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

Changes in brain water, sodium, potassium, and albumin contents and blood-brain barrier (BBB) permeability were determined at various times between 1 hour and 6 weeks following occlusion of the middle cerebral artery (MCA) in rats. In the center of the infarct, brain edema increased to a maximum level by 12 hours, remained elevated for 7 days, and then returned to normal. The change in water content was accompanied by a parallel increase in sodium and decrease in potassium contents; however, the increase in sodium always exceeded the decrease in potassium, resulting in a net gain in brain cations during edema formation which returned to normal with edema resolution. The BBB permeability to 3H-alpha-aminoisobutyric acid was increased by 24 hours after MCA occlusion and returned to normal by 1 week after the edema had resolved. The time course for changes in brain albumin content was different than that for brain edema formation. Large increases in brain albumin content were not apparent until 6 hours after the onset of ischemia, rose to a peak at 3 days after occlusion of the MCA, and returned to normal several weeks after the edema had resolved. Albumin appeared to spread from the central infarct zone to surrounding, less ischemic areas. The relative contributions of the osmotic force produced by the increase in brain cations and the oncotic force produced by the increase in brain albumin to the observed change in water content were calculated. At all time points, the increase in brain cations accounted for nearly all of the observed brain edema, while the increase in albumin played essentially no role in edema development.
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PMID:Contributions of ions and albumin to the formation and resolution of ischemic brain edema. 842 Dec 8

Transvascular clearance of labeled rabbit albumin was measured in gastrocnemius muscle and heel skin from anesthetized rabbits after 1 or 2 h of tourniquet ischemia. Albumin clearance, calculated as a 1-h extravascular uptake, was 4.7 +/- 0.4 and 29 +/- 1 microliter.h-1 x g dry wt-1 for control gastrocnemius muscle and heel skin, respectively. During the first hour of reperfusion, the clearance was 101 +/- 23 and 56 +/- 6 microliters.h-1 x g dry wt-1 in the muscle and skin, respectively. The clearance in skin during the second and third hour of reperfusion was not different from control. The increased clearance in muscle persisted during 2 h of reperfusion but returned to control levels during the third hour of reperfusion. The solvent drag reflection coefficient was measured by increasing venous pressure during reperfusion in one leg after bilateral ischemia. In skin, the reflection coefficient, calculated as 1 minus the change in clearance divided by the change in water weight, was 0.94 +/- 0.05 and did not change with tourniquet ischemia. The reflection coefficient in muscle was 0.98 +/- 0.01 for control animals and decreased to 0.66 +/- 0.11 during the first hour of reperfusion. The reflection coefficient was not different from control during the third hour of reperfusion. The transitory increase in microvascular permeability to albumin in skeletal muscle is more indicative of an acute inflammatory response than of endothelial injury.
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PMID:Transvascular albumin flux in rabbit hindlimb after tourniquet ischemia. 845 91

The purpose of this study was to define the differences in heat shock protein (hsp)70, albumin, alpha(-1)-acid glycoprotein (AGP), and CCAAT enhancer binding proteins (C/EBP) alpha and beta mRNA between hepatic ischemia and reperfusion, and to begin to explore C/EBP protein production. These genes have been found important in the hepatic response to lipopolysaccharide and inflammation. In two experiments, Sprague-Dawley rats underwent temporary occlusion of the median and left hepatic lobe vasculature. The first experiment included a single sham-operated group and ligation of the right hepatic lobes during reperfusion. It compared 30 and 60 min ischemia to 2 h reperfusion. The second experiment included a sham-operated group for every time point, and the right hepatic lobes were not ligated during reperfusion; a 30-min ischemia group was compared to 2-, 5-, and 24-h reperfusion groups. Total RNA from the ischemic lobes was analyzed by Northern hybridization for hsp70, albumin, AGP, and C/EBPalpha and beta. C/EBPalpha and beta proteins were compared by Western blotting. Differences in experimental design played an important role in interpretation of results. hsp70 mRNA began to increase during ischemia. Albumin mRNA remained constant during ischemia and reperfusion. The ischemic hepatocyte nucleus is not quiescent and retains the ability to upregulate certain genes, e.g., hsp70. Changes in mRNA in response to hepatic ischemia/reperfusion occur rapidly. Hepatic ischemia/reperfusion does not recapitulate the classic acute phase response; albumin is not down regulated during reperfusion.
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PMID:Early gene response to hepatic ischemia reperfusion. 866 Nov 80

