acid-phosphatase and Ischemia

Topics: Acid Phosphatase; Animals; Autophagy; Ischemia; Liver; Lysosomes; Microscopy, Electron; Myocardium; Temperature; Time Factors

Topics: Acid Phosphatase; Aged; Carcinoma; Cardiovascular Diseases; Cerebrovascular Disorders; Clinical Trials as Topic; Diethylstilbestrol; Electrocardiography; Heart Failure; Humans; Ischemia; Male; Myocardial Infarction; Neoplasm Metastasis; Placebos; Plasminogen; Prognosis; Prostate; Prostatic Neoplasms; Pulmonary Embolism

Cold preservation of the liver before transplantation may change uptake and excretory functions of hepatocytes. We hypothesized that an increase in the duration of preservation would result in a progressive decrease in the hepatic uptake and/or biliary excretion of indocyanine green (ICG), which would be attenuated by pharmacologic interventions.. Donor rats (n = 40) were administered saline (control) or single 5 mg/kg doses of methylprednisolone (MP) or its liver-targeted prodrug (DMP) 2 h prior to liver harvest. Following preservation in cold University of Wisconsin solution for 0, 24, 48, or 72 h, livers were reperfused in a single-pass manner for 30 min in the presence of ICG (approximately 4 microg/ml), followed by 60 min of ICG-free perfusion. The inlet, outlet, and bile concentrations of ICG were measured periodically by high performance liquid chromatography (HPLC), and kinetic parameters were estimated.. Effects of duration of preservation: In unpreserved livers, a significant portion of ICG dose (16%) was effluxed from the liver during the washout period. Cold preservation for 24-72 h progressively increased (p < 0.05) the efflux of ICG (>2-fold at 72 h). Similarly, average extraction ratio showed a modest (30-40%) decrease with increasing preservation time (p < 0.05). However, biliary excretion of ICG showed the most sensitivity to the preservation time (14 to >800-fold decline). Effects of pretreatment: DMP caused significant (p < 0.05) increases in biliary ICG levels (>12-fold) and bile flow rates (6-15-fold) of preserved livers. Although MP pretreatment significantly (p < 0.05) increased (6-fold) bile flow rates in 48-h preserved livers, its effects on biliary ICG levels were not significant (p > 0.05).. Biliary excretion of ICG is the most sensitive kinetic parameter to prolonged cold ischemia-reperfusion injury in a rat liver perfusion model. The injury may be significantly attenuated by pharmacologic pretreatment of the liver donors.

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Bile; Cryopreservation; Dextrans; Drug Combinations; Indocyanine Green; Ischemia; L-Lactate Dehydrogenase; Liver; Liver Failure; Liver Transplantation; Methylprednisolone Hemisuccinate; Organ Preservation; Organ Preservation Solutions; Perfusion; Prodrugs; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Time Factors; Tissue Donors

We studied the state of lysosomal apparatus and pro- and antioxidant activity in the liver of rats with different resistance to hypoxia during postischemic recovery. Under normal conditions the lysosomal apparatus did not differ in highly and low resistant animals. During ischemia and reperfusion the damage to hepatic lysosomal membranes in rats highly resistant to hypoxia was less pronounced than in low resistant animals. These differences also concerned labilization of lysosomes during exposure to damaging factors (hypotonia and Triton X-100). The rats highly resistant to hypoxia differed from low resistant animals by higher stability of lysosomal membranes, lower prooxidant activity (malonic dialdehyde content), and higher tissue concentration of alpha-tocopherol during reperfusion.

Topics: Acid Phosphatase; alpha-Tocopherol; Animals; beta-Galactosidase; Hypoxia; Intracellular Membranes; Ischemia; Liver; Lysosomes; Male; Malondialdehyde; Octoxynol; Oxidative Stress; Rats; Rats, Wistar; Reperfusion Injury; Ribonucleases; Time Factors

The paper compares the effects of ozone therapy and conventional balneological methods on health condition of patients with obliterative atheromatosis and on serum activity of three lysosomal enzymes.. Sixty-four patients with lower limb ischaemia in the course of obliterative atheromatosis (without diabetes) were enrolled in the study. Thirty-two patients were treated with ozone administered by intravenous infusions and 30-minute aerosol oxygen-ozone baths. A comparative group was formed of 32 patients treated with traditional balneology. There was also a control group made up of 30 healthy subjects. Ozone therapy as well as traditional balneology were administered daily for the period of 10 days, excluding Saturdays and Sundays. Blood for biochemical analysis was collected from elbow vein in the following time intervals: 24 hours before ozone therapy or classical balneology, one hour after therapy and on the 10th day of treatment. The activity of cathepsin D, acid phosphatase and arylsulphatase as well as the levels of a-1-antitrypsin (protease inhibitor) were determined in blood serum of patients with obliterative atheromatosis.. In patients who received ozone therapy the activity of analysed lysosomal hydrolases returned to the values typical for healthy subjects. Patients' general condition also improved. The use of traditional balneological methods did not result in any significant change either in the activity of lysosomal hydrolases, the level of a-1-antitrypsin or general condition of patients.. Ozone therapy administered by intravenous infusions and aerosol oxygen-ozone baths of lower extremities yields much better therapeutic results in comparison with classical balneology.

Topics: Acid Phosphatase; Aged; alpha 1-Antitrypsin; Arteriosclerosis; Arylsulfatases; Cathepsin D; Female; Humans; Ischemia; Leg; Lysosomes; Male; Middle Aged; Ozone

The mechanisms by which heparin protects the liver during induced episodes of liver ischemia-reperfusion are poorly understood. Previous work in a swine model demonstrated that serum levels of glycohydrolases and lipid peroxide peaked within 3 h after 45 minutes of hepatic ischemia followed by reperfusion. Serum levels of lactate dehydrogenase and aspartate aminotransferase peaked 20-24 h later. The aim of this study was to evaluate the effect of heparin on these two-phases of enzyme release, using a pig model of hepatic ischemia-reperfusion injury. Twenty male swine were divided into control (n = 8) and heparin (n = 12) groups. In the heparin group, heparin was administered prior to and concurrent with ischemia-reperfusion. Following 45 min of hepatic ischemia, the levels of beta-galactosidase, beta-glucosidase, acid phosphatase, purine nucleoside phosphorylase, lipid peroxides, lactate dehydrogenase, and aspartate aminotransferase in serum were monitored for up to 166 h and compared to pre-ischemic and control levels. With heparin infusion, the peak levels of beta-galactosidase, beta-glucosidase, and the lipid peroxide were reduced to 50-60% of the control levels. Acid phosphatase and purine nucleoside phosphorylase activities in serum were reduced to 25% and 60%, respectively. The peak concentrations of lactate dehydrogenase and aspartate aminotransferase were reduced to about 25% of the control level. In addition, the serum enzymes of control pigs did not return to pre-ischemic levels until 2 weeks after hepatic ischemia, while they normalized in less than 1 week in the heparin-treated animals. Systemic heparinization had different protective effects on the first and secondary phases of liver injury. These differences may reflect heparin protection of different types of liver cells. The protection of the parenchymal cells may be the combined result of reduced sinusoidal cell injury and the anticoagulant properties of heparin.

