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

Classical forms of degenerative changes of neurocytes, defined by Nissl and Spielmeyer as neuronal diseases were produced experimentally in rats. The individual neuronal changes were induced with the aid of X-ray irradiation, TET administration, ligation of the carotid artery followed by oxygen deficient breathing (anoxia), and by sectioning of the sciatic nerve. The so produced experimental models of neuronal diseases were the subject of morphological and cytochemical studies with special attention payed to enzymic and autoradiographic reactivity. Basing on the results of performed investigations, the author inferred that from a pathogenetic point of view, not all of the respective forms of neuronal diseases postulated by the classification of Nissl and Spielmeyer can be regarded as separate, distinct forms of degenerative changes. From the results obtained it would appear that pathogenetically distinct are only the following diseases: acute nerve cell swelling, shrinkage of perikaryons, homogenizing changes of Purkinje cells and axonal degeneration. The so called severe disease as well as the ischemic disease should be regarded as transitory forms of neuronal changes developing from shrunken neurocytes. It has also been suggested that the pathogenesis of homogenizing changes in Purkinje cells is distinct from that responsible for the development of ischemic changes in the course of cerebral anoxia and ischemia. This suggestion is substantiated by the observed differences in cytoenzymic reactivity between homogenized Purkinje cells and ischemically changed neurocytes.
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PMID:Histochemistry of neuronal degenerative changes. 17 15

It has been suggested that unstable angina at rest, like acute myocardial infarction, might be associated with a thrombotic process. In order to study the hypothesis that myocardial ischemia during exercise could also be associated with an activation of blood coagulation and/or fibrinolysis, we investigated the presence of plasma markers of a prethrombotic or thrombotic state (thrombin-antithrombin III complexes TAT, prothrombin fragment F1 + 2, and D-dimers DD) in 100 consecutive patients with confirmed or suspected coronary artery disease during ergometric test with myocardial thallium-201 scintigraphy. Symptoms and scintigrams allowed to define three groups of patients: those showing no ischemia (n = 79) and those with symptomatic (n = 8) or silent myocardial ischemia (n = 13). Before exercise, DD and TAT levels were not significantly different among the three groups. On the other hand, the F1 + 2 levels were slightly albeit significantly higher in the patients without ischemia than in the patients with symptomatic or silent ischemia. After exercise, no significant difference was found between the three groups. Exercise induced a significant and parallel increase in both the TAT and the F1 + 2 levels (but not of the DD levels) in the three groups. Thus, our study does not support the hypothesis that myocardial ischemia, silent or symptomatic, is associated with an activation of plasma coagulation and fibrinolysis that can be distinguished from the exercise-induced thrombin generation.
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PMID:Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia. 160 40

The state of water in cerebral ischemia was studied by using the proton nuclear magnetic resonance (1H-NMR) method. Cerebral ischemia was induced experimentally in Mongolian gerbils by unilateral ligation of the common carotid artery. Longitudinal (T1) and transverse (T2) relaxation times of the ischemic brain were measured with a pulse FT-NMR spectrometer and the water content was determined by the wet/dry method. Quantitative analysis of the relaxation times was performed sequentially during the initial 7 hours following ligation and the data were compared with those of brain edema previously reported by S. Naruse in the rat. Characteristic findings in brain ischemia include prolongation of the slow component of T2 and increase in the water content. A quantitative comparison of relaxation rate and water content demonstrates that ischemic brain edema in Mongolian gerbils is different from cytotoxic and vasogenic types of brain edema. When R2 (1/T2) was plotted against the water content, the slope value of ischemia in the gerbil was between the slope values of the TET intoxication and cold injury induced edemas reported previously. From these results, it might be said that ischemic brain edema includes both the cytotoxic and vasogenic types of brain edema. Glycerol was demonstrated to affect brain ischemia by decreasing the water content and by shortening the slow component of T2. By analysis of the relaxation times and water content, we examined the pathophysiological characteristics of water molecules in ischemic brain tissue.
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PMID:Proton NMR relaxation times in ischemic brain edema. 381 Jul 13

