Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two days after an iv infusion of norepinephrine (NE) (4 micrograms.kg-1.min-1 X 60 min) in rabbits, patchy myocardial damage in frozen cross sections of right and left papillary muscles was associated with loss of staining for alkaline phosphatase (ALP), an enzyme present in normal capillary endothelium, whereas a regular pattern of staining was observed in control normal muscles. Semithin cross sections of the same muscles after resin embedment gave comparable estimates of capillary density in control muscles and undamaged regions of norepinephrine-treated muscles. In damaged regions the complete absence of ALP staining corresponded with an apparent reduction in number, but not absence, of capillaries identifiable in semithin sections with light microscopy. Electron microscopy, however, revealed capillaries present in these regions in numbers similar to control undamaged tissue. Around 90% of these capillaries exhibited marked morphological abnormalities, with an 18% increase in endothelial cell volume density and a corresponding reduction in luminal volume density. These changes are similar to those reported after ischemia in cardiac and skeletal muscle. Myocardial damage induced by a high dose of NE is therefore associated 48 hr later with loss of ALP staining and endothelial cell disruption and edema, which may impair capillary perfusion and contribute to limited working cardiac performance observed previously.
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PMID:Capillary density and fine structure in rabbit papillary muscles after a high dose of norepinephrine. 318 97

The development of optimal methods for preservation is important for the advancement of liver transplantation. This study compares hypothermic storage (HS) and hypothermic pulsatile perfusion (HPP) with various solutions, using an isolated normothermic perfusion model (LIPM). Canine livers were removed from mongrel dogs without warm ischemia and flushed with either heparinized Ringer's lactate (control and HPP-preserved groups) or the solution used for hypothermic storage (TP-V or modified Collins). The type of preservation and solution for each of the experimental groups was as follows: group I (n = 7), no preservation, fresh; group II (n = 7), 24-h HS with TP-V (a hyperosmolar colloid solution containing sucrose, dextrose, and ATP-MgCl2); group III (n = 7), 24-h HS with modified Collins (C-2), an intracellular crystalloid solution; group IV (n = 5), 24-h HP with TP-V; group V (n = 6), 24-h HPP with Belzer solution, containing ATP-MgCl2; group VI (n = 3), 24-h HPP with albumin. After the preservation period, livers were placed on HPP at 37 degrees C with albumin-mannitol solution for 3-h testing in an LIPM. Perfusate samples were taken at 1-h intervals to assess liver function. LDH, SGOT, alkaline phosphatase, lactic acid, LAP, GGT, pO2, pCO2, pH, osmolarity, AMP, ADP, and ATP were studied. Histologic studies were performed, as were representative HIDA scans. Using the LIPM, livers preserved by HS and HPP with TP-V solution appeared to be superior to those preserved with modified Collins, Belzer, and albumin solutions. In these non-TP-V groups, the greatest cellular and organ damage was observed. TP-V HPP appeared to give the best overall liver functional response and histologic results and is recommended as the preferred method for 24-h liver preservation.
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PMID:Liver preservation techniques for transplantation. 330 26

This study was undertaken to determine whether pretreatment of the donor rat with coenzyme Q10 (CoQ10) would protect against hepatic ischemia induced for 30 minutes at normothermic body temperature. Fresh liver transplants were used as controls (minus warm ischemia of 30 minutes) and gave a 1-week survival rate of 84.6%. CoQ10 was administered intravenously (10 mg/kg body weight) to the donor rat 1 hour before induction of warm ischemia (group A). In another group (B), the same dose was given intravenously not only to the donor rat but also to the recipient rat 1 hour before grafting. None of the placebo group survived more than 2 days. The 1-week survival rates of the groups pretreated with CoQ10 were 45.5% for group A and 50% for group B. There was no significant difference between groups A and B. A statistically significant difference was demonstrated between the placebo group and both CoQ10-treated groups (p less than 0.05). It was therefore assumed that CoQ10, accumulated in the donor liver, was a primary factor in improving survival. Serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), serum alkaline phosphatase (SALP), total bilirubin, and total protein were measured by means of light and electron microscopic examination of the liver 6 months after transplantation. Long-term-surviving rats with transplanted, ischemically damaged liver that was pretreated with CoQ10 showed a decrease in the activity of SGOT and SGPT and an increase in levels of total protein to the normal range (as well as to those levels exhibited by fresh-liver-transplanted rats) with practically no change in levels of SALP, total bilirubin, or in histologic findings. These results indicate that donor pretreatment with CoQ10 is useful for increasing survival after warm ischemic damage of rat liver grafts.
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PMID:Ischemic damage prevention by coenzyme Q10 treatment of the donor before orthotopic liver transplantation: biochemical and histologic findings. 331 78

