Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemorrhage and shock gave rise to quantitative determination of serum protein changes by means of the two-dimensional immunoelectrophoresis according to Laurell. 5 proteins showed significant changes. There were no new protein peaks or products of decomposition of other serum proteins. The liver injured by ischemia can not alone be responsible for the shift of serum proteins. Rather probably the majority of lost proteins remains in the splanchnic area.
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PMID:[Serum protein changes in liver transplantation in the dog]. 18 68

Focal cerebral ischemia was produced by occluding the left middle cerebral artery in 769 rats. Permeability of the blood-brain barrier to small or large molecules was evaluated qualitatively using Evans blue or sodium fluorescein and quantitatively using the transfer indexes of iodine-125-labeled bovine serum albumin or [14C]sucrose. Water content was determined using wet and dry weights and sodium and potassium contents using flame photometry. Cortical tissue in the middle cerebral artery territory was sampled less than or equal to 14 days after occlusion. A significant increase in the albumin transfer index was first found 12 hours after occlusion, and the index remained approximately the same until water content peaked 3 days after occlusion. In contrast, the sucrose transfer index increased gradually, significantly correlated with increases in the water and sodium contents. Tissue staining by sodium fluorescein was more extensive than that by Evans blue. As edema fluid decreased gradually 4-10 days after occlusion, the albumin and sucrose transfer indexes increased markedly. These findings indicate that disruption of the blood-brain barrier to small molecules is accompanied by accumulation of edema fluid during the later stages of ischemia. Opening of the barrier to serum protein is probably related to the resolution of edema.
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PMID:Brain edema and cerebrovascular permeability during cerebral ischemia in rats. 169 34

To study selectively the dilutional aspects of severe blood loss on the serum complement system, we developed an animal model consisting of isovolumic phlebotomy and reinfusion of washed autologous erythrocytes. This model avoided hypoperfusion, ischemia, and transfusion of foreign antigen. We measured total serum protein, C3 antigen, total complement hemolytic activity, and alternative pathway hemolytic activity. Each of the first three parameters dropped to 55% of initial value (P less than 0.005) by the end of the phlebotomy/reinfusion procedure and returned to normal levels by Day 1 or 2. C3 antigen and total complement hemolytic activity then rose to 150% of normal by Day 4 and gradually returned to normal within 2 weeks. Alternative pathway activity, by contrast, fell by more than 80% (P less than 0.005) within the first 6 hr, recovered by Day 4, and gradually rose to about 140% of normal by Day 21. Trauma patients treated for heavy blood loss who suffer depletion of hemolytic complement during the first few hours may be at greater risk of infection due to immune deficiencies. The implication of the results presented here is that the alternative pathway may be particularly weakened during blood loss and transfusion by simple dilution in addition to the effects of processes omitted in this model. Knowledge of the kinetics of complement recovery, independent of other effects usually accompanying trauma, may be helpful in determining whether these patients might benefit from exogenous manipulation of the complement system.
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PMID:Effects of plasmapheresis and autotransfusion on complement recovery in dogs. 235 91

The biochemical characterization of experimental acute pancreatitis was performed by determination of the secretory enzymes lipase and alpha-amylase, of the cytoplasmic ALAT (alanine aminotransferase), of total protein and calcium concentration in serum of rats. The moderate and protracted course of the pathological process in the small animal model presented allowed to study the initial phase from 1-24 h. In the first 4-8 h most massive enzyme release into the intravasal space was observed. The level of enzyme activities was correlating with the severity of assault. One noxa alone (ischemia or juice edema) resulted in a moderate enzyme release (lipase : 2-2.5 fold of control). The action of both noxae caused a drastical increase in enzyme activities in the initial phase lipase : 8-20 fold, ALAT: 7 fold, alpha-Amylase: 2.5 fold). 24 h postoperatively the serum enzyme activities were at distinct pathological level. At this time acute pancreatitis provoked already a decreased serum protein content. A hypocalcemia was not observed.
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PMID:Contribution of pancreatic edema and short-term ischemia to experimental acute pancreatitis in the rat. II. Behaviour of serum parameters. 349 93

