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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxic oil syndrome is a multisystemic disease caused by the ingestion of adulterated rapeseed oil. The basic lesion is a peculiar vasculitis that affects mainly the intima, showing the features of an endovasculitis. Vessels of every type and size are involved, affecting practically every organ. The vascular lesions begins with endothelial damage that varies from cellular swelling to cellular necrosis. It then progresses by mixed cellular inflammatory infiltration of the intima and, in some cases, of the media and adventitia. In some cases the infiltrate is rich in eosinophils and a few show foamy histiocytes. Proliferation of myointimal cells and in advanced stages fibroblastic proliferation causes narrowing or obliteration of the vascular lumen. Thromboembolic complications perpetuate the vascular lesion and compound the ischemia and parenchymal atrophy of several organs. The peripheral nerve lesions begin with an inflammatory neuropathy with lymphocytic perineuritis and progress to perineural fibrosis with secondary axonal degeneration. Skeletal muscle lesions exhibit an interstitial inflammatory myopathy at first, followed by a neurogenic muscular atrophy. A direct effect of unidentified toxic substances, possibly free radicals, may cause the endothelial lesion. Other factors, such as immunopathologic mechanisms of delayed hypersensitivity, may contribute to the progression of the vascular lesions.
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PMID:Extracardiac vascular and neural lesions in the toxic oil syndrome. 165 52

The present paper has been written in order to determine the morphological alterations in the sural nerve from patients with chronic arteriosclerotic occlusive disease. Eight patients with Peripheral Vascular Disease (PVD) and six age-matched control subjects were studied. Morphometric data revealed two groups of patients, one of them with mild disease (n = 5), and the other one with severe damage (n = 3), consisting in loss of myelinated fibres and increase in the number of small fibres (p less than 0.05). Teased nerve fibres and electron microscopic studies also showed two types of patients, with respect to the myelin or the axonal alterations. The unmyelinated fibre population was affected equally in both groups. In conclusion, this study supports the idea that ischemia is able to cause structural alterations in the peripheral nerve, and that it can play a role in the development of neuropathy.
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PMID:Morphological abnormalities in the sural nerve from patients with peripheral vascular disease. 166 55

Cerebral ischemia can be caused by many diverse conditions such as cardiac arrest and severe hypotension and is often the cause of secondary brain damage following head injury or infantile birth trauma. The inadequate cerebral blood flow can result in permanent loss of essential brain circuitries and neurological deficits. The CA1 region of the hippocampal formation is the region of the brain that is most often lesioned following transient forebrain ischemia and is associated with impairments of learning and memory. Furthermore, the loss of such a large target area can lead to detrimental post-trauma synaptic reorganization. Since methods are not currently available for the prevention of neuronal loss following cerebral ischemia, a number of anatomical methodologies were utilized to investigate whether transplanted neurons had the potential to afford some measure of repair. The hippocampal CA1 region of the rat brain was lesioned by transient forebrain ischemia and subsequently repopulated with suspensions of fetal hippocampal tissue. The ability of the transplanted neurons to remain viable when placed into a degenerating environment was confirmed by the histological demonstration of 3H-thymidine labelled neurons in the lesioned region. Histological and immunohistochemical techniques showed that the transplanted neurons developed cytological features that were indistinguishable from their normal CA1 counterparts, often showed a remarkable degree of organization, and expressed some of the same neuron specific proteins; specifically calbindin-D28K and parvalbumin. Acetylcholinesterase histochemistry and retrograde axonal transport of Fluorogold demonstrated that some afferent and efferent fibre projections to and from the septal nucleus could be reinstated. The data have shown that the transplanted neurons can demonstrate many of the anatomical properties that are characteristic of the adult cells they have replaced and therefore have great potential for the reconstruction of severe focal lesions due to ischemia.
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PMID:Hippocampal neurons transplanted into ischemically lesioned hippocampus: anatomical assessment of survival, maturation and integration. 172 74