Topics: Acid Phosphatase; Animals; Aspartate Aminotransferases; beta-Galactosidase; beta-Glucosidase; Heparin; Ischemia; L-Lactate Dehydrogenase; Lipid Peroxides; Liver; Male; Purine-Nucleoside Phosphorylase; Reperfusion Injury; Swine

Abundant fat in the liver has been implicated in poor outcome after liver transplantation or liver surgery, but the reasons for this association are still unclear. The aim of the present study was to examine mechanisms that may be involved in hepatic dysfunction after ischemia-reperfusion (I/R) of the steatotic rat liver. Steatosis was produced by a choline-methionine-deficient (CMDD) diet. In the first experiment, isolated perfused rat livers, subjected to 24-hour cold storage followed by 120-minute reperfusion, were used to investigate hypothermic I/R injury of the steatotic rat liver. In the second experiment, livers were subjected to 60-minute partial left lobar vascular clamping to allow study of normothermic I/R injury. In the first experiment, compared with normal nonsteatotic liver, steatotic livers showed significantly greater injury, as assessed by amounts of hepatic enzymes released into the perfusate, bile production, the concentrations of reduced glutathione (GSH) in the perfusate, as well as in the livers themselves, and electron microscopic findings of sinusoidal microcirculatory injury. The addition of N-acetylcysteine (NAC), a precursor of glutathione, to the liver before cold storage significantly improved these parameters in steatotic livers. The second experiment showed that, compared with nonsteatotic livers, steatotic livers had lower concentrations of GSH and impaired rates of bile production. There was also evidence of increased oxidative stress in polymorphonuclear leukocytes (PMNLs) in liver or peripheral blood of rats with fatty livers. An anti-rat intercellular adhesion molecule-1 (ICAM-1) monoclonal antibody inhibited neutrophil infiltration into pericentral sinusoids and improved these parameters in the steatotic rats. We conclude that sinusoidal microcirculatory injury is involved in hypothermic I/R injury, that oxidative stress produced by PMNLs is involved in normothermic I/R injury, and that NAC and anti-rat ICAM-1 monoclonal antibody restore liver integrity in I/R injury.

Topics: Acetylcysteine; Acid Phosphatase; Alanine Transaminase; Animals; Antibodies, Monoclonal; Aspartate Aminotransferases; Bile; Choline Deficiency; Fatty Liver; In Vitro Techniques; Intercellular Adhesion Molecule-1; Ischemia; L-Lactate Dehydrogenase; Liver; Male; Malondialdehyde; Methionine; Microscopy, Electron; Neutrophils; Perfusion; Rats; Rats, Wistar; Reperfusion Injury

The study was performed on rats divided into 9 groups. Groups 1-3 served as controls. In groups 4 and 5 rat livers were subjected to 90-min ischemia followed by 12- or 24-hour reperfusion. In groups 6 and 7 rats were injected with intraperitoneal chlorfenvinphos (2 mg/kg b.w.) and sacrificed after 12 or 24 hours. In groups 8 and 9 rat livers were subjected to 90-min ischemia, 12- or 24-hour reperfusion and then rats were injected with chlorfenvinphos (2 mg/kg b.w.). Liver sections were evaluated morphologically, histochemically (SDH, LDH, G6Pase, glycogen, Mg2+ ATPase and AcP). The microsomal fraction of the liver was evaluated for cytochrome P450 content and NADPH-cytochrome P-450 reductase activity. It has been found that liver ischemia and reperfusion result in extensive necrosis, enzymatic disturbances, particularly in acinar zone 3. Ischemia as well as reperfusion decrease the cytochrome P450 content of hepatocytic microsomes and the activity of NADPH-cytochrome P-450 reductase. Intraperitoneal injection of chlorfenvinphos during ischemia and reperfusion dramatically intensifies damage to the liver, although chlorfenvinphos alone produces only mild nonspecific effects on the morphological and enzymatic structure of the liver.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Biomarkers; Chlorfenvinphos; Cytochrome P-450 Enzyme System; Glucose-6-Phosphatase; Ischemia; L-Lactate Dehydrogenase; Liver; Male; NADP; NADPH-Ferrihemoprotein Reductase; Necrosis; Periodic Acid-Schiff Reaction; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Succinate Dehydrogenase

Adult male Wistar rats were divided in 3 groups. In the first group, infrarenal abdominal aorta was occluded for 6 hours and reperfused thereafter. In the second group, the reperfusion was not made, and the third group underwent a sham operation. Lysosomal enzymatic activities were assessed in serum tissues. Lysosomal membrane fragilities were estimated also in these tissues. Finally, 14C-aminopyrine breath test (ABT) was studied to define the possible liver dysfunction caused by limb ischemia. As a result, release of lysosomal enzymes from ischemic muscle was confirmed in vitro experiments, and the increase in the serum was statistically significant in the first and second groups as compared to the third group. Particularly prominent was a marked elevation of cathepsin-D in the first group which was observed immediately after the release of occlusion. Results of liver lysosomal enzymes and ABT revealed significant cellular damages and depression of microsomal function of the liver both in the first and second groups. These studies suggest that lysosomal enzymes derived from ischemic muscle exert a possible toxicity on the liver, and liver damage thus resulted may play a roll on the pathogenesis of whole body injury associated with acute and critical lower limb ischemia.

Topics: Acid Phosphatase; Animals; Cathepsin D; Glucuronidase; Ischemia; Leg; Liver; Lysosomes; Male; Muscles; Osmotic Fragility; Rats; Rats, Wistar

The alterations of several small-intestinal mucosal enzymes have been examined in cats that underwent different periods (1-4 hr) of occlusion of the superior mesenteric artery, followed by 4 hr of reperfusion. The damage progressed during ischemia and reperfusion from the villus tips to the crypts: first, there was a rapid decrease in the activity of maltase, a brush-border enzyme; a slower decline occurred in two cytoplasmic enzymes, aldolase A (with preferential location in feline villus cells) and lactate dehydrogenase (with an ubiquitous distribution); a lag preceded the decrease in aldolase B (a cytoplasmic enzyme shown to occur mainly in feline crypt cells). For all these enzymes, the initial period of reperfusion was associated with a greater decrease in enzyme activity than persisting ischemia. By determination of the unsedimentable proportion of glutamate dehydrogenase (a mitochondrial matrix enzyme) and of acid phosphatase (a lysosomal enzyme) it was demonstrated that ischemia caused important mitochondrial damage before the cells were lost, whereas no lysosomal damage was observed in any condition. These sensitive parameters of cell damage can serve as a criterion for an adequate evaluation of potential cytoprotective agents.