Ischemia of the stria vascularis in the cochlea associated with temporal hearing loss was found in guinea pigs with intravenous othacrynic acid injection. Using this animal model, we studied the therapeutic value of low power density microwave on the ischemic stria vascularis. Experimental findings confirmed that microwave irradiation on the ear might prompt a quicker recovery of hearing. Meanwhile, milder pathological changes of the stria vascularis were shown either on light microscopy or on TEM in the microwave treated animals. Hence, it is suggested that microwave irradiation causes an improvement of microcirculation and an alleviation of lesions in the stria vascularis. The study has provided an experimental basis of microwave treatment for the hearing impairment due to microcirculation disorder in the inner ear.
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PMID:[Experimental study on the therapeutic value of microwave on hearing loss due to ethacrynic acid ototoxicity]. 816 43

The efficacy of preventing ischemia-reperfusion damage by employing native or modified (mPEG-SOD) superoxide dismutase in an experimental model of acute ischemia was tested in the left hind limb of 43 Wistar rats. A significative difference (p=0.004) of the survival leg rate was found in the group treated with mPEG-SOD (86.6%) compared with the control group (30%). This difference was confirmed both clinically and by TEM analysis of muscular specimens.
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PMID:Prevention of ischemia-reperfusion damage with polymerized superoxide dismutase. 851 86

Decreasing progressive dermal ischemia after burning could theoretically limit the amount of skin necrosis. It is controversial whether the use of free radical scavengers could prevent the progressive dermal ischemia of the postburn stasis zone. We evaluated the effect of superoxide dismutase (SOD) on preventing postburn dermal ischemia in animal models by the India ink perfusion and skin transparent preparation techniques. The closely clipped backs of guinea-pigs were bathed in 75 degrees C water for 10 s. Within 5 min postburn, SOD-treated groups were administered SOD (10,000 u/kg) intra-peritoneally every 6 h. All animals were perfused with 70 per cent India ink via cervical artery cannula by 16 kPa constant pressure at 0, 8, 16, 24 h postburn, and the skin transparent preparations were made, while the level of malonyl dialdehyde (MDA) in skin tissue was assessed. The results showed that with prolongation of postburn time, the rate of filling of India ink in skin capillary plexuses decreased gradually (p < 0.01). MDA increased continuously, which was related to postburn dermal ischemia (r = 0.689, p < 0.01). Though the level of MDA decreased in SOD-treated groups, the India ink filling rates showed no significant difference between controls and experimental groups (p > 0.05). The results were also confirmed by observation of skin transparent preparations and TEM. This study suggests that superoxide dismutase fails to prevent progressive dermal ischemia after burning.
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PMID:Can superoxide dismutase prevent postburn dermal ischemia? 923 83

In this study, we evaluated the role of proteolytic enzymes belonging to the coagulation, fibrinolytic, and plasma contact systems in the early postoperative phase after orthotopic liver transplantation (OLT). Twenty-nine patients were studied at the time of OLT and during the first 2 postoperative weeks. Blood samples were collected daily after OLT and analyzed for kallikrein-like activity (KK), functional kallikrein inhibition (KKI), plasmin-like activity (PL), and alpha2-antiplasmin (AP). In addition, prekallikrein (PKK), prothrombin (PTH), antithrombin III (AT III), plasminogen (PLG), prothrombin/antithrombin III complexes (TAT), prothrombin fragment 1 + 2 (F1 + 2), and plasmin/alpha2-antiplasmin complexes (PAP) were measured. Nineteen patients experienced biopsy-verified acute rejections (AR) and ten patients had uneventful courses and served as controls. Plasma analyses showed that the contact, coagulation, and fibrinolytic systems were activated during OLT. Following OLT, continuous thrombin and plasmin generation was observed, and these effects were more pronounced in the group having an uneventful course than in patients with AR. Factors that could possibly affect plasma proteolytic activity, such as blood product usage during and after OLT and cold ischemia time of the liver graft, did not differ between the groups, nor did the routine liver function tests, alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
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PMID:Plasma proteolytic activity in liver transplant rejection. 1036 91