An early change following mild renal ischemia is the loss of the renal microvilli, which then regenerate morphologically within 6 h. We studied microvillar regeneration in rats with 25 min of renal artery occlusion and subsequent reflow. At subsequent intervals the rats were injected intraperitoneally with [14C]choline and [3H]leucine; 25 min later they were killed and their renal brush border membranes isolated. At 30 min of reflow of blood there was a 77% reduction in the incorporation of [3H]leucine into microvillar protein compared with that of the opposite control kidney (P less than 0.02). The incorporation rose to normal within 60 min. At 30 min of reflow, the incorporation of [14C]choline into phospholipids increased twofold (P less than 0.005), then returned toward normal values after 2 h. The altered incorporation of tracers was not due to change in membrane turnover or substrate pools. The activities of alkaline phosphatase, gamma-glutamyl transpeptidase, and alpha-glucosidase decreased 50% following ischemia (P less than 0.02) and returned to control values within 2 h. Thus, renal damage severe enough to partly efface microvilli is repaired metabolically within several hours.
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PMID:Regeneration of the renal brush border after renal ischemia in rats. 611 66

Tissue sections of kidneys from 172 patients with various pathologic conditions, such as hydronephrosis, interstitial nephropathies, ischemia, chronic graft rejection and renal cancer, were evaluated by an image analysis technique. Structurally defined kidney alterations were monitored for enzymatic, immunologic and other histochemical changes. Indicator enzymes of the proximal tubule, alanine-aminopeptidase (AAP), alkaline phosphatase (AP), beta-glucoronidase (beta-Gl) and gamma-glutamyltranspeptidase (GGTP), were used as parameters for screening. Enzyme concentrations were found to be significantly decreased in kidney sections of patients with various renal diseases (AP less than 15%, AAP less than 55% and beta-Gl less than 60%) as compared to normal kidney tissues (100%). AAP concentration was measured quantitatively by specific immunofluorescence using an antienzyme antibody. Immunofluorescence of AAP was comparable to that of AAP calculated by the colorimetric technique (substrate: DL-alanine-beta-naphthylamide-HCl) and decreased to less than 50% in altered kidney tissues. Furthermore, kidney cancer (less than 20%) and kidney tissue adjacent to tumours (less than 65%) displayed significantly decreased levels of kidney marker enzyme activity. This study suggests that (1) the diseased kidney is characterized by a defined change in key enzymes of the cell surface and (2) renal cancer exhibits partial depletion of these constituents. Image analysis of the pattern of enzyme activity appears to be a useful tool in the analysis of renal pathology.
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PMID:Quantitative enzymatic, immunologic and histochemical studies of clinically relevant human kidney alterations using image analysis. 611 96

The tissue concentration of tubular marker enzymes were evaluated in sections of kidneys from 86 patients with various underlying diseases such as hydronephrosis, interstitial nephropathies, ischemia due to renal arterial stenosis and chronic allograft rejection. In addition, as an experimental model, kidney tissue sections of 166 Wistar rats were analyzed due to hydronephrosis caused by ureteral obstruction, ischemia and obstruction of the renal vein. The tissue concentration of indicator enzymes, such as alkaline phosphatase (AP) and alanine-aminopeptidase (AAP), was considered as a parameter describing the extent of kidney tubule damage. Quantitative evaluation of enzymatic activity was performed by histophotometry using a computed image analysis device technique. As compared to normal human kidney (enzyme activity 100%), the concentrations of brush border enzymes were significantly (p less than 0.001) lower under pathological conditions (AP less than 15%, AAP less than 55%). In similar manner investigations of kidneys in animal experiments with rats exhibited lower enzyme concentrations following kidney injury caused by ureteral obstruction for 10 and 21 days (AP less than 12%, AAP less than 65%; 2p less than 0.01). Kidneys after an ischemic period of 2 h and a subsequent 14-day recirculation period displayed a significant (2p less than 0.01) decrease of normally present indicator enzyme concentrations (AP less than 22%, AAP less than 77%) as compared to normal renal organs (100%). Computed image analysis of kidney tissue sections might be a useful aid in evaluating morphologic and enzymatic patterns of human and animal kidney alterations.
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PMID:Quantitative enzymatic histophotometry of morphologic alterations caused by urologically relevant tubular kidney damages using computed image analysis device technique. 611 5