Topics: Acid Phosphatase; alpha-Glucosidases; Animals; Cats; Female; Fructose-Bisphosphate Aldolase; Glutamate Dehydrogenase; Intestinal Mucosa; Intestine, Small; Ischemia; Male; Reperfusion; Tissue Distribution

The effect of ischemia on the stability, i.e. the permeability of the lysosomal membrane of rat liver has been studied using quantitative histochemical analysis of acid phosphatase activity. Ischemia in vitro was performed for 0-240 min at 37 degrees C and ischemia in vivo for 60 min was followed by 1, 5, 24 and 48 h of reperfusion. Acid phosphatase activity was demonstrated in cryostat sections using naphthol AS-BI phosphoric acid as substrate and polyvinyl alcohol was added to the incubation medium to counteract diffusion phenomena. Ischemia in vitro up to 240 min did not affect the localization nor the total activity of acid phosphatase activity. After 60-min ischemia in vivo followed by 1-h reperfusion distinct areas showed decreased acid phosphatase activity. A further decrease in activity was observed after 5 h reperfusion. Final reaction product generated by acid phosphatase activity was rather diffusely distributed in border zones between normal and damaged tissue after 24 and 48 h of reperfusion following 60 min ischemia in vivo. It is concluded that not ischemia itself but rather reperfusion affects the stability of the lysosomal membrane due to the occurrence of oxygen-derived free radicals and/or imbalanced Ca2+ concentration. Restoration of the blood flow causes leakage of acid phosphatase from the lysosomes into the cytoplasm of liver parenchymal cells and from there to the blood.

Topics: Acid Phosphatase; Animals; Cytophotometry; Frozen Sections; Histocytochemistry; Intracellular Membranes; Ischemia; L-Lactate Dehydrogenase; Liver; Lysosomes; Male; Rats; Rats, Inbred Strains; Reperfusion; Time Factors

Topics: Acid Phosphatase; Animals; Ischemia; Ligation; Liver; Lysosomes; Male; Portal Vein; Postoperative Complications; Rabbits

Acid phosphatase (APh) activity has been experimentally studied on 69 dogs in the musculus soleus during ischemic and postischemic periods. Absence of an essential APh activation demonstrates a complete adaptation and stabilization of the intracellular mechanisms of homeostasis under an acute 3 hours' ischemia. Under a prolonged (6, 9, 12 h) ischemia APh activity in sarcoplasm of the muscle fibers increases considerably. This is, probably, one of the signs demonstrating structural-metabolic disadaptation and beginning of irreversible lesions. The data obtained make it possible to conclude that it is necessary to perform operative restoration of the blood stream in the extremities at early stages of ischemia.

Topics: Acid Phosphatase; Acute Disease; Animals; Dogs; Hindlimb; Histocytochemistry; Ischemia; Microscopy, Electron; Muscles; Time Factors

On the basis of previous (n = 23) and current muscle biopsies (n = 25) as well as five animal-experimental investigations, the paper deals with the cause and the manifestation of perifascicular muscle-fiber atrophy. A deteriorated trophic situation of the subfascial or marginal muscle fibers in patients suffering from immunocomplex vasculopathies in connection with a reduced supply of blood to the muscles is seen as the cause of the areactive weight loss (atrophy). This is accompanied by a considerably reduced capillary supply of blood to the muscle fibers. Even in normal conditions, the portion of collateral vessels and capillaries is lower in the subfascial region than in the center of the fascicle. When the blood supply is disturbed, the marginal fibers are in a trophic situation worse than that of the central muscle fibers. They become atrophied. In responsive patients, the muscle fibers regenerate and recapillarize during the convalescence period. This can be shown histochemically by means of the alkaline phosphatase reaction. The extent of perifascicular musclefiber atrophy can be fixed in quantitative terms by the method of Baumli and Mumenthaler. Where a second biopsy is indicated, results can be obtained regarding the changes in the perifascicular atrophy as a consequence of the therapy provided.

Topics: Acid Phosphatase; Adolescent; Adult; Aged; Animals; Basement Membrane; Biopsy; Capillaries; Child; Dermatomyositis; Female; Fluorescent Antibody Technique; Humans; Immune Complex Diseases; Immunoglobulins; Ischemia; Male; Middle Aged; Muscle, Smooth, Vascular; Muscles; Muscular Atrophy; Muscular Dystrophies; Myositis; Rats; Rats, Inbred Strains

Intracellular enzyme activities can be greatly influenced by alterations of pH, and non-physiologic pH may inhibit cell metabolism. The study was undertaken to examine the influence of pH values in preservation solution on ischemic tolerance time of the liver. BDE rat livers were used. Livers were preserved for 20 min or 2 h in warm ischemia after an initial perfusion with Ringer's solution at pH 9.0, 7.4, and 6.0. The values of total adenine nucleotide (TAN) and energy reserve (ER) in the livers were determined at the end of the preservation. After 20 min of warm ischemia, TAN values at pH 9.0 and 7.4 fell to 2.727 +/- 0.255 and 2.410 +/- 0.164 mumol/g, respectively (normal values: 3.414 +/- 0.270 mumol/g) and ER values to 0.786 +/- 0.186 mumol/g at pH 9.0 and to 0.446 +/- 0.095 mumol/g at pH 7.4 (normal values: 2.962 +/- 0.214 mumol/g). A similar trend was also observed after 2 h of warm ischemia. The preservation with a solution at pH 6.0 did not present any difference as compared to that at pH 7.4. Four-hour preservation in cold ischemia with Ringer's solution at pH 9.0 rendered higher values of TAN (2.635 +/- 0.085 mumol/g) and ER (0.336 +/- 0.026 mumol/g) than those in preservation at pH 7.4. No significant difference between TAN and ER values was found when 4-h preservation at pH 7.4 and 6.0 was compared. In another group an intermittent liver perfusion at 1-h interval was performed with chilled Ringer's solution; afterwards GOT, GPT, beta-glucuronidase, and acid phosphatase values in the effluents were evaluated. All of these enzymes showed higher concentration in the effluent with solution at pH 7.4 than that at 9.0. These results suggested that better intracellular energy reserve and organ viability can be maintained by preservation with alkaline solution. Furthermore, ER values seemed to be an excellent indicator of the organ viability during preservation. These were also confirmed by orthotopic hepatic transplantation in pigs. Livers were successfully preserved with alkaline Ringer's solution for up to 12 h. However, without change of pH, livers could not be preserved for more than 4.5 h.