Thickening of vessel walls resulting from endothelial proliferation was observed in the vasa nervorum of eleven patients with peripheral neuropathy associated with dysglobulinemia. Electron microscopy showed endothelial proliferation accompanied by abnormal accumulation of masses of intracytoplasmic filaments in each case. Of the eleven patients with dysglobulinemia, nine had monoclonal gammopathy and two were found to have polyclonal elevation of gamma globulin levels. Symptoms of neuropathy characteristically preceded detection of serum protein abnormalities by months to years. Nerve fiber lesions involved primarily the axon in four cases; segmental demyelination was the principal abnormality in the other seven. Both abnormalities were present to some degree in all eleven patients. Biphasic myelinopathy with uniform separation of myelin lamellae attributable to globulin deposition was observed in four cases. The microvascular changes included endothelial cytoplasmic enlargement, virtually obliterating the vessel lumen in many instances, with thickening of pericytes, in which intracytoplasmic filaments were prominent and pinocytotic vesicles numerous. No extracellular filaments were noted, and amyloid stains were negative. Possible effects of these microvascular changes include ischemia resulting from severe vascular luminal narrowing, and altered vascular permeability. Severe loss of axons in this group of neuropathies may be the result of ischemia, whereas altered vascular permeability may admit globulin into the endoneurium, where it may directly affect the myelin sheath and precipitate demyelination.
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PMID:Microangiopathy of vasa nervorum in dysglobulinemic neuropathy. 633 Dec 77

Brain free fatty acids (FFAs) and brain water content were measured in gerbils subjected to transient, bilateral cerebral ischemia under brief halothane anesthesia (nontreated group) and pentobarbital anesthesia (treated group). Mortality in the two groups was also evaluated. In nontreated animals, both saturated and mono- and polyunsaturated FFAs increased approximately 12-fold in total at the end of a 30-min period of ischemia; during recirculation, the level of free arachidonic acid dropped rapidly, while other FFAs gradually decreased to their preischemic levels in 90 min. In treated animals, the levels of total FFAs were lower than the nontreated group during ischemia, but higher at 90 min of reflow, and the decrease in the rate of free arachidonic acid was slower in the early period of reflow. Water content increased progressively during ischemia and recirculation with no extravasation of serum protein, but the values were consistently lower in the treated group. None of the nontreated animals survived for 2 weeks; in contrast, survival was 37.5% in the treated group. It is suggested that barbiturate protection from transient cerebral ischemia may be mediated by the attenuation of both membrane phospholipid hydrolysis during ischemia and postischemic peroxidation of accumulated free arachidonic acid.
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PMID:Brain free fatty acids, edema, and mortality in gerbils subjected to transient, bilateral ischemia, and effect of barbiturate anesthesia. 640 69

The definition of blood-brain barrier (BBB) damage in cerebral ischemia using contrast-enhanced MRI has not been clearly correlated to the spread of edema or other histological measures of barrier disruption. In this study, we used a rabbit model of focal cerebral ischemia to compare GdDTPA-enhanced MRI with spin-echo images of brain injury and immunocytochemical detection of BBB damage and vasogenic edema. After 4 h of transient ischemia followed by 6 h of reperfusion, in vivo T2W and T1W images were obtained in a 1.5 T magnet using a 3-inch surface coil. After MRI, the animals were sacrificed and anti-serum protein (IgG) monoclonal antibodies were used to detect regions of increased BBB permeability to serum proteins. Ischemic neuronal damage was confirmed with cresyl-violet histology. T2W scans showed focal regions of increased signal intensity in the ischemic hemisphere (17.0 +/- 4.1%) that primarily involved the cortex and striatum. T1W scans showed corresponding regions of hypointensity but demonstrated, in general, smaller lesion sizes (10.1 +/- 2.9%). GdDTPA-enhanced images showed variable areas of BBB disruption that included regions of intense leakage as well as lesions that only showed subtle enhancement along the periphery of damaged tissue. It appeared that large and more severe lesions corresponded to peripheral enhancement whereas smaller lesions showed central parenchymal enhancement. The extent of MR contrast enhancement did not correlate well with immunocytochemical images of serum protein leakage. Anti-IgG stains demonstrated widespread regions of BBB damage corresponding with areas of damaged neurons that appeared pyknotic on cresyl-violet sections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood-brain barrier disruption in experimental focal ischemia: comparison between in vivo MRI and immunocytochemistry. 800 69