In order to learn more about the vulnerability of nerve fibres to ischemia, a quantitative study of nerve fibre abnormalities was performed on biopsy specimens of the superficial branch of the peroneal nerve from 26 patients with vasculitic neuropathy: 20 had necrotizing arteritis, 5 a lymphocytic, and 1 a leucocytoclastic vasculitis on nerve and/or muscle biopsy. The density of myelinated fibres ranged from 25 to 7880 per mm2 (n = 8470 +/- 706 (SD]. There was a marked inequality in the density of nerve fibres between the fascicles of individual nerves with a mean coefficient of variation of 41 +/- 37 (SD) % versus 7.4 +/- 3.0% in controls. Loss of myelinated fibres, which was greater for fibres larger than 7 microns in diameter, was more severe than that for unmyelinated axons. Regeneration, which was assessed by the number of clustered axons, decreased when the density of myelinated fibres decreased, suggesting that severe nerve ischaemia precludes axonal regeneration. Wallerian degeneration affected on average 58% (range 5-100%) and segmental demyelination, mainly of the secondary type, on average 1.94% (range 1-10%) of teased fibres. It was concluded that (1) myelinated fibres are more vulnerable to ischaemia than unmyelinated axons; (2) large myelinated fibres are affected before the smaller ones; (3) segmental demyelination is uncommon in this context; (4) severe nerve ischaemia precludes axonal regeneration.
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PMID:Vulnerability of nerve fibres to ischaemia. A quantitative light and electron microscope study. 188 86

An autopsied patient with Menkes' kinky hair disease, who showed unusually long survival until the age of five years with typical neuropathological changes, was examined for distribution of neuronal depletion in the cerebral cortex, and the cerebellar changes were compared morphologically and immunohistochemically with those found in a younger patient (1 year 8 months old) reported previously. Neuronal loss in the cerebral cortex in the both cases, which was ill-defined and unassociated with gliosis, was preferentially distributed in the fifth and sixth layers, especially of the gyral bottom in almost all lobes in the older case. Therefore, this change was thought to be secondary to local ischemia caused by mechanical distortion at the stage of gyrus formation in addition to abnormal development. Ultrastructurally, a prominent increase of confronting cisternae (CC) complexes was found in the perikaryon and processes of Purkinje cells in both cases, and in the older patient CC complexes were arranged more densely and were transformed into concentric lamellar structures in the swollen dendrites. Immunohistochemically, the stainability of neurofilaments (NF, 200 kDa) in Purkinje cells, with or without somatic sprouts was faint or negative in the older patient compared with the marked or moderate positivity in the younger patient and age-matched controls. Empty baskets were absent and NF-positive axonal terminals and synaptophysin-positive granules on Purkinje cells were markedly decreased in both cases. These changes suggest that Purkinje cells degenerate progressively with time and that basket cells also are simultaneously involved.
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PMID:Menkes' kinky hair disease: morphological and immunohistochemical comparison of two autopsied patients. 202 48

We have developed a method for producing chronic regional nerve ischemia in rats by creating proximal limb arteriovenous shunts. This procedure results in a 50 to 75% reduction in endoneurial blood flow within the distal sciatic nerve as measured by the iodoantipyrine method. Nerve conduction velocities in sciatic nerves ipsilateral to the shunt fell by 25 to 30% within 2 weeks after creation of the shunt and did not recover for up to 10 months after the procedure. Morphological studies of the ischemic nerves showed structural abnormalities at nodes of Ranvier and mild axonal atrophy. Neither segmental demyelination nor axonal degeneration were evident. These results indicate that reduced endoneurial blood flow, insufficient to cause infarction, may result in measurable functional and morphological abnormalities in peripheral nerves.
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PMID:Peripheral neuropathy after chronic endoneurial ischemia. 204 44