Topics: Acid Phosphatase; Adenine Nucleotides; Alanine Transaminase; Animals; Aspartate Aminotransferases; Energy Metabolism; Glucuronidase; Hydrogen-Ion Concentration; Ischemia; Liver; Perfusion; Rats; Time Factors; Tissue Preservation

Topics: Acid Phosphatase; Animals; beta-Galactosidase; Chlorpromazine; Cold Temperature; Ischemia; Lysosomes; Male; Rats; Rats, Inbred Strains

The structure-linked latency of acid phosphatase and beta-galactosidase was studied in rat liver lobes made ischaemic for 1 or 2 h and then recirculated with blood for increasing periods. Free activity of acid phosphatase and unsedimentable activity of beta-galactosidase are increased in homogenates of ischaemic livers. When ischaemia had been maintained for 1 h, the recovery of normal latency for both enzymes was observed 1 h after re-establishment of the blood flow. After a 2 h period of ischaemia, unmasked activity markedly decreases during the first 1 h after restoration of blood flow; after that, a large and irreversible secondary rise takes place. Chlorpromazine, injected 30 min before or just after induction of ischaemia, extensively prevents the latency decrease occurring during restoration of blood flow. Modifications of the hydrolase distribution pattern obtained after differential centrifugation are in agreement with the latency changes. These results suggest that a 2 h ischaemia causes an alteration of the liver lysosomes that is largely reversible and that restoration of blood flow induces an irreversible alteration of these organelles. Chlorpromazine treatment prevents the irreversible lesion from taking place.

Topics: Acid Phosphatase; Animals; beta-Galactosidase; Centrifugation; Chlorpromazine; Galactosidases; Ischemia; Liver; Male; Rats

Renal cortex was studied during experimentally induced ischemia. A transient increase in anerobic glycolysis occurred with concomitant swelling of both the Golgi apparatus and mitochondria. These intracytoplasmic organelles underwent marked changes in their intracellular positions. Infolding of cytoplasmic membrane at the basal side of proximal tubule cells increased in complexity and proceeded to enclose various intracytoplasmic microorganelles such as mitochondria and the Golgi apparatus. Piling up in layers was particularly marked around mitochondria. This piling up appeared as myelin-like structures on the free surface of, and within, proximal tubule cells, and followed disruption of the brush border at the free surface. Histological examination of thin sections showed that the fused portions of this brush border were actually brush border cytoplasmic membrane piled up in layers giving the appearance of myelin-like structures. After two hours of ischemia, parts of the membrane of these myelin-like structures were disrupted. Large vacuoles developed and these were thought to be related to the large vacuoles seen during cell degeneration.

Topics: Acid Phosphatase; Animals; Glucuronidase; Histocytochemistry; Ischemia; Kidney; Kidney Tubules, Proximal; Lipids; Rabbits; Time Factors

Topics: Acid Phosphatase; Animals; Chlorpromazine; Galactosidases; Hydrolases; Ischemia; Liver; Lysosomes; Male; Rats

After ligationof the vascular arcades of the upper jejunum in rats ischemic damage to the intestinal mucosa and its regenerative behavior were investigated by histology, morphometry, enzyme-histochemistrym, autoradiography and electron microscopy. The process of ischemic damage begins at the tips of the villi and progresses to the crypts. After ischemia lasting 300 min the mucosa, submucosa and muscularis propria are necrotic, which means, that the small intestine is at this time completely infarcted. Whilst sthe ischemic damage to the crypt epithelia is similar to that of other kinds of epithelia, the ischemic damage to the enterocytes is different. The enterocytes are shed to the intestinal lumen without any signs of irreversible damage by a blebformation at their cell base. After 2 h ischemia -- the basal epithelia of the crypts are not irreversible damaged yet at this time--and a 12 h period of restored blood flow, the mucosal surface is completely covered again by a flat epithelium. This is achieved 1) by an above-normal proliferation of the epithelia derived from the residual crypts, 2) by the appearance of flat epithelia with an increased diameter. After 8 days of repair the small intestinal mucosa shows morphologically, autoradiographically and enzyme-histochemically a normal picture again.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Basement Membrane; Epithelium; Intestinal Mucosa; Intestine, Small; Ischemia; Necrosis; Rats; Succinate Dehydrogenase; Wound Healing

The uses of histochemistry in pathology (experimental and clinical), pharmacology and toxicology are considered and their restrictions are discussed. In time-course studies of drug effects in animals the research worker must choose an appropriate histochemical technique for evaluating the changes seen in the tissues, if any, during the study. Acid phosphatase is shown to be a marker enzyme which may be active in both cell multiplication and tissue necrosis; results obtained with it must therefore be interpreted with caution. The need for histochemical techniques to match experimental conditions is emphasized. The restrictions of fixation and tissue preparation are also emphasized. Histochemical and biochemical techniques should be used together where appropriate, and the results should be analysed carefully. Indiscriminate use of histochemistry and quantitation is deplored.

Topics: Acid Phosphatase; Animals; Cell Division; Dose-Response Relationship, Drug; Histocytochemistry; Ischemia; Liver; Necrosis; Pathology; Pharmacology; Toxicology

Topics: Acid Phosphatase; Animals; Cathepsins; Female; Glucuronidase; Ischemia; Kidney Cortex; Male; Microscopy, Electron; Proteins; Rats; Renin

1. The changes with the time of the activities of some energy-supplying enzymes and of the hydrolytic enzyme, acid phosphatase, were studied over 2 weeks of complete ischaemia, produced in the rat soleus muscle by section of the abdominal aorta and terminal devascularization, leaving nerve and tendon intact. 2. Activities of glycolytic enzymes, oxidative enzymes, hexokinase and acid phosphatase are affected in a different manner. Activities of the glycolytic enzymes, lactate dehydrogenase, triosephosphate dehydrogenase and glycerolphosphate dehydrogenase, are lowest on the 1st day and increase thereafter. The first two reach the control values again on the 4th and 14th day, respectively, while glycerolphosphate dehydrogenase reaches about 50% of the control value on the 14th day. The maximum decrease in activity of the oxidative enzymes, citrate synthase, beta-hydroxyacyl-CoA-dehydrogenase and malate dehydrogenase occurs later (4th day); thereafter their activity returns slowly to control values, but does not reach them even on the 14th day. Hexokinase activity is slightly decreased on the 1st day; then it increased and reached on the 7th day twice the control value. Thus on the 1st day the activity of the enzymes of aerobic metabolism prevail, and on the 4th day those of anaerobic carbohydrate (glucose) metabolism; the recovery of enzyme activity of aerobic oxidation occurs later. 3. Acid phosphatase activity increased from the 2nd day onwards, reaching up to 3 times the control value on the 4th day and still twice that value on the 14th day. This agrees well with the histochemical picture of acid phosphatase. 4. Histochemical changes of alkaline phosphatase activity reveal destruction of capillary endothelial cells during the first few days after operation and their later proliferation from the periphery, correlating with the loss and recovery of oxidative enzyme activity.

