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

Oligo-elements such as zinc (Zn), selenium (Se) and copper (Cu) have a significant influence on the function of the immune system. Various immunological and inflammatory changes are known to occur in patients undergoing cardiopulmonary bypass. The aim of this study was to evaluate changes in serum oligo-elements levels during and following cardiopulmonary bypass. The serum levels of Zn, Se and Cu were determined in 67 consecutive patients, with coronary artery disease admitted for coronary artery bypass grafting. Blood samples for oligo-elements, analysis were withdrawn into metal-free tubes just prior to the start of cardiopulmonary bypass; at 30, 60 and 90 min into cardiopulmonary bypass; following weaning from cardiopulmonary bypass; 30 min after termination of cardiopulmonary bypass; at 24 h; and on the 5th postoperative day. Trace elements analyses were performed using atomic absorption spectrophotometry. Interleukin 6 and 8, as well as serum albumin, creatine phosphokinase, lactate dehydrogenase and creatine phosphokinase-MB fractions were also analyzed. The mean age was 63 +/- 9 years and 91% (61) were men. The mean preoperative left ventricular function was 52 +/- 12%, Canadian Cardiovascular Society (CCS) angina class was 3.7 +/- 0.5 and 30% (20) of the operations were re-do's. All patients had normothermic cardiopulmonary bypass. Mean cardiopulmonary bypass-time was 85 +/- 31 min. One patient was lost for the recovery sampling (hospital mortality, 1.5%). Nine patients had a postoperative cardiac index < 2.0 liter/min per m2, which required pharmacological support and additional intra-aortic balloon pump in two of them. Other postoperative complications were few. There was a rapid depletion of S-selenium and S-Zn levels, which were halved at 30 min after cardiopulmonary bypass and remained low throughout the study period. The Cu/Zn ratio increased significantly at the start of cardiopulmonary bypass, which indicated an inflammatory reaction and was not normalized until the 5th postoperative day. Length of ischemia time, presence of diabetes. hypertension and hyperlipidemia did not influence the results, while a prolonged cardiopulmonary bypass-time > 120 min resulted in a higher Cu/Zn ratio than observed for shorter cardiopulmonary bypass-times. This indicates a more profound inflammatory response. Inflammatory parameters responded in the same manner as described earlier by others. These data indicate that severe loss of various oligo elements occur in patients undergoing coronary artery bypass grafting and suggests that a supplementary administration of zinc and perhaps also selenium could be appropriate during cardiopulmonary bypass.
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PMID:Inflammatory response and oligo-element alterations following cardiopulmonary bypass in patients undergoing coronary artery bypass grafting. 972 21

We have shown that high-concentration albumin therapy is markedly neuroprotective in focal cerebral ischemia. The present study was conducted to ascertain the degree to which hemodynamic alterations are responsible for this therapeutic effect. Normothermic, physiologically regulated male Sprague-Dawley rats received a 2-h period of middle cerebral artery occlusion (MCAo) by insertion of an intraluminal suture coated with poly-L-lysine. Albumin (25% human serum albumin solution) or vehicle (0.9% sodium chloride) was administered intravenously at a dose of 1% of body weight immediately after suture withdrawal following 2-h MCAo. Local cerebral blood flow (LCBF) was measured autoradiographically with 14C-iodoantipyrine after 1 h of recirculation. Novel image-processing methods were used to compare average LCBF data sets against previously obtained infarction-frequency data on a pixel-by-pixel basis. Albumin therapy reduced mean hematocrit by 42% but produced no other systemic alterations. Pixel-based histopathological analysis revealed large, consistent cortical and subcortical infarcts in saline-treated rats with MCAo; albumin therapy reduced mean cortical infarct volume by 85%. Within regions showing albumin-associated neuroprotection, numbers of pixels having LCBF in the upper ischemic-core flow range (0.12-0.24 ml g-1 min-1) were reduced by 8.6-fold by albumin therapy when compared to saline-treated rats; and numbers of pixels with LCBF in the lower penumbral flow range (0.24-0.36 ml g-1 min-1) were reduced by 3. 1-fold in albumin-treated rats (p=0.04 by repeated-measures analysis of variance). Analysis of the [albumin-saline] 3-dimensional difference-image data set revealed a circumferential zone of statistically significant albumin-associated LCBF increase within the posterior portion of the ischemic hemisphere, surrounding the core-region of prior ischemia. Thus, high-concentration albumin therapy improves local perfusion to regions of critical LCBF reduction. The spatial extent of this LCBF effect, however, appears too small to account fully for the marked neuroprotective efficacy of this therapy. We suggest that other, non-hemodynamic mechanisms may also be contributory.
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PMID:The effect of high-dose albumin therapy on local cerebral perfusion after transient focal cerebral ischemia in rats. 972 10