Alterations in pulmonary surfactant have been reported to be associated with ischemia/reperfusion injury in experimental and clinical lung transplantation. It is unknown whether these alterations are due to damage to surfactant synthesizing type II pneumocytes during hypothermic ischemic storage. The aim of the present study was to examine the effects of hypothermic ischemic storage of the lung on canine type II pneumocytes by means of conventional (CTEM) and energy filtering TEM (EFTEM) and stereology. The lungs of 18 dogs were fixed for TEM immediately after cardiac arrest (6 double lungs) and after storage in Tutofusin at 4 degrees C for 20 min, 4 hr, 8 hr, and 12 hr (6 single lungs, respectively). Using a systematic uniform random sampling scheme, type II pneumocytes were analyzed qualitatively and stereologically. The relative phosphorus content of cell organelles, especially the surfactant containing lamellar bodies, was investigated by EFTEM. By CTEM, no major qualitative alterations could be observed in type II pneumocytes of the experimental groups. Stereologically, no significant changes in the volume densities or the volume-to-surface ratios of type II pneumocytes and their lamellar bodies were found. By EFTEM, the highest intracellular phosphorus signals were recorded over lamellar bodies in all experimental groups. No changes in the phosphorus signals were observed during ischemia. These results indicate that the ultrastructure of canine type II pneumocytes and their lamellar bodies is not affected by hypothermic ischemia of the lung up to 12 hr. Structural preservation of intracellular surfactant is possible during prolonged ischemic lung storage.
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PMID:Ultrastructure of canine type II pneumocytes during hypothermic ischemia of the lung: a study by means of conventional and energy filtering transmission electron microscopy and stereology. 1136 Feb 29

Studies of ischemia/reperfusion (I/R) injury and preconditioning have shown that ion homeostasis, particularly calcium homeostasis, is critical to limiting tissue damage. However, the relationship between ion homeostasis and specific cell death pathways has not been investigated in the context of I/R. Previously we reported that calpain cleaved Bid in the absence of detectable caspase activation (1). In this study, we have shown that an inhibitor of the sodium/hydrogen exchanger prevented calpain activation after I/R. Calpain inhibitors prevented cleavage of Bid as well as the downstream indices of cell death, including DNA strand breaks, creatine kinase (CK) release, and infarction measured by triphenyl tetrazolium chloride (TTC) staining. In contrast, the broad spectrum caspase inhibitor IDN6734 was not protective in this model. To ascertain whether mitochondrial dysfunction downstream of these events was a required step, we utilized a peptide corresponding to residues 4-23 of Bcl-x(L) conjugated to the protein transduction domain of HIV TAT (TAT-BH4), which has been shown to protect mitochondria against Ca2+-induced deltaPsi(m) loss (2). TAT-BH4 attenuated CK release and loss of TTC staining, demonstrating the role of mitochondria and a pro-apoptotic Bcl-2 family member in the process leading to cell death. We propose the following pathway. (i) Reperfusion results in sodium influx followed by calcium accumulation. (ii) This leads to calpain activation, which in turn leads to Bid cleavage. (iii) Bid targets the mitochondria, causing dysfunction and release of pro-apoptotic factors, resulting in DNA fragmentation and death of the cell. Ischemia/reperfusion initiates a cell death pathway that is independent of caspases but requires calpain and mitochondrial dysfunction.
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PMID:Calpain and mitochondria in ischemia/reperfusion injury. 1204 24

The delivery of proteins across the blood-brain barrier is severely limited by the proteins' size and biochemical properties. Eleven-amino acid human immunodeficiency virus TAT protein is able to cross cell membranes even when coupled with larger peptides. We evaluated whether TAT-Bcl-X(L) fusion protein is protective in focal ischemia. Mice underwent 30 or 90 minutes of intraluminal middle cerebral artery thread occlusion. TAT-Bcl-X(L), TAT-beta-galactosidase, or TAT-GFP (0.6 nmol each) were applied intravenously over 10 minutes either 1 hour before or immediately after ischemia. Additional animals received no TAT protein infusions. We show that the brain tissue is progressively transduced with TAT proteins within 3 to 4 hours after intravenous delivery. We provide evidence that TAT-Bcl-X(L) treatment reduces infarct volume and neurological deficits after long ischemic insults lasting 90 minutes, when applied both before and after ischemia. After short insults, lasting only 30 minutes, TAT-Bcl-X(L) further diminishes the number of caspase-3-reactive and DNA fragmented cells and increases the number of viable neurons in the striatum. Our results indicate that TAT fusion proteins are elegant and powerful tools that might be of clinical interest for stroke treatment, because factors may be intravenously applied. Thus, fusion proteins may open fascinating perspectives for future research.
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PMID:Intravenous TAT-Bcl-Xl is protective after middle cerebral artery occlusion in mice. 1240 59


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