Topics: 3-Hydroxyacyl CoA Dehydrogenases; Acid Phosphatase; Animals; Citrate (si)-Synthase; Female; Glucosephosphate Dehydrogenase; Glyceraldehyde-3-Phosphate Dehydrogenases; Hexokinase; Histocytochemistry; Ischemia; L-Lactate Dehydrogenase; Malate Dehydrogenase; Muscles; Rats

After ligation of the vascular arcades of the upper jejunum in rats, the ischemic damage to the intestinal mucosa and its regenerative behavior after ischemia lasting 120 minutes were investigated with histological and enzyme-histochemical methods. During the ischemic injury of the jejunal mucosa, there is rejection of hydropically swollen epithelial cells into the intestinal lumen advancing from the tip to the base of the villi without a previously detectable loss of activity of the enzymes investigated. At the end of ischemia lasting 120 minutes, there is complete destruction of the villi as well as the upper portions of the crypts. After rapid re-epithelialization of the mucosal surface by a flat epithelium, reformation of villi begins already after a 24 h period of regeneration. On the third day of regeneration, the intestinal mucosa has plump villi again. Their epithelia already show the morphological characteristics of mature enterocytes. On the other hand, enzymatic maturation of the enterocytes is only concluded between the first and second week of regeneration. An altered proliferation kinetics of the crypt epithelia due to the repair process is discussed as cause of this delayed enzymatic maturation of the enterocytes relative to the morphological differentiation. Although the intestinal mucosa has a regular villous structure again after regeneration lasting 8 days, enzyme histochemical finding in the lamina propria indicate that the process of repair is only complete here in the sixth week of regeneration.

Topics: Acid Phosphatase; Alkaline Phosphatase; alpha-Glucosidases; Animals; Esterases; Histocytochemistry; Intestinal Mucosa; Ischemia; Jejunum; Leucyl Aminopeptidase; Male; Oxidoreductases; Rats; Regeneration

The role of lysosomal enzymes in ischemic retinal pigment epithelial cells (RPE) of albino rabbits was examined with the modified Gomori technique for acid phosphatase. Ischemia was produced by cutting the lateral posterior ciliary artery and short posterior ciliary arteries (PCA). Five days after PCA-cut RPE in the ischemic region were disorganized by increased enzymatic digestion. In RPE of the border between the ischemic and normal region a lot of fragmented outer segments were phagocytosed 24 h to 7 days after PCA-cut. At this time phagosomes appeared much more frequently than in the normal retina, showing several variations in their shape, localization, and histochemical reaction. However, after 10 and 14 days, RPE in the border had a tendency to reduce the phagocytic activity. A strong acid phosphatase activity was encountered in the phagosomes of macrophages, which was considered to be derived from RPE, and seemed to play the major role in scavenging destructed retinal elements.

Topics: Acid Phosphatase; Animals; Ciliary Body; Epithelium; Female; Histocytochemistry; Ischemia; Male; Phagocytosis; Rabbits; Retina; Retinal Pigments; Retinal Vessels

The action of Trasylol on the lysosomal and ATP changes after renal-stalk clamping in rats was examined. It was found that, in the presence of an effective Trasylol concentration, a distinct stabilization of the lysosomal membrane can be detected after 30 min of renal-stalk clamping. It was also found that there is only an indirect relationship between lysosomal changes and ATP metabolism under the action of Trasylol. The more rapid regeneration of the ATP is a result of the better microcirculation. The results confirm the earlier belief that Trasylol acts primarily on the lysosomal membrane.

Topics: Acid Phosphatase; Adenosine Triphosphate; Animals; Aprotinin; Cathepsins; Cerebroside-Sulfatase; Glucuronidase; Ischemia; Kidney; Lysosomes; Male; Microcirculation; Rats; Shock

Topics: Acid Phosphatase; Animals; Choroid; Histocytochemistry; Ischemia; Phagocytosis; Pigment Epithelium of Eye; Rabbits

Dog kidneys were subjected to one, two, or three hours' normothermic ischemia in situ and were then excised for biochemical and histological evaluation. The uptake of para-aminohippurate (PAH) by cortical slices progressively decreased with prolongation of the ischemia, but active transport was never abolished. Glycine uptake and oxygen consumption were only reduced to a modest extent by the ischemia. The intracellular ion levels were drastically altered, with loss of potassium and gain of sodium and chloride, and considerable increases in tissue water were observed. Acid phosphatase was liberated by the whole organ into the venous blood and by the incubated slices into the incubation medium, but both biochemical and histochemical techniques showed that the total quantity of the enzyme in the cells was hardly changed. The histochemical reaction product was localized exclusively in the lysosomes. Morphological damage was slight after one or two hours' ischemia, but more pronounced after three hours, when some cells were seen to be detached from the basement membrane. These relatively minor changes seem insufficient to predict the ultimate fate of the organ after ischemia.

Topics: Acid Phosphatase; Animals; Dogs; Epithelium; Glycine; Ischemia; Kidney; Kidney Tubules; Lysosomes; Oxygen Consumption; p-Aminohippuric Acid; Time Factors

The lactate and pyruvate levels, as well as acid and alkaline phosphatase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, glutaminic acid-oxalacetic acid transaminase and aldolase levels of rat liver homogenizates were measured at 24 degrees C and 38 degrees C during 120 min ischaemia from 0 to the 120th min. With the exception of transaminase and aldolase, the other enzymes were also enzyme-histochemically studied. The early lesions of the liver can be detected, both the quantitative laboratory tests and enzyme histochemical studies. The deviations from normal, observed at 24 degrees C between the 60th and 100th min, and at 38 degrees C between the 30th and 60th min, might be signs of irreversible lesions. Fractionated study of the liver homogenizate improves the assessability of enzyme determinations. In the course of "warm" ischaemia, the liver lysosomal lesions are early symptoms. Parallel to the breakdown of aerobic glycolysis lactic acid, fermentation, and an active pentose phosphate cycle can be detected. Quantitative testing of the liver homogenizate and enzyme histochemical observation of the hepatic tissue, might be a suitable method for the assessment of ischaemic liver lesions.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Esterases; Fructose-Bisphosphate Aldolase; Glucosephosphate Dehydrogenase; Histocytochemistry; Ischemia; Isoenzymes; L-Lactate Dehydrogenase; Lactates; Liver; Male; Pyruvates; Rats; Subcellular Fractions; Temperature; Time Factors

The effect of the anabolic hormone 19-nortestosterone propionate (Superanabolon Spofa) on the metabolism of chronically ischaemic striated muscle (anterior tibial m.) was studied in a described model in the rat. Metabolic changes were estimated in terms of the activities of a number of enzymes in muscle fibres. Enzyme activities (AcP, ATPase, CE, LDH, MDH) were determined both biochemically and histochemically excepting SDH, which was determined only by the histochemical way. Morphological changes were investigated by routine histology. Administration of 19-nortestosterone propionate prevented enzymatic changes which are typical for chronic ischaemia, primarily the decrease in the activities of dehydrogenases of Krebs' cycle tricarboxylic acides (MDH, SDH). In addition, the ratio of red to white muscle fibres increased. Administration of anabolic hormone has a similar favourable action on ischaemic muscle as training, studied previously.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Carboxylic Ester Hydrolases; Citric Acid Cycle; Female; Ischemia; L-Lactate Dehydrogenase; Malate Dehydrogenase; Muscles; Nandrolone; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Dogs; Female; Glomerular Filtration Rate; Glycine; Hypothermia, Induced; Ischemia; Kidney; Kidney Cortex; Kidney Transplantation; Kidney Tubules; Male; Methylglucosides; Time Factors; Transplantation, Autologous