Nitroxide free radicals are known to protect cells from oxidative damage. Diffusion-weighted and perfusion-weighted magnetic resonance imaging was used to evaluate the effects of polynitroxyl albumin (PNA) in a middle cerebral artery intraluminal suture model of transient focal cerebral ischemia in the rat. Three groups of Sprague-Dawley rats were investigated: (1) PNA (N=6), (2) human serum albumin (N =6), and (3) saline (N=7). The middle cerebral artery was occluded for 2 hours. Treatment was started 30 minutes after induction of ischemia. A total dose of 1% body weight (volume/weight) of PNA (23.5 mg/dL protein and 110 mmol/L nitroxide), albumin (23.5 mg/dL), or saline was injected intravenously at three time points: 0.5% at 0.5 hours, 0.25% at 2 hours (i.e., just before reperfusion), and 0.25% at 4 hours after occlusion. Six sets of diffusion- and perfusion-weighted magnetic resonance images were acquired throughout the 2 hours of ischemia and the 2 hours of reperfusion. The rats were killed at 24 hours, and the brains were stained with 2,3,5-triphenyltetrazolium chloride (TTC). Diffusion-weighted imaging showed that the growth of the ischemic lesion was suppressed in the PNA-treated group. The 4 hours diffusion-weighted imaging--derived hemispheric lesion volume in the PNA-treated group (25%+/-9%) was significantly smaller than that in the saline-treated (43%+/-13%; P=0.016) or albumin-treated groups (38%+/-6%; P=0.017). A larger difference was observed for the 24-hour TTC-derived lesion volumes in the PNA (8%+/-7%), saline (35%+/-8%; P < 0.001), and albumin (31%+/-6%; P < 0.001) groups. Perfusion-weighted imaging demonstrated a marked improvement in cerebral perfusion in the PNA-treated group during ischemia and reperfusion. In conclusion, treatment with PNA results in an improvement in perfusion and a reduction of infarct volume in a model of transient focal cerebral ischemia in the rat.
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PMID:Polynitroxyl albumin reduces infarct size in transient focal cerebral ischemia in the rat: potential mechanisms studied by magnetic resonance imaging. 974 Jan 6

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

The effects of permanent focal ischemia on specific proteins of the cerebral hemisphere were studied by unilateral occlusion of the middle cerebral artery (MCAO) in rat. Brain proteins were prepared 72 h after the occlusion and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The proteins were identified by their interaction with rabbit antibodies against rat serum proteins and anti-transferrin antibodies. SDS-PAGE analysis of the proteins prepared from ischemic tissue showed significant increase in the 66 and 80 kDa components; where a marked decrease in the 260 kDa protein occurred in the ischemic and para-ischemic tissues. The 66 kDa and 80 kDa proteins stained intensely with anti-serum protein antibodies, indicating that they are related to plasma components. Moreover, the 66 kDa band had the same electrophoretic mobility as bovine serum albumin used as a standard molecular size marker. The 80 kDa band was identified as transferrin by staining with the specific antibody. Transferrin was immunolocalized in the penumbra of cerebral cortex, hippocampal CA1 region and dentate gyrus of the ischemic cerebral hemisphere. The present results suggest that alteration in the brain content of 66 kDa (albumin), 80 kDa (transferrin) and 260 kDa (unidentified) proteins may reflect early effects of focal ischemia.
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PMID:Alteration in brain proteins following occlusion of the middle cerebral artery in rat. 1046 76

