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

Renal function and morphology were studied before and after 60 min of renal ischemia and contralateral nephrectomy in two groups of rabbits. The animals were pretreated with ginsenosides (n = 22) and saline (n = 22) respectively, the latter as control. Results showed that ginsenosides (30 mg/kg body wt.) pretreatment by intravenous injection 10 min before warm ischemia resulted in the survival of all the animals with better renal function, 1, 3 and 7 days after blood urea nitrogen, fraction of excreted sodium and urine protein were observed in the control rabbits and a less pronounced increase was noted (P less than 0.05) after pretreatment with ginsenosides. The appearance of kidney tissue taken from surviving rabbits with Ginsenosides pretreatment was found to be normal under light microscope. Severe tubular necrosis was observed in kidneys of the control group. Tissues were examined with a transmission electron microscope. ginsenosides have protective effects on the epithelial cells of the proximal convoluted tubules, and microvilli and mitochondria were less damaged by ischemia than those of the control animals. There was also a large amount of ribosome on rough surfaced endoplasmic reticulum in the cells of ginsenosides-treated kidney, reflecting their ability to stimulate ribonucleic acid and protein synthesis. This is considered to be the basis of improvement of renal function.
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PMID:[Protective effects of ginsenosides on warm ischemic damages of the rabbit kidney]. 132 38

In a light microscopical study, we previously showed that more than 80% of somatostatin (SS) immunoreactive (-i) neurons in the hilus of the dorsal part of the rat dentate gyrus are lost 4 days after ischemia. In order to verify that the loss of SS immunostaining is due to an actual loss of the SS-i neurons and not merely a loss in expression of SS immunoreactivity, we have now performed an ultrastructural study of these neurons before and 40 h after 20 min of global cerebral ischaemia in adult rats. The normal SS-i neurons were multipolar and fusiform in shape. The SS-i product was associated with the endoplasmic reticulum and occasionally the Golgi apparatus. The cell nuclei had indentations of the nucleolemma and contained intranuclear rods. After ischaemia, many SS-i neurons in the dentate hilus showed increased electron density of both the cell nucleus and the cytoplasm. In addition the cytoplasm was heavily vacuolated with the SS-i associated with some of these vacuoles. Other SS-i neurons had, in addition to the vacuoles a more homogeneous, and abnormal electron lucent nucleus and cytoplasm. These ultrastructural changes correspond to previously reported irreversible, ischaemic cell changes of neurons. Based on this we conclude that the SS immunoreactivity in the dentate hilus of the dorsal hippocampus is lost after ischaemia because of neuronal necrosis. As a minor part of this study, we examined whether the ischaemia-susceptible SS-i neurons in dentate hilus had commissural axonal projections. This was done utilizing double fluorescence microscopy of retrograde axonal transport of the fluorescent dye, Fluoro-Gold, and the observation that vulnerable SS-i neurons display homogeneously dispersed immunostaining 40 h after ischaemia. Fluoro-Gold was injected unilaterally into the dorsal dentate gyrus 5 days prior to ischaemia. Then, 40 h after ischaemia, sections were stained for SS immunofluorescence, and examined, in the dentate hilus contralateral to the injection, for neuronal co-localization of both events. Cell counts revealed double-labelling of 13% of all neurons which displayed one of the events. This observation suggests that at least some of the ischaemia-susceptible SS-i neurons in dentate hilus do project commissurally. The pathophysiological significance of ischaemic loss of commissurally projecting SS-i neurons in dentate hilus remains to be determined.
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PMID:Ultrastructure of neurons containing somatostatin in the dentate hilus of the rat hippocampus after cerebral ischaemia, and a note on their commissural connections. 135 89