Topics: Acid Phosphatase; Adult; Aged; Alkaline Phosphatase; Brain; Cerebral Hemorrhage; Cerebrovascular Disorders; Electron Transport Complex IV; Female; Glycogen; Histocytochemistry; Humans; Ischemia; Ischemic Attack, Transient; Leukocytes; Male; Middle Aged; Peroxidases

A mechanical obstruction was produced in the dog ileum, and four days later, loop of intestine above and below the occlusion were subjected to one hour's ischaemia. This led to widespread morphological and functional damage of the epithelium, indistinguishable from the response of the normal intestine. The recovery of the mucosa of both loops after the ischaemia followed exactly the same pattern as when there was no occlusion superimposed: The transport capacity for phenylalanine in vitro was entirely restored, whereas that of beta-methyl-glucoside, together with oxygen consumption and lactate production, remained depressed; morphometric examination revealed that the recuperating mucosa had smaller villi, shorter crypts and smaller epithelial cells than the contiguous untouched tissue. These results suggest that the regenerative potential of the crypts could not be obliterated by one hour's ischaemia, either in the presence of a noxious obstruction fluid above the occlusion, or in the atrophic mucosa below it.

Topics: Acid Phosphatase; Animals; Dogs; Ileum; Intestinal Absorption; Intestinal Mucosa; Intestinal Obstruction; Ischemia; Lactates; Methylglucosides; Oxygen Consumption; Phenylalanine; Regeneration

Topics: Acid Phosphatase; Animals; Choroid; Ischemia; Macrophages; Pigment Epithelium of Eye; Rabbits; Retina

1. The function and structure of dog ileal mucosa was examined immediately after arterial ischaemia for 1 h and 1, 3 or 7 days after the trauma. 2. Immediately after the ischaemia, there was a net movement of water and ions into a luminal perfusate in vivo. One day later, there was no net movement of water and electrolytes but net absorption returned on the third day. 3. Active transport of phenylalanine or beta-methylglucoside by mucosal strips in vitro was abolished immediately after the trauma but was largely restored 1 day later. There was a close correlation between glucose absorption in vivo and beta-methylglucoside uptake in vitro. 4. Morphological study revealed pronounced desquamation of enterocytes immediately after the trauma. The regenerating mucosa had shorter villi and crypts, and lower enzyme activities assessed histochemically 1 day later. Most parameters had returned to normal by the third post-operative day.

Topics: Acid Phosphatase; Animals; Biological Transport, Active; Body Water; Glucose; Ileum; Intestinal Absorption; Intestinal Mucosa; Ischemia; Lactates; Methylglucosides; Oxygen Consumption; Phenylalanine; Potassium; Sodium

The experiments were performed in 56 albino rats (15of them served as a control. The small intestine was excluded from the blood circulation for 45minutes and then pieces of the proximal and distal parts of the intestine were taken forhistological and histochemical study. It was shown that such a term of anemia resulted indeep but reversible changes in the mucous sheath and in the intramural nervous apparatus of thesmall intestine. The state of the organ wall became normal in 15 days after operation.

Topics: Acid Phosphatase; Animals; Female; Histocytochemistry; Intestine, Small; Ischemia; Male; Microtomy; Mitosis; Neurons; Oxidation-Reduction; Rats; Regeneration; Staining and Labeling; Succinate Dehydrogenase; Time Factors

A histochemical study of the effect of ischaemia on rat kidneys showed that changes were demonstrable in adenosine triphosphatase, alkaline phosphatase and succinic dehydrogenase within 2 h. Further changes occurred with increasing time. The activity of acid phosphatase was little affected up to 24 h although at this time there was marked tubular disruption. Paraffin embedded H and E sections also showed marked changes within 2 h. Enzyme histochemical and histological changes in kidneys taken at varying periods after the death of the animal showed very similar changes to those in ischaemic kidneys. Differences were mainly in the rate and extent of the changes.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Histocytochemistry; Ischemia; Kidney; Kidney Tubules, Distal; Kidney Tubules, Proximal; Ligation; Male; Postmortem Changes; Rats; Succinate Dehydrogenase

The ischaemic lesion of the pancreaticoduodenal graft prepared for transplantation was studied by enzyme histochemical methods. Estimation of lactate dehydrogenase, non-specific acid and alkaline phosphatases and esterases and of glucose-6-phosphatase pancreas. While in the pancreas, lesions due to warm ischaemia will appear after one hour, the same can be observed in the duodenum after 30 minutes and in both organs the lesions progress rapidly. Lesions resulting from cold effects appear in the pancreas after three hours and remain unchanged for 15 to 18 hours, while in the duodenum they will appear after one hour and deteriorate considerably after three hours. Continuous perfusion for more than 30 minutes or the glucose perfusion test performed after cold ischaemia of more than two hours duration considerably affected the enzymes of the organs.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Dogs; Duodenum; Esterases; Glucosephosphate Dehydrogenase; Histocytochemistry; Ischemia; L-Lactate Dehydrogenase; Methods; Pancreas; Pancreas Transplantation; Refrigeration; Tissue Preservation; Transplantation, Homologous

Segments of dog colon were subjected to one hour's ischaemia, and their morphology and function were studied either immediately after the ischaemia or 24 hours later. As functional tests, net sodium transport across the mucosa in vitro, the transport capacity in vitro for sugars and amino-acids, tissue respiration, lactate production, and the liberation of acid phosphatase were applied. Immediately after the ischaemia, all parameters differed significantly from the control mucosa: net sodium transport was abolished; amino-acid and sugar uptake, oxygen consumption and lactate production were reduced; and lysosomal enzyme release was increased. All parameters, except sugar uptake, had normalised 24 hours after the trauma. Histological examinations revealed much variation in the lesions occurring after the ischaemia, varying from slight epithelial desquamation to considerable mucosal destruction. In most cases, the mucosa had almost normalised 24 hours later. Morphometric analysis revealed decreased mean mucosal thickness immediately after the trauma, though 24 hours later, there was again no significant difference with the control group.