We used an isolated, blood-perfused rat lung model to evaluate the separate roles of ischemia and reperfusion time, the changes in pulmonary artery pressure (Ppa), and the circulating neutrophil number in mediating ischemia-reperfusion lung injury. Extravascular albumin accumulation was used to quantify changes in the permeability of the alveolar capillary membranes. In animals subjected to 30 and 45 min of ischemia without reperfusion, extravascular albumin accumulation was significantly higher than in controls subjected to continuous perfusion (P < 0.05). Albumin accumulation in animals subjected to 45 min of ischemia was greater compared with those undergoing 30 min of ischemia followed by 30 min of reperfusion (P < 0.05). In animals undergoing 45 min of ischemia followed by 30 min of reperfusion, a linear relationship was demonstrated between changes in Ppa and extravascular albumin accumulation. Reducing Ppa with a thromboxane antagonist (ICI-192605) and a smooth muscle relaxant (papaverine) produced, in both cases, a significant decrease in albumin extravasation (P < 0.05). No significant difference in extravascular albumin accumulation or change in Ppa was shown in neutrophil-depleted animals compared with nondepleted animals. We conclude that ischemia time contributes significantly to ischemia-reperfusion lung injury and that transient changes in Ppa after reperfusion exacerbate and injury in this model. This early injury demonstrated here was neutrophil dependent.
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PMID:Ischemia-reperfusion lung injury: contribution of ischemia, neutrophils, and hydrostatic pressure. 925 39

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

The objective of the present study was to determine whether long-term arterial hypertension renders the microvasculature more vulnerable to the deleterious inflammatory responses elicited by ischemia and reperfusion (I/R). Intravital fluorescence microscopy was used to monitor leukocyte adherence and emigration, platelet-leukocyte aggregation, and albumin extravasation in mesenteric postcapillary venules of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) after 10 minutes of ischemia and subsequent reperfusion. Significant and comparable increases in leukocyte adherence/emigration and the formation of platelet aggregates were elicited by I/R in both WKY and SHR. Albumin extravasation was enhanced after I/R in SHR, but not in WKY. Monoclonal antibodies directed against the adhesion glycoproteins CD18, P-selectin, or ICAM-1 showed similar patterns of protection against the I/R-induced inflammatory responses in WKY and SHR. The enhanced albumin extravasation noted in postischemic venules of SHR was prevented by immunoneutralization of either CD18 on leukocytes or ICAM-1 on endothelial cells. These results suggest that, whereas long-term arterial hypertension does not significantly modify the leukocyte and platelet recruitment normally elicited in venules by I/R, it does result in an exaggerated albumin leakage response, which is mediated by an interaction between beta(2) (CD18) integrins on leukocytes and ICAM-1 on endothelial cells.
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PMID:Microvascular responses to ischemia/reperfusion in normotensive and hypertensive rats. 1045 43

