described in Renaut bodies and neurofibromas. Despite suturing of transected nerves to prevent sprouting, occasional regenerating sprouts were noted in the Schwann cell columns. These axons were surrounded in a sheath-like fashion by pre-existing endoneurial cell fascicles covered by a basal lamina. In the reinnervating nerves the endoneurial space gradually lost its compartmentized structures consisting of collagen fibrils and endoneurial fibroblast-like cells. After 20 weeks the endoneurial cells were inconspicuous and the extracellular matrix consisted mainly of 50- to 60-nm collagen fibrils. During axonal growth and maturation, Schwann cells containing unmyelinated axons surrounded large, myelinated axons in a collar-like fashion. Close to these collars of Schwann cells, thin 25- to 30-nm collagen fibrils were noted in focal areas, even after 50 weeks. Occasionally, numerous clusters of regenerating axonal sprouts were noted in the perineurium. These were surrounded by multiple layers of cells possessing basal lamina. The present results show that after nerve transection the distal stump of the severed nerve shows dynamic changes in the endoneurial space, especially in nerves where reinnervation is prevented.(ABSTRACT TRUNCATED AT 400 WORDS)
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Quantitation of Schwann cells and endoneurial fibroblast-like cells after experimental nerve trauma.
Schwann cells and endoneurial fibroblast-like cells were quantitated for 30 weeks in both nonregenerating and freely regenerating, transected rat sciatic nerve. Immunocytochemical recognition of S-100 protein was used as a marker for Schwann cells and other immunocytochemical and histological methods in the differentiation of S-100 protein-negative endoneurial cells in cross sections of the distal stump 10 mm distal to the site of transection. A marked increase in the total number of cells was observed during the first 4 weeks after the injury in both operative groups. The quantitative relationships between cell populations remained essentially the same as in normal nerves, although the proliferation of the S-100 protein-negative cell population was proportionately slightly stronger when compared to the number of these cells in normal nerves. After the initial proliferation, a gradual decrease occurred in the total number of cells per cross section. This was most marked in the non-regenerating nerves, whereas in the regenerating nerves the decrease in cell number ceased at 16 weeks. The number of Schwann cells was 3.5 times as high as in the control nerves in this phase. The method used in the present study is less laborious than morphometry employing electron microscopy. Furthermore, electron microscopic characteristics of endoneurial cells are not always reliable after nerve trauma, because normal anatomical relationships have become disturbed. This study demonstrates that S-100 protein immunocytochemistry is useful in the study of traumatic lesions of peripheral nerve.
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Reversible endoneurial changes after nerve injury.
Endoneurial changes in the rat sciatic nerve were studied during Wallerian degeneration and subsequent regeneration. After total axotomy two different experimental models were used. In the first the cut ends of the sciatic nerves were left free to allow reinnervation. In the second model the distal end of the transected nerve was sutured to the adjoining muscle to prevent regeneration. Within 2 weeks after the axomoty, a Wallerian type of degeneration was seen with axonal destruction and phagocytosis of myelin sheaths. After 4 weeks endoneurial fibroblastic cells formed circular structures around the Schwann cell columns, i.e., the bands of Buengner in both groups. These fascicle-like structures became more pronounced in the non-regenerating nerves up to 8 weeks, while during reinnervation the cellular reaction in the endoneurium nearly disappeared within this time. Ultrastructurally, the endoneurial fibroblast-like cells showed marked phagocytotic activity and also fragments of basement membrane on their surface. The appearance of thin (25-30 nm in diameter) collagen fibrils closely related to the basement membrane was noted around the bands of Buengner, as well as the appearance of an amorphous extracellular gap between the newly synthetized thin collagen fibrils and normal endoneurial collagen (50-60 nm). The reversible endoneurial compartmentation seems to be important for maintaining the nerve structure, serving as a support for axonal regeneration in addition to the bands of Buengner.
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The effects of nerve transection on the endoneurial collagen fibril sheaths.