Topics: Acid Phosphatase; Amino Acids; Animals; Biological Transport; Colon; Dogs; Intestinal Mucosa; Ischemia; Lactates; Lysosomes; Methylglucosides; Oxygen Consumption; Sodium

The experiments with a compression of the hepato-duodenal ligament for 10, 15, 20, 30, 40, 50, 60 and 70 minutes were conducted on 75 dogs. A correlation of the data obtained in bio-histoenzymatic studies on the liver condition after various terms of compression of the hepato-duodenal ligament allowed a conclusion as to irreversible changes in the liver after 50 minutes of exsanguination.

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Constriction, Pathologic; Dogs; Duodenum; Ischemia; Ligaments; Liver; Liver Function Tests; Mitochondria, Liver; Ornithine Carbamoyltransferase; Peritoneum; Succinate Dehydrogenase

Topics: Acid Phosphatase; Animals; Choroid; Ischemia; Pigment Epithelium of Eye; Rabbits; Retina

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Disease Models, Animal; Esterases; Female; Histocytochemistry; Iliac Artery; Ischemia; Ligation; Malate Dehydrogenase; Muscles; Nucleotidases; Physical Exertion; Rats; Regeneration; Succinate Dehydrogenase; Time Factors

Topics: Acetylcholinesterase; Acid Phosphatase; Acute Disease; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Chronic Disease; Female; Histocytochemistry; Ischemia; Male; Microscopy, Electron; Mitochondria, Muscle; Muscle Denervation; Muscles; Muscular Dystrophies; Myofibrils; Necrosis; Phosphorylases; Rats; Regeneration; RNA; Time Factors

Topics: Acid Phosphatase; Acute Disease; Adenosine Triphosphatases; Animals; Biological Transport; Colon; Dogs; Extracellular Space; Female; Ileum; Intestinal Mucosa; Ischemia; Male; Methylglucosides; Phenylalanine; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Dogs; Histocytochemistry; Ischemia; L-Lactate Dehydrogenase; Liver; Perfusion

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Dogs; Histocytochemistry; Hypothermia, Induced; In Vitro Techniques; Ischemia; L-Lactate Dehydrogenase; Liver; Perfusion

Topics: Acid Phosphatase; Animals; Female; Glucuronidase; Hindlimb; Histocytochemistry; Ischemia; Lymph; Lysosomes; Male; Muscles; Rabbits; Time Factors; Wound Healing

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Amidohydrolases; Animals; Aspartate Aminotransferases; Dogs; Glomerular Filtration Rate; Glutamate Dehydrogenase; Ischemia; Isoenzymes; Kidney; L-Lactate Dehydrogenase; Lymph; Malate Dehydrogenase; Thoracic Duct; Urination

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Biological Transport, Active; Creatinine; Dogs; Glomerular Filtration Rate; Glycine; Hypothermia, Induced; Ischemia; Kidney; Kidney Transplantation; Phenolphthaleins; Potassium; Sodium; Tissue Preservation; Transplantation, Autologous

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Amidohydrolases; Animals; Aspartate Aminotransferases; Blood Proteins; Dogs; Ischemia; Kidney; L-Lactate Dehydrogenase; Leucine; Lymph; Malate Dehydrogenase; Oxidoreductases; Phosphoric Monoester Hydrolases; Potassium; Proteins; Renal Artery; Transaminases

Topics: Acid Phosphatase; Adrenal Glands; Animals; Cell Membrane Permeability; Dimethylamines; Female; Histocytochemistry; Inclusion Bodies; Ischemia; Lysosomes; Microscopy, Electron; Necrosis; Polyamines; Polymers; Rats

Topics: Acid Phosphatase; Animals; Cats; Dihydrolipoamide Dehydrogenase; Electron Transport Complex IV; Esterases; Female; Glucosephosphate Dehydrogenase; Ischemia; Lipase; Male; NAD; Necrosis; Pancreas; Succinate Dehydrogenase

Topics: Acid Phosphatase; Animals; Galactosidases; Hexosaminidases; Ischemia; Isomerism; Lysosomes; Male; Muscles; Rabbits; Time Factors

Topics: Acid Phosphatase; Animals; Aorta, Abdominal; Detergents; Glucosidases; Glucuronidase; Ischemia; Ligation; Male; Muscles; Rats; Ribonucleases; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Cell Membrane; Cell Membrane Permeability; Chlorpromazine; Cold Temperature; Computers; Dogs; Hypoxia; Ischemia; Isoproterenol; Liver; Membrane Potentials; Methylprednisolone; Microelectrodes; Oxygen; Perfusion; Potassium; Time Factors; Tissue Preservation; Tissue Survival; Tromethamine

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Cholinesterases; Enzymes; Ischemia; Kidney; Kidney Diseases; L-Lactate Dehydrogenase; Leucyl Aminopeptidase; Malate Dehydrogenase; Male; Pyelonephritis; Rabbits; Transaminases

Short loops of dog small intestine, filled with a buffered glucose solution, were subjected to one hour's total ischaemia by clamping the corresponding mesenteric artery and vein as well as the intestinal wall at each end of the loop. Immediately after the ischaemic period and 24 hours later, their functional capacity, together with that of neighbouring control loops, was determined by studying the absorption of phenylalanine and beta-methyl-glucoside in vitro and by measuring the levels of Na(+)-K(+)-ATPase in the mucosa. The release of lysosomal enzymes after the ischaemia was studied by gauging the levels of acid phosphatase in the venous blood draining the ischaemic loop. The state of the mucosal microcirculation was investigated by injection of indian ink into the mesenteric artery removal of the loop. Immediately after ischaemia, considerable structural damage was observed in the intestinal mucosa, with desquamation of the villous tips, oedema, vascular stasis, and haemorrhagic infiltration in the lamina propria. No dye was observed in the mucosal capillaries. All transport capacity was abolished, but ATPase levels were unchanged. A significant release of lysosomal enzymes into the venous blood was noted. One day later structural and functional recovery was complete, and vascularization of the villous core was restored.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Biological Transport, Active; Capillaries; Carbon; Dogs; Female; Glycosides; Intestinal Absorption; Intestinal Mucosa; Intestine, Small; Ischemia; Lysosomes; Male; Mesenteric Arteries; Mesenteric Veins; Microcirculation; Phenylalanine

Topics: Acid Phosphatase; Acute Kidney Injury; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Blood Pressure; Central Venous Pressure; Dogs; Esterases; Hemodynamics; Ischemia; Kidney; Kidney Tubules; Lysosomes; Mitochondria; Mitochondrial Swelling; Pulse; Shock, Hemorrhagic; Succinate Dehydrogenase; Time Factors

Topics: Acid Phosphatase; Animals; Blood Platelets; Centrifugation; Copper; Dogs; Erythrocytes; Ischemia; Leukocytes; Liver; Liver Circulation; Lysosomes; Microsomes, Liver; Mitochondria; Naphthalenes; Nitrophenols; Phosphorus; Sulfates; Tartrates