The effect of vitamin B2 (riboflavin) on oxidant-mediated acute lung injury has been examined in three different rat models. Pulmonary injury was induced by intravenous injection of cobra venom factor (CVF), by the intrapulmonary deposition of IgG immune complexes, or by hind limb ischemia-reperfusion. In each of the three models, injury was characterized by increases in vascular permeability (leakage of 125I-labeled bovine serum albumin), alveolar hemorrhage (extravasation of 51Cr-labeled rat erythrocytes), and neutrophil accumulation (myeloperoxidase activity). Intraperitoneal administration of riboflavin at a dose of 6 micromoles/kg body weight reduced vascular leakage by 56% in the CVF model, by 31% in the immune complex model, and by 53% in the lung injury model following ischemia-reperfusion of the hind limbs. Similar treatment reduced hemorrhage by 76%, 51%, and 70% in the three models of lung injury. In the CVF model, riboflavin was also shown to decrease products of lipid peroxidation (conjugated dienes) in lungs (by 45%) and in plasma (by 74%). Neutrophil accumulation in the lungs was not influenced by riboflavin administration in any of the three models. The studies demonstrate that riboflavin can mount a significant protection against oxidant-mediated inflammatory organ injury.
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PMID:Protection by vitamin B2 against oxidant-mediated acute lung injury. 1046 81

Albumin is used to provide colloid osmotic pressure in some resuscitation and organ preservation protocols. These solutions are expensive and carry the risks of using high concentrations of blood products. Used as a carrier of drugs and substrates, the concentration of albumin present in perfusates may be considerably lower in experimental ischemia. The present study examined if trace amounts of albumin (0.0004%) reduce injury from ischemia and reperfusion in isolated rat hearts. Hearts were perfused by the Langendorff technique (60 mmHg) with an intraventricular balloon. Zero-flow ischemia (20 min, 37 degrees C) was followed by reperfusion (35 min, 37 degrees C). Recovery of contractile function during reperfusion was significantly improved by the presence of fatty acid-free bovine serum albumin (BSA) (22 290+/-1280 mmHg/min, pressure-rate product) or rat serum albumin (RSA) (21 095+/-2836 mmHg/min) compared with Krebs-Henseleit buffer with no albumin (KHB) (9660+/-2324 mmHg/min). Release of lactate dehydrogenase activity, formation of tissue edema and accumulation of tissue malonyldialdehyde were significantly reduced in hearts receiving BSA or RSA compared with KHB alone. These parameters were not altered by the presence of albumin in non-ischemic control hearts or in the pre-ischemic values of the hearts subjected to ischemia and reperfusion. Development of ischemic contracture with an extended period of ischemia (27 min) was not altered by the presence of BSA, suggesting that protection observed with albumin occurred during reperfusion, rather than during ischemia. Reperfusion following 45 min of ischemia with bovine serum albumin resulted in similar myocardial injury to hearts that were reperfused following 20 min of ischemia without bovine serum albumin. Thus, trace amounts of albumin provide significant reduction in myocardial injury from ischemia and reperfusion, probably via antioxidant mechanisms.
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PMID:Trace amounts of albumin protect against ischemia and reperfusion injury in isolated rat hearts. 1047 49