The connective tissue changes during Wallerian degeneration and subsequent regeneration were studied in the distal stump of transected sciatic nerves of Wistar rats. In half of the animals regeneration was prevented by suturing the distal stump to muscle and in the rest spontaneous regeneration was allowed. Intact contralateral nerves served as controls. By 4 weeks after transection the Schwann cell columns became surrounded by a layer of thin collagen fibrils that were, on average, 25-30 nm in diameter. This was only half of the fibril diameter observed elsewhere in the endoneurium or in control nerves. The layer of thin fibrils diminished in thickness when axonal regeneration reached the distal stump, especially as the axons became myelinated. At all stages of the experiment the fibril diameter distribution in the surrounding normal endoneurial stroma was comparable with that observed in control nerves. Segments of Schwann cell basement membrane were observed to be closely associated with collagen fibrils both in freely regenerating, as well as in non-regenerating, nerves. The diameter of these fibrils corresponded to that observed in the zone of thin fibrils surrounding the Schwann cell columns. Such areas were not found in control nerves. The data obtained show that deposition of thin collagen fibrils occurs around the Schwann cell columns as a reaction to transection. Our observations on the regenerating nerves indicate that this connective tissue reaction does not prevent regeneration in the early phases following injury and that its progression is limited concomitantly with axonal regeneration.
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Laminin in traumatized peripheral nerve: basement membrane changes during degeneration and regeneration.
The changes in Schwann cell basement membrane associated with degeneration and regeneration during 50 weeks after transection of rat sciatic nerve were studied immunohistochemically with antibodies to laminin. In half of the animals, regeneration was prevented by suturing the nerve stumps aside, whereas in the rest spontaneous regeneration was allowed. Axonal regeneration was monitored with anti-neurofilament protein antibodies. In control nerves, basement membranes surrounding Schwann cells were visualized as circular, laminin-positive structures within the endoneurium. By 8 weeks after transection, Schwann cells had formed columns which were laminin-positive throughout their cross-sectional area and indistinguishable from basement membrane zones in both non-regenerating and regenerating nerves. As axons repopulated the distal stump, the normal shape of Schwann cell basement membrane tubes was slowly restored in freely regenerating nerves. In non-regenerating nerves, however, a striking atrophy of Schwann cell columns was observed. Regenerating axons were only seen inside laminin-positive tubular structures in all phases after 8 weeks in regenerating nerves. On the other hand, restoration of normal shape in laminin-positive basement membrane zones was coincident with appearance of axons in the distal stump, but it did not take place in chronically degenerating nerves. The results show that chronic degeneration leads to an atrophy of Schwann cell columns and results in a decrease in laminin immunoreactivity associated with them.
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Changes in intramuscular collagen and fibronectin in denervation atrophy.
The distribution of collagen types I, III, and V and fibronectin was investigated by means of immunofluorescent techniques in denervated and normal rat skeletal muscle. During a period of 28 days, a distinct atrophy developed in the denervated gastrocnemius muscle and was accompanied by an increase in types I and III collagen in the endomysium and perimysium. The amount of type V collagen showed little change, whereas fibronectin increase closely parallelled types I and III collagen. The results indicate that denervation atrophy in muscles is accompanied by striking fibrotic changes due to mesenchymal types I and III collagen.
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Endoneurial fibrosis following nerve transection. An immunohistological study of collagen types and fibronectin in the rat.
Indirect immunofluorescent techniques with antibodies to type I, III, and V collagens and fibronectin were used to study rat sciatic nerve tributaries after transection with intact contralateral nerves as controls. Codistribution of type I and III collagens characterized the epineurium of normal nerve. In the perineurium, however, type I collagen was absent, but type III and V collagens and fibronectin were detected. Type I and III collagens were codistributed in the endoneurial stroma where a homogeneous staining by antibodies to fibronectin was also observed. During the 4-week observation period after transection the perineurium reacted by slight thickening which was most clearly demonstrated by staining with antibodies to fibronectin and to type V collagen. A widening of the type I-negative cleft also occurred. Endoneurial, type V collagen-positive cuffs around the nerve fibers became disorganized, and a concomitant increase of the stroma containing type I and III collagens and fibronectin was observed. The codistribution of the fibrous collagen types appeared similar in normal epineurium and endoneurium. Type V collagen was located in the perineurium and in endoneurial cuffs surrounding the nerve fibers. The present data indicate that collagen accumulation takes place in the perineurium and endoneurium of transected nerve. The cell type responsible for the synthesis of the connective tissue material is discussed.
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