Animal experiments were made to study and compare enzymatic activity of brain tissue mitochondria and microsomes treated and untreated with Tween-80 and Triton-X-100. In Mongolian gerbils, the 10-minute brain ischemia induced by bilateral carotid occlusion led to the labilization of the membranes of microsomal fractions, which did not return to normal an hour after resuscitation. The destructive effect of ischemia combined with clinical death from mechanical aspnyxia was similar to that of Triton-X-100. The ten-minute clinical death from ventricular fibrillation due to electroshock in dogs labilized lysosomal membranes. During the first hour after resuscitation and especially during the first 24 hours, the treatment of crude mitochondria with Tween-80 did not activate alkaline phosphatase and plasminogenic activator as compared with the control group.
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PMID:[Membrane damage in brain subcellular structures in terminal states and in the postresuscitation period]. 685 85

Though difficult, early diagnosis of acute intestinal ischemia is essential in order to improve the prognosis of this major affection. The possibility that early modifications in biological parameters could provide such data was explored. Serum alkaline phosphatase levels were unaltered, whereas blood phosphorus concentrations were increased during AII of arterial or venous origin in the rat. The latter test therefore provides an early specific indication of the diagnosis, the mechanism involved being liberation of phosphate ions from the intestine, enhanced by a functional renal insufficiency.
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PMID:[Early biological disorders in acute intestinal ischemia in the rat. Determination of blood phosphorus and serum alkaline phosphatase]. 715 64

Left kidneys of rats were made ischemic for 25 minutes and proximal tubule brush border alterations studied in the S1 and S2 segments. Scanning electron microscopy revealed that brush border microvilli became unstable, fused with one another, and were interiorized into proximal tubule cytoplasm soon after reflow of blood following ischemia. Rapid regeneration followed; scanning electron microscopy showed that regeneration occurred in a fashion whereby clusters of microvilli in flower-like configurations were extruded from the cell interior toward the surface. Such unique patterns of microvillus formation have not been reported before. Activity of the brush border enzymes, alkaline phosphatase and maltase, were not significantly depressed throughout the cycle of brush border loss and regeneration. Likewise, there were no alterations in the activity of beta-glucuronidase, a lysosomal enzyme. Alkaline phosphatase cytochemistry showed that microvillus membranes that were interiorized into the cell cytoplasm retained enzyme activity on their surfaces during the early period of brush border loss as well as during regeneration. These results strongly suggest that in reversibly injured proximal tubule cells regeneration of the brush border occurs primarily by a process of recycling of damaged, previously incorporated membrane. The nature of the initial membrane damage and the mechanism of recycling remain unknown.
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PMID:Mechanism of proximal tubule brush border loss and regeneration following mild renal ischemia. 730 Feb 48

In an ischemic Thiry-Vella colonic segment which was constructed to facilitate the serial measurement of submucosal blood flow by radioxenon clearance, we found that, after producing ischemia, the submucosal xenon clearance fell from 68+/-3 to 21+/-4 percent. In the succeeding two hours, a further fall in xenon clearance to 16+/-3 per cent occurred as a result of vasoconstriction in the peripheral mesenteric bed. From 24 hours onward, the submucosal flow increased. However, throughout the 96 hours, no healing of the ischemic necrosis was seen in the mucosa, and submucosa. Serial alkaline phosphatase levels showed a great rise from 24 hours onward, and began to fall as submucosal blood flow increased. This rise in the alkaline phosphatase value appears a useful marker of the degree of ischemia of the intestinal wall.
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PMID:Correlation of alkaline phosphatase with submucosal blood flow and morbid histology of the ischemic colon. 740 17


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