Therapeutic cerebral hypothermia is widely used for the treatment of severe head injury and cerebral ischemia. The effects of cerebral hypothermia on the cerebral blood flow (CBF) and metabolism, and cerebral vasculature in the normal brain were investigated. Thirty-four adult cats were divided into four groups. CBF was monitored by hydrogen clearance. Arteriovenous oxygen difference (AVDO2) and cerebral venous oxygen saturation (ScvO2) were measured in blood samples from the superior sagittal sinus. The cerebral metabolic rate of oxygen (CMRO2) and cerebral vascular resistance (CVR) were calculated. The cerebral blood volume (CBV) was measured using technetium-99m-labeled human serum albumin in 12 cats. Deep cerebral temperature was cooled from 37 degrees C to 25 degrees C using a water-circulating blanket. In the hypothermia group (Group A: n = 10), CBF (51.2 +/- 8.3 ml 100 g-1 min-1 at 37 degrees C) decreased with lower brain temperature (6.1 +/- 2.7 at 25 degrees C). CMRO2 (2.24 +/- 0.75 ml 100 g-1 min-1 at 37 degrees C) was also decreased (0.52 +/- 0.20 at 25 degrees C). AVDO2 (4.3 +/- 1.0 ml 100 g-1 min-1 at 37 degrees C) increased significantly at 31 degrees C (6.6 +/- 1.8; p < 0.05) and ScvO2 (67.8 +/- 7.9% at 37 degrees C) decreased significantly at 29 degrees C (53.7 +/- 9.7; p < 0.05). CBV (5.3 +/- 1.2% at 37 degrees C) decreased significantly at 29 degrees C (3.7 +/- 1.0; p < 0.05) and CVR (3.2 +/- 0.7 mmHg ml-1 100 g-1 min-1 at 37 degrees C) increased significantly at 29 degrees C (13.8 +/- 5.2; p < 0.01). The combined effect of hypothermia with vasopressor (noradrenalin) (Group B: n = 6) or barbiturate (thiopental) administration (Group C: n = 6) on the cerebral metabolic parameters were also examined. Hypothermia with noradrenalin administration significantly improved the ischemic parameters (AVDO2 was 4.7 +/- 1.4 ml 100 g-1 min-1 at 31 degrees C and ScvO2 was 72.2 +/- 6.4% at 29 degrees C). However, hypothermia with barbiturate administration did not improve these metabolic parameters. These results suggest that hypothermia may cause vasoconstriction and misery perfusion in the brain. This potential risk of relative ischemia can be avoided by combination with vasopressor administration.
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PMID:Misery perfusion caused by cerebral hypothermia improved by vasopressor administration. 1049 21

The purpose of this study was to determine whether treatment with high-dose human serum albumin (HSA) would offer protection in a model of high-grade transient forebrain ischemia. Twenty-six fasted Wistar rats underwent bilateral common carotid artery occlusion and severe hypotension (50 mmHg) for 10 min. The agent (25% HSA) or vehicle (0.9% NaCl) was administered i.v. 5 min after termination of ischemia. HSA-treated rats showed significantly improved neurological deficits throughout a 7-day survival period. Histologically, HSA-treated rats showed 2.4- to 5.3-fold increases in numbers of surviving CA1 hippocampal pyramidal neurons compared to saline-treated animals. These results document that high-dose albumin therapy instituted 5 min after global ischemia significantly improves neurological score and reduces histological damage.
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PMID:Neuroprotective effect of high-dose albumin therapy against global ischemic brain injury in rats. 1052 50

The effects of three hemoglobin solutions were compared with those of iso-oncotic human serum albumin in rats with ischemic renal failure and sham-operated controls. Unmodified and alpha-alpha cross-linked hemoglobins both increase mean arterial pressure and systemic vascular resistance and reduce cardiac output substantially and to a comparable extent. In contrast, omicron-raffinose cross-linked hemoglobin has no deleterious effect on any of these parameters. In sham-operated rats unmodified hemoglobin reduces the glomerular filtration rate (GFR) by approximately 30%, whereas neither of the two cross-linked hemoglobins has any adverse effect on GFR in this group. None of the three hemoglobin solutions exacerbated the degree to which GFR was reduced by ischemia-reperfusion injury. Also, the degree of tubular necrosis induced by ischemia-reperfusion injury was also comparable in all groups. We conclude the following: (1) omicron-raffinose cross-linking, but not alpha-alpha cross-linking, ameliorates the effects of unmodified hemoglobin on vascular resistance and cardiac output; (2) both forms of cross-linking reduce the nephrotoxicity exhibited by unmodified hemoglobin in sham-operated rats; and (3) none of the hemoglobin solutions exacerbate renal injury induced by ischemia-reperfusion.
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PMID:Effects of hemoglobin-based oxygen-carrying solutions in anesthetized rats with acute ischemic renal failure. 1063 97


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