Using laser Doppler measurements of nerve blood flow and electron microscopy, we determined that removal of the vasa nervorum from the surface of rat peripheral nerve results in an immediate 58.4% +/- (SD) 12.6% reduction in nerve blood flow (p less than 0.017) and subsequent subperineurial demyelination. To further assess the role of ischemia in demyelination, a second group of Sprague-Dawley rats (250 to 300 gm) was anesthetized and oxygen tensions were recorded with platinum microelectrodes in the tibial epineurial and endoneurial spaces before and 30 minutes after epineurial devascularization. Normal epineurial oxygen tension was 40.4 +/- (SD) 6.5 mm Hg before devascularization and 26.3 +/- 12.3 mm Hg after (p less than 0.012). Normal endoneurial oxygen tension was 22.9 +/- 6.0 mm Hg before devascularization and 14.3 +/- 5.4 mm Hg after (p less than 0.003). The topography of nerve fiber injury in this experimental model is identical with the changes induced in the sciatic nerve by circumferential compression at 30 mm Hg which is also thought to impede epineurial circulation. This subperineurial pattern of demyelination and axonal degeneration is associated with experimental interference with the epineurial circulation and may be contrasted with the central fascicular degeneration caused by microsphere embolization of the vasa nervorum via the common iliac artery. The data suggest that ischemia is the mechanism for subperineurial fiber injury after epineurial devascularization and highlight the importance of the transperineurial vessels which connect the epineurial anastomotic circulation and endoneurial capillary network.
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PMID:Subperineurial demyelination associated with reduced nerve blood flow and oxygen tension after epineurial vascular stripping. 207 64

Peripheral sensory nerve abnormalities were investigated in long-term streptozotocin diabetic rats using quantitative analysis. To determine whether the characteristic structural changes occur with a proximodistal gradient, three levels of the sensory peripheral nervous system were investigated: the postganglionic segment of the dorsal root, the midportion of the sciatic nerve, and the distal sural nerve. Reduction of myelinated fiber size due to reduced axonal caliber was the most characteristic change at both proximal and distal levels of the peripheral nerve. The relationship between axonal size and myelin spiral length indicated a more severe axonal atrophy in the distal portion. The axonal atrophy was related to a proportional loss of axonal neurofilaments at proximal levels, whereas in the distal sural nerve the loss of neurofilaments exceeded that which would be expected for axonal size. The universal reduction of axonal size in diabetic nerve may be accounted for by impaired supply of neurofilaments or reduced neurofilament synthesis. Such cytoskeletal defects may, in turn, lead to distal axonal degeneration or contribute to the susceptibility of diabetic nerve to various external noxi, including ischemia and hypoglycemia.
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PMID:Reduced myelinated fiber size correlates with loss of axonal neurofilaments in peripheral nerve of chronically streptozotocin diabetic rats. 214 49

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82

Myocardial infarction, myocardial scar tissue formation, and cardiac arrhythmogenesis seem to be associated. There are electrophysiological data suggesting that myocardial nerves are involved in arrhythmia development; however, there are no morphologic studies describing the fate of these nerves following necrotizing myocardial injuries. To describe the reactions of Schwann cells and axons following such injuries, we induced lesions in rat hearts with ischemia or transdiaphragmatic freeze-thawing and examined the acutely necrotic, healing, and healed lesions with light and electron microscopy. Antibodies to Schwann cell-associated S-100 protein were used to facilitate histologic detection. Both forms of injury produced focal lesions in which Schwann cells were killed and axonal segments destroyed; however, the basal lamina sheaths of cardiac myocytes and capillaries, and probably also of nerve fibers, remained largely intact. During 4 weeks of sequential observations, Schwann cells and axons were components of a hypercellular healing front that began at the periphery and moved toward the center of each lesion. Their proliferation and growth may have occurred within the original nerve basal lamina sheaths, and reparative axonal enlargements contained an abundance of 50- to 100-nm clear and dense storage granules. Fully developed nerve fibers were not only present in newly formed scar tissue but also appeared to be present in significantly greater density than in uninjured myocardial tissue. These findings demonstrate that proliferative nerve fiber regeneration occurs from the edges of necrotizing myocardial injuries, that healing results in relatively large number of nerve fibers in newly formed scars, and that axons in these scar-associated nerve fibers contain an abundance of neurosecretory granules. The functional significance of these observations remains to be determined.
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PMID:Fate of nerve fibers in necrotic, healing, and healed rat myocardium. 223 3


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