Photodynamic therapy has been used in the management of patients with malignant brain tumors even though the effects of this form of treatment on the adjacent normal brain are incompletely characterized. The authors examined, in sequential experiments, morphologic alterations affecting the cerebral cortex in rats injected with Photophrin II and exposed to light. Initially, minimal cell alterations, including cisternal swelling of both endoplasmic reticulum and Golgi apparatus, involved only neurons located in the superficial layers of the cerebral cortex exposed to light. These changes spread, over a period of several hours, from the surface to the bottom of the cortex and eventually involved the entire cortical segment exposed to light. The earliest structural signs of lethal injury to neurons developed over a period of 18 hours after porphyrins had been photoactivated and astrocytes had been severely damaged. Signs of lethal injury to neurons included an increase in the number of mitochondrial cristae and appearance of amorphous electron-dense deposits within swollen mitochondria. The appearance of these alterations was followed by segregation of intracytoplasmic organelles and fragmentation of nuclear and cytoplasmic membranes. The tissue changes, including those involving neurons, eventually progressed to coagulation necrosis at 48 hours. These observations suggest that prophyrins injected to rats (48 hours before photoactivation) cause swelling and necrosis of astrocytes. This is followed by neuronal necrosis, which appears at two time intervals; the initial neuronal necrosis occurs after the astrocytic disintegration. A second type of neuronal alteration appears after microvessels become thrombosed and ischemia is likely to develop.
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PMID:Neuronal injury after photoactivation of photofrin II. 141 89

The effect of RSM on ultrastructural alterations of the cortical, hippocampal and caudate neucleus areas brought about by forebrain ischemia in rats were studied. In both RSM-treated and saline-treated groups the ischemic damage was detected in nearly all animals three hours after bilateral common carotid artery ligation, while it was much more mild in RSM-treated animals. The ultrastructural changes consisted of swollen mitochondria, partial loss of cristae, dilatation of rough endoplasmic reticulum and Golgi's complex. In addition, some dark neurons were present, capillary endothelial cells and processes of astrocytes were swollen and active pinocytosis appeared in the endothelial cells. Their presence was most severe in the hippocampus region and the least in the caudate nuclear area. No ultrastructural changes exhibited in the sham-operated animals. The findings of the present experiment demonstrate that RSM can reduce ultrastructural abnormalities of cerebral ischemia and are also direct evidence of the protective effect of RSM on cerebral ischemia.
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PMID:The effect of radix Salviae miltiorrhizae on the changes of ultrastructure in rat brain after cerebral ischemia. 145 56

Prompt dendritic damage has been observed in the hippocampus of the gerbil brain after transient cerebral ischemia. In the present study, we studied the frontoparietal cortex of the gerbil brain electron microscopically after brief bilateral carotid occlusion to assess the vulnerability of dendritic processes. After ischemia for 5 min, there was swelling of the periphery of dendrites accompanied by swelling of mitochondria, cytoplasmic vacuolation and disintegration of microtubules in layer I, which spread to layer III after ischemia for 20 min. After reperfusion for 3-24 h following ischemia for 20 min, swelling in the periphery of dendrites and of mitochondria inside receded but vacuole formation and disintegration of microtubules propagated proximally. In neuronal perikarya, polyribosomal disaggregation was observed after ischemia for 20 min and persisted thereafter, while fragmentation of rough endoplasmic reticulum (ER) and microvacuolation occurred after reperfusion for 3 h. Electron-dense clumping of neuronal perikarya was observed after reperfusion for 6 h particularly in layers III and Vb, which increased in number for up to 72 h. The observed progressive damage in dendrites may be common to neurons vulnerable to cerebral ischemia and may significantly contribute to development of delayed neuronal death.
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PMID:Electron microscopic investigation of the cerebral cortex after cerebral ischemia and reperfusion in the gerbil. 148 6