Chronic hyperglycemia may cause growth factor alterations that are likely to participate in tissue remodeling typical for diabetic late complications. However, few details of such events are known. The ocular vitreous fluid allows studies of growth factor levels in human eyes (after vitrectomy). The vitreous is highly inert and protected by the blood-retina barrier and thus probably reflects growth factor production by the normal retina. Vitreous from patients with proliferative diabetic retinopathy (PDR) was compared with vitreous obtained from patients with nonproliferative eye disease and with vitreous from patients without diabetes but with marked neovascular proliferations due to ischemia. This design permits us to distinguish diabetes-related from non-diabetes-related alterations. Insulin-like growth factor I (IGF-I), IGF-II, IGF binding protein 2 (IGFBP-2), and IGFBP-3 were elevated 3- to 13-fold in nondiabetic retinal ischemia and 1.5- to 3-fold in PDR, indicating that the changes were not restricted to diabetes. These changes may partially be explained by leakage of serum into the vitreous, since IGFs and IGFBPs are 20- to 50-fold higher in serum than in vitreous, and vitreous protein content was 1.5-fold elevated in PDR subjects and 5-fold in ischemia patients compared with control subjects. TGF-beta is a proposed antiangiogenic factor in the eye. TGF-beta2 was the predominant subtype in vitreous, and its total amount was not altered in PDR patients. More importantly, the active fraction of TGF-beta was decreased by 30 and 70% in PDR and nondiabetic retinal ischemia patients, respectively. Since plasmin may control TGF-beta activation, the serum protein alpha2-antiplasmin was measured and found to be significantly elevated to 150 and 250% of control values in PDR and ischemia patients, respectively. Thus, influx of serum proteins due to microvascular disturbances and hypoxia is proposed as a possible cause for vitreous alterations of IGF-I and of active TGF-beta. These changes seem to occur late in the sequence of events leading to PDR and are not specific for diabetes, but they were also observed in other diseases characterized by retinal hypoxia.
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PMID:Growth factor alterations in advanced diabetic retinopathy: a possible role of blood retina barrier breakdown. 928 95

Elevated serum lactate dehydrogenase (LDH) is a characteristic finding in patients with thrombotic thrombocytopenic purpura (TTP). It is widely accepted that total serum LDH principally rises due to the release of red blood cell LDH as a consequence of intravascular hemolysis. To identify the cellular source of serum LDH in TTP, we prospectively analyzed total serum LDH and LDH isoenzyme profiles in 10 consecutive patients with classic, acute idiopathic TTP within 5 days of clinical presentation. Total LDH was quantitated on a Hitachi 911 Analyzer (Indianapolis, IN), using the lactate to pyruvate reaction. LDH isoenzymes were measured by serum protein electrophoresis, using the Beckman LDH Isoenzyme Kit (Anaheim, CA). Isoenzymes attributable to erythrocytes (LDH1, LDH2) were not disproportionately elevated in 9 of 10 patients. LDH3 was below or within normal limits for all 10 patients, and one patient showed a slightly increased LDH4. Serum LDH5, the isoenzyme derived primarily from liver and skeletal muscle, was elevated 1-2 times normal in all patients. Evidence supporting hemolysis as the major contribution to the elevated total serum LDH frequently encountered in acute TTP was not identified in this study. The isoenzyme fractions LDH and LDH2 elevated by erythrocyte injury were not disproportionately elevated in this series. LDH 5, the isoenzyme found in skeletal muscle and liver, was consistently 1- to 2-fold greater than normal in all patients. We propose that the elevation of serum LDH seen in patients with TTP is due to release of LDH from a variety of tissues damaged as a result of systemic ischemia.
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PMID:Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura. 959 Apr 92

Accumulation of serum protein has been demonstrated in injured brain cells following vasogenic brain edema. The present study was conducted to test whether this phenomenon is also observed in apoptotic cells as well as in necrotic cells. Apoptotic cell death has been implicated in a variety of brain injuries, including ischemia and trauma. Cold injury and focal cerebral ischemia-reperfusion were used to induce both vasogenic edema and apoptotic cell death. Evans blue extravasation was used to determine the cellular accumulation of serum albumin. Apoptotic cell death was evaluated by both morphological alterations and by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining. Evans blue accumulation in cells was observed not only in the surrounding zone of the lesion after cold injury and in the entire ischemic area after focal ischemia, but was also detected in the regions remote from the primary injury site. Some of these cells demonstrated nuclei fragmentation. TUNEL staining confirmed that apoptosis was induced in the region where apoptotic cells were morphologically detected. These observations suggest that accumulation of the extravasated serum component is accompanied by apoptotic cell death following vasogenic brain edema.
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PMID:Cellular accumulation of extravasated serum protein and DNA fragmentation following vasogenic edema. 981 38


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