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

This review evaluates the various causes and management of acute renal failure (ARF) in children. ARF is defined as an abrupt decline in the renal regulation of water, electrolytes and acid-base balance, and continues to be an important factor contributing to the morbidity and mortality of critically ill infants and children. The common causes of ARF in children include acute tubular necrosis secondary to various causes (including congestive heart failure and sepsis), haemolytic uremic syndrome, and glomerulonephritis and urinary tract obstruction. Ischaemia, toxins (including drugs) as well as primary parenchymal disease, have to be considered and ARF can also be a complication of systemic disease. The basic principles of management are avoidance of life-threatening complications, maintenance of fluid and electrolyte balance, and nutritional support. Only a few patients require specific management of the underlying disorder, although it is important to diagnose these conditions. Knowledge about the use of drugs for the prevention of ARF is scarce. Mannitol, low-dose dopamine, calcium channel antagonists, atrial natriuretic peptide and albumin have been evaluated and, where possible, meta-analyses are cited. Mannitol treatment appears to be warranted prophylactically after paediatric renal transplantation. Albumin infusion can reverse prerenal ARF in children with nephritic syndrome. For treatment of the complications of hyperkalaemia and volume overload, salbutamol, insulin and glucose infusion and diuretics such as furosemide and sodium bicarbonate, are discussed. All of the major dialysis modalities (peritoneal dialysis, haemodialysis and continuous haemofiltration) can be used to provide equivalent solute clearance and ultrafiltration. The indication for, and the choice of the modality depend on the patient requirements and on local resources, and should involve the care of a paediatric nephrologist. Peritoneal dialysis requires minimal equipment and infrastructure, is easy to perform and remains the favoured modality of renal replacement therapy in children. However, continuous haemofiltration is an excellent alternative to peritoneal dialysis in patients with ARF and severe fluid overload. Dialysis remains the most important tool to bridge the time needed for recovery of renal function. There is increasing evidence that more intense use of dialysis may improve the overall prognosis.
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PMID:Acute renal failure in children: aetiology and management. 1173 64

Reported causes of pancreatitis in pregnancy include: gallstone disease, hyperlipidemia, alcohol ingestion, viral, and idiopathic. Few reports associate pancreatitis with pregnancy-induced hypertension. A 35-year-old women with pregnancy-induced hypertension and spontaneous rupture of membranes was admitted for induction of labor. Her postpartum course was complicated by acute renal failure that responded well to treatment with Lasix and Albumin. Subsequently, the patient developed acute pancreatitis and recovered following conservative treatment. It is possible that the pancreatic ischemia due to generalized vasoconstriction of preeclampsia and loop diuretics in the setting of oliguria with renal failure, had a synergistic effect on the pancreas. Therefore, we suggest that in postpartum women with pregnancy-induced hypertension and acute renal failure, diuretics should be cautiously used because they may increase the risk of pancreatitis.
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PMID:Pregnancy-induced hypertension complicated by postpartum renal failure and pancreatitis: a case report. 1201 78

Multiple organ dysfunction syndrome (MODS) is mediated by complex mechanisms in which interactions between activated leukocytes and endothelial cells play a central role. ICAM-1 (intercellular adhesion molecule-1) mediates firm adhesion and transendothelial migration of activated leukocytes from postcapillary venules into the tissue. The present study evaluated the ICAM-1 expression in various organs after 40 min of intestinal ischemia and 1, 3, 6, 12 h of reperfusion (I/R) in the rat, using a dual monoclonal antibody technique (n = 36). Endothelial barrier permeability, using the vascular leakage of radiolabeled human serum albumin was also assessed (n = 12). Neutrophil sequestration in the lungs was quantitated by myeloperoxidase activity and plasma protease inhibitor levels were measured with electroimmunoassay. Significant regional differences were found in ICAM-1 expression between organs, both constitutively and after I/R-injury. The highest constitutive levels were observed in the liver and lungs, followed by the kidneys. The constitutive ICAM-1 expression in the intestines and in the heart was about 1/20 compared with that found in the liver and lungs. The brain and muscle had levels of about 1/150 of that in the liver and lungs. After intestinal I/R, significant increases (17-45%) were found in the lungs, intestines, brain, heart, and muscle. Albumin leakage index (ALI) in all examined organs and myeloperoxidase activity in the lungs increased after I/R-injury. Serum levels of albumin and most protease inhibitors decreased significantly after I/R challenge. Intestinal I/R results in an increase of systemic ICAM-1 expression with marked organ variability. The upregulation of ICAM-1 could represent a crucial step in the adherence- and migration process of activated leukocytes and potentially in the development of tissue injury.
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PMID:The effect of intestinal ischemia and reperfusion injury on ICAM-1 expression, endothelial barrier function, neutrophil tissue influx, and protease inhibitor levels in rats. 1209 41


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