Ethanol was injected intraperitoneally to dd-strain mice (20-25 g) with a dose of 5 g/kg body weight. The animals were sacrificed by the cervical dislocation at 4, 8, 12 and 24 hr after the ethanol injection. The changes of the ultrastructure of liver, heart, lung and kidney were examined by a transmission electron microscope. The results; from 4 hr to 24 hr after ethanol injection, deposition of fat droplets, swelling of mitochondria, enlargement of rough endoplasmic reticulum and loss of glycogen granules were observed in hepatocytes. Also, the edema of hepatocytes and intravascular hemostasis were found. These changes were aggravated with time course. In the heart, intravascular hemostasis, edema of myocardium, remarkable decrease of glycogen, swelling of mitochondria and appearance of I bands of myocardial fibers were observed. The damage to the myocardium by ethanol injection was similar to that associated with ischemia and anoxia. In the lung and the kidney, at early time after ethanol injection intravascular hemostasis and cell edema were observed but no other electron microscopical changes were found during the experiment. At 4 hr and 24hr after ethanol injection the edema of sinusoidal endothelial cell of liver and at 24hr that of endothelial cell of capillaries of heart were observed. These histological results suggest that the cell damages and intravascular hemostasis would be caused mainly by a direct action of ethanol. The damages of the liver and the heart, however, on the time blood ethanol was not detected would be caused by the disturbance of metabolism owing to ethanol oxidation.
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PMID:[Ultrastructural changes of liver, heart, lung and kidney of mice in a large dose of ethanol injection]. 158 89

To evaluate possible involvement of phospholipid metabolism and related second messenger systems in the selective neuronal damage after ischemia, we measured changes of polyphosphoinositides (PPIs) and free fatty acids (FFAs) in a model of 5-min or 10-min ischemia and reperfusion in gerbils. The binding activity of 3H-phorbol 12,13-dibutyrate (PDBu) for protein kinase C (PKC) and 3H-inositol 1,4,5-triphosphate (IP3) for IP3 receptors was demonstrated autoradiographically. Induction of 70 KDa heat shock protein (HSP70) mRNA and amyloid precursor protein (APP) mRNA was also examined using Northern blot analysis. In the parietal cortex (an area resistant to transient ischemia), PPIs decreased during ischemia and recovered rapidly after reperfusion. However, recovery did not occur in the hippocampal CA1 area (an area more vulnerable to transient ischemia). In the cortex, arachidonic acid (AA) increased during ischemia and returned to baseline by 7 days after reperfusion; in the CA1 area, the AA level remained elevated even after 7 days of reperfusion. PDBu binding decreased in CA1 cells after 2 days of reperfusion. IP3 binding began to decrease at 5 hr of reperfusion, which is far earlier than either the onset of decreased PDBu binding or the observation of neuronal damage by light microscopy. The induction of HSP70 mRNA occurred, but the induction of APP mRNA did not. Regional differences in the induction of HSP70 mRNA were found; CA1 cells produced less HSP70 mRNA than cortical cells 8 hr after transient ischemia. These results suggest that CA1 cell membranes may not recover after transient ischemic attack, and that the membranes of the endoplasmic reticulum, which have IP3 receptors, may undergo alterations earlier than cytoplasmic membranes. The variable induction of HSP70 mRNA may be related to regional differences in vulnerability in cortical and hippocampal CA1 cells after transient ischemia. Involvement of excitatory neurotransmission in the induction of HSP70 has been suggested. The combined data may support a role for inositol phospholipid metabolism, changes in related second messenger systems, and induction of HSP70 in the excitotoxic mechanism of hippocampal CA1 neuronal damage, death, and repair.
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PMID:Phospholipid metabolism and second messenger system after brain ischemia. 163 89