Topics: Acid Phosphatase; Alkaline Phosphatase; Ammonia; Amylases; Animals; Body Fluids; Cathepsins; Creatine Kinase; Dogs; Fructose-Bisphosphate Aldolase; Glucuronidase; Intestinal Obstruction; Intestine, Small; Ischemia; L-Lactate Dehydrogenase; Lactates; Leucyl Aminopeptidase; Sulfatases

Topics: Acid Phosphatase; Animals; Blood Proteins; Capillary Permeability; Female; Glucuronidase; Hindlimb; Ischemia; L-Lactate Dehydrogenase; Lymph; Male; Muscles; Necrosis; Rabbits; Time Factors; Tourniquets

Topics: Acid Phosphatase; Animals; Coronary Vessels; Dogs; Female; Glycogen; Hydrogen-Ion Concentration; In Vitro Techniques; Ischemia; Ligation; Lysosomes; Male; Muscles; Myocardial Infarction; Papillary Muscles; Potassium; Time Factors

Topics: Acid Phosphatase; Animals; Aorta, Abdominal; Dogs; Glucuronidase; Hepatic Veins; Intestine, Small; Ischemia; Jejunum; Kidney; Liver; Lymph; Lysosomes; Mesenteric Vascular Occlusion; Portal Vein; Renal Veins; Spleen; Splenic Vein; Thoracic Duct

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Esterases; Histocytochemistry; Ischemia; Kidney; Kidney Tubules; Male; Rats; Renal Artery; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Femoral Artery; Femoral Vein; Glutamate Dehydrogenase; Guinea Pigs; Histocytochemistry; Ischemia; L-Lactate Dehydrogenase; Ligation; Malate Dehydrogenase; Succinate Dehydrogenase; Vascular Diseases

Topics: Acid Phosphatase; Acid-Base Equilibrium; Alanine Transaminase; Animals; Buffers; Chlorpromazine; Glucuronidase; Hydrogen-Ion Concentration; Hypothermia, Induced; Ischemia; Liver; Liver Transplantation; Male; Methods; Organ Size; Perfusion; Phenoxybenzamine; Rats; Temperature; Tissue Preservation; Transplantation, Homologous

Increased fibrinolytic activity and consumption coagulopathy are common consequences of liver transplantation and are a major cause of morbidity and death. In the present investigation the effects of hepatic ischemia on the coagulation mechanism were studied in the stump-tail monkey. The results suggest that, although fibrinolytic activity is induced by both major intraabdominal operations as well as one hour of hepatic ischemia, consumption coagulopathy, presumably due to intravascular clotting, is enhanced by the revascularization of the ischemic liver, possibly because of clotting within the liver itself. Release of a plasminogen activator from the liver due to hepatic ischemia alone is not demonstrated by these studies. It is believed that the first phase of intravascular coagulation after liver transplantation is due to release of tissue activators from vascular endothelium, which may be minimized by the action of ganglionic blocking agents. The severity of fibrinolysis in this stage is aggravated by the "liverless state," in which no clearance of plasminogen activators occurs. The degree of liver injury directly affects the ability of the liver to control hypercoagulability in the second phase. Thrombus formation which we believe occurs during this phase may be minimized by use of continuous controlled heparinization.

Topics: Acid Phosphatase; Animals; Blood Coagulation; Fibrinolysis; Ischemia; Liver; Liver Transplantation; Macaca; Platelet Count

Topics: Acid Phosphatase; Animals; Atrophy; Ischemia; Liver Circulation; Liver Diseases; Liver Glycogen; Portal Vein; Rats

Topics: Acid Phosphatase; Animals; Cathepsins; Chlorpromazine; Dextrans; Electron Transport Complex IV; Endoplasmic Reticulum; Fasting; Female; Glucose-6-Phosphatase; Glucuronidase; Hydrolases; Ischemia; Liver; Lysosomes; Malate Dehydrogenase; Male; Mitochondria, Liver; Organ Size; Oxidoreductases; Rats; Stimulation, Chemical; Time Factors

Topics: Acid Phosphatase; Animals; Cholesterol; Coronary Vessels; Dogs; Electron Transport Complex IV; Hypoxia; Ischemia; Microscopy, Electron; Mitochondria; Myocardium; Oxygen Consumption; Phospholipids; Proteins; Triglycerides

Topics: Acid Phosphatase; Animals; Cathepsins; Deoxyribonucleases; Ischemia; Liver Diseases; Lysosomes; Male; Rats; Ribonucleases; Solubility; Sulfatases

1. Lymph was collected directly from the hind limb of cats anaesthetized with pentobarbitone before and for several hours after the limb was injured.2. After the limb was subjected to very mild injury such as hot water at 50 degrees C or ischaemia for 1 hr there was no increase in protein or enzyme concentrations in the lymph, although after the ischaemia there was an increase in lymph flow.3. After burning the limb at 60 degrees C there was a significant increase in the concentrations of the cytoplasmic enzymes glutamic-oxalacetic transaminase and lactic dehydrogenase, as a result of an increased permeability of the cell membrane.4. When the limb was burned at 80 degrees C there was a marked increase not only in the cytoplasmic enzymes but also in the mitochondrial enzyme glutamic pyruvic transaminase. Thus with the stronger burn the permeability of the intracellular mitochondrial membrane was also increased.5. Not until the most severe injury of all, i.e. freezing the limb solid, was there an increase in the concentration of lysosomal enzymes in the lymph.6. It is concluded that estimation of intracellular enzymes in the lymph draining an injured tissue affords a method of assessing the extent of cellular injury.

Topics: Acid Phosphatase; Animals; Burns; Cats; Cell Membrane Permeability; Freezing; Glucuronidase; Ischemia; L-Lactate Dehydrogenase; Lymph; Potassium; Proteins; Transaminases; Wounds and Injuries

Topics: Acid Phosphatase; Adrenal Gland Diseases; Adrenal Glands; Animals; Cytoplasm; Esterases; Histocytochemistry; Hydroxysteroid Dehydrogenases; Ischemia; Necrosis; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Axons; Brain Edema; Cerebrovascular Disorders; Dendrites; Female; Histocytochemistry; Hypoxia, Brain; In Vitro Techniques; Ischemia; Lysosomes; Male; Neuroglia; Neurons; Oxidoreductases; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Animals; Esterases; Histocytochemistry; Hypertrophy; In Vitro Techniques; Ischemia; Liver; Liver Circulation; Lysosomes; Male; Rats

Topics: Acid Phosphatase; Adaptation, Physiological; Animals; Cathepsins; Cortisone; Cytoplasm; Endotoxins; Enzymes; Erythrocytes; Glucuronidase; Histocytochemistry; Humans; Ischemia; Liver; Lysosomes; Mesenteric Arteries; Mitochondria; Mononuclear Phagocyte System; Protective Agents; Rabbits; Rats; Research; Salmonella Infections; Salmonella Infections, Animal; Shock, Septic; Shock, Traumatic; Stress, Physiological; Thorium; Thorium Dioxide