Cryopreserved allograft valves are increasingly being used as valvular replacements. Leaflet fibroblast viability has been suggested to influence clinical durability. The warm ischemic time is thought to be a critical determinant of this cell viability. The purpose of this study was to apply quantitative morphometric methods to characterize, by transmission electron microscopy, valvular cellular injury resulting from progressive warm ischemic time. Porcine aortic valves were harvested with a spectrum of warm ischemic times (40 minutes and 2, 6, 12, 24, and 36 hours; five valves per warm ischemic time; n = 30) and processed by standard electron microscopic methods. To ensure randomized tissue selection within each warm ischemic time interval, we randomly selected one thin section from each leaflet. The first ten cells in each thin section were photographed and cellular injury was assessed (cell disruption, dilation of endoplasmic reticulum, cytoplasmic edema, nuclear and mitochondrial changes). Nine hundred micrographs have been analyzed by Cochran-Mantel-Haenszel statistics to determine if a significant association between warm ischemic time and cellular injury exists. Our findings indicate a significant association between reversible cell injury through 24 hours of warm ischemic injury (p less than 0.0001). Furthermore, a significant association between irreversible cell injury and progressive warm ischemia through 36 hours was also found. These findings indicate that the ischemic interval after donor death is associated with progressive leaflet cell injury. Cellular damage begins shortly after donor death and continues incrementally throughout 36 hours. After 2 hours of warm ischemic injury 37% of the cells had morphologic evidence of injury. After 6 hours of warm ischemic injury the number of injured cells increased to 73%. By 36 hours 22% of the cells appeared normal. Irreversible cell injury increases with prolonged ischemia and becomes quantitatively impressive at 24 hours, by which time 26% of cells are so affected. Conversely, some cells are resistant to irreversible injury for a prolonged ischemic interval.
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PMID:Donor heart valves: electron microscopic and morphometric assessment of cellular injury induced by warm ischemia. 173 90

The ultrastructure of the progressive testicular involution with advancing age in men is reviewed. There is no definite age at which testicular involution begins, and the onset and severity of testicular lesions are subjected to pronounced individual variations. Hormone studies also indicate great individual variations, and subtle changes in both the testis and the pituitary develop progressively with age. Testicular size, sperm quality, and numbers of all germ cell types, Sertoli cells, and Leydig cells decrease with age. The volume occupied by the seminiferous tubules decreases, whereas that occupied by the testicular interstitium remains constant. The most frequent histological pattern of the aging testis is a mosaic of different seminiferous tubule lesions, varying from tubules with complete, although reduced, spermatogenesis, to completely sclerosed tubules. The tubules with complete spermatogenesis may show numerous morphological abnormalities in the germ cells, including multinucleation. Abnormal germ cells degenerate causing Sertoli cell vacuolation. These vacuoles correspond to dilations of the extracellular spaces resulting from the premature exfoliation of germ cells. Degenerating cells that are phagocytosed by the Sertoli cells give rise to an accumulation of lipid droplets in the Sertoli cell cytoplasm. The loss of germ cells begins with the spermatids, but progressively affects the earlier germ cell types, and tubules with maturation arrest at the level of the spermatocytes or spermatogonia are observed. The Sertoli cells show morphological abnormalities such as dedifferentiation, mitochondrial metaplasia, and multinucleation. Germ cell loss is associated with thickening of the tunica propria. When all seminiferous epithelial cells have disappeared, only an intensely collagenized tunica propria with myoid cells remains (sclerosed tubules). The Leydig cells progressively dedifferentiate with a decrease in the quantity of both smooth endoplasmic reticulum and mitochondria, together with an accumulation of lipid droplets, crystalline inclusions, and residual bodies, and formation of multinucleate cells. The development of tubular involution with age is similar to that observed after experimental ischemia, suggesting that vascular lesions may play an important role in age-related testicular atrophy.
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PMID:Ultrastructure of the aging human testis. 174 4

Plasma membrane potential generated by Na+, K(+)-ATPase provides the driving force for high-affinity, Na(+)-dependent uptake of glutamate into the cytoplasm of glutamatergic nerve endings and glial cells. Ca2(+)-calmodulin-dependent ATPase in the plasma membrane and Ca2(+)-ATPase in the endoplasmic reticulum influence the intracellular [Ca2+] and, therefore, the exocytotic release of neurotransmitter glutamate. The membrane potential across the membrane of the synaptic vesicles, generated by a H(+)-ATPase, provides the driving force for synaptic vesicular uptake of glutamate as well as that of GABA and glycine. Hypoxia and ischemia lead to release of glutamate, perhaps in consequence of an increased endogenous pool of glutamate and/or lack of substrate (ATP) for the ATPases. This release, rather than being exocytotic, is believed to result mainly from a reversal of the Na(+)-dependent high-affinity glutamate transporter in the plasma membrane.
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PMID:Interrelationship between glutamate and membrane-bound ATPases in nerve cells. 198 May 85


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