acid-phosphatase and Shock--Septic

Mitochondria and lysosomes were evaluated by assessment of changes in activity of selected enzymes: lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), adenosinetriphosphatase (ATPase), acid phosphatase (AcPase) and beta-glucuronidase (BG) in rats under profound hypoxia induced by endotoxemic shock. The study was conducted on adult male Wistar rats. The animals formed the following four groups of 15 rats each: control animals (C);-rats receiving intraperitonally O(2)/O(3) (CO), rats receiving of Escherichia coli toxin (LPS) (CL); rats receiving LPS plus oxygen-ozone mixture (OL). Histoenzymatic examinations of liver, kidney, lungs, and heart muscle were performed. Lipopolysaccharide suppressed activities of all the enzymes except for LDH, the activity of which as high as a fourfold increase. The results demonstrated potent, stabilizing and regenerative effects of ozone therapy on body enzymatic processes in course of induced endotoxemic shock in rats, which might prove to be of clinical significance.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Biomarkers; Glucuronidase; Hypoxia; Infusions, Parenteral; Kidney; L-Lactate Dehydrogenase; Lipopolysaccharides; Lung; Lysosomes; Male; Mitochondria; Myocardium; Oxidants, Photochemical; Oxygen; Ozone; Rats; Rats, Wistar; Shock, Septic; Succinate Dehydrogenase

UR-12670 is a novel and potent PAF antagonist, eg., it displaces [3H]WEB-2086 from PAF receptors in rabbit platelet membranes (Ki = 0.6 nM) and inhibits PAF-induced increase in vascular permeability in rat trachea (100%), thymus (44%), seminal vesicles (100%) and stomach (54%) at a dose of 0.01 mg/kg i.v. Since PAF is thought to be an important mediator in endotoxic shock, the effect of pretreatment with UR-12670 on changes in vascular permeability, disseminated intravascular coagulation (DIC) and plasma biochemical parameters were determined in a rat model of acute endotoxemia. UR-12670 and the reference PAF antagonist, lexipafant (10 mg/kg i.v.), strongly inhibited lipopolysaccharide (LPS, 25 mg/kg i.v.)-induced plasma leakage in the trachea (49 and 100%, respectively) and seminal vesicles (81 and 100%), as assessed by the Evans blue extravasation method. Only lexipafant inhibited the increase in vascular permeability in the thymus (36%). Neither PAF antagonist was effective in the stomach. Both UR-12670 and lexipafant at 10 mg/kg i.v. attenuated the LPS-induced variation of some DIC markers, such as activated partial thromboplastin time increase (56 and 58%, respectively) and the fibrinogen concentration decrease (53 and 31%), whereas the increase in prothrombin time was not affected. Increased plasma acid phosphatase (ACP, a lysosomal activation marker) and lactate dehydrogenase (LDH, a tissue damage marker) activity elicited by LPS was attenuated by pretreatment with 10 mg/kg i.v. of either UR-12670 or lexipafant (ACP: 55 and 48%; LDH: 50 and 33%). LPS-induced hyperglycemia (46 and 37%) and hyperlactacidemia (100% both) were also inhibited. UR-12670 protected against several shock symptoms, confirming the role of PAF in the pathogenesis of rodent endotoxemia.

Topics: Acid Phosphatase; Animals; Blood Glucose; Capillary Permeability; Evans Blue; Extravasation of Diagnostic and Therapeutic Materials; Imidazoles; L-Lactate Dehydrogenase; Lactic Acid; Lipopolysaccharides; Male; Partial Thromboplastin Time; Platelet Activating Factor; Platelet Aggregation Inhibitors; Prothrombin Time; Pyridines; Rats; Rats, Sprague-Dawley; Shock, Septic

To study the clinical significance of the decrease of glucocorticoid receptor (GR) in stress and shock, GR was blocked about 80% by mifepristone (RU38486), and the effects of the blockade on the pathological changes of endotoxemia were studied in rats. The results revealed that GR blockade may exacerbate the pathological and pathophysiological changes of endotoxemia: (1) the more rapid drop in arterial blood pressure, (2) the more severe pathological changes involving multiple organs, especially the lung and small intestine, (3) the increase of leukocyte adherence in venules and more pronounced rheological changes in the mesenteric microcirculation, and (4) the striking elevation of serum acid phosphatase (ACP), phospholipase A2 (PLA2) activity, and lipoperoxide (LPO). The changes of serum ACP, PLA2, and LPO in the rats with 80% GR blockade were more marked than in those with 50% GR blockade. Based on these findings, we propose that the decrease in GR during stress and shock might be a contributing factor in the pathogenesis of shock and multiple organ failure (MOF). The possible mechanisms of the above noted findings are discussed.

Topics: Acid Phosphatase; Animals; Blood Pressure; Cell Adhesion; Endotoxins; Intestine, Small; Kinetics; Leukocytes; Lipid Peroxides; Lung; Mifepristone; Phospholipases A; Phospholipases A2; Rats; Rats, Sprague-Dawley; Rats, Wistar; Receptors, Glucocorticoid; Shock, Septic; Splanchnic Circulation

The preventive effects of a traditional Chinese medicine Sho-saiko-to (Kampo prescription, TJ-9) were determined from oxygen toxicity and membrane damage in liver during endotoxemia. The liver lipid peroxide level and xanthine oxidase activity 18 h after administration of endotoxin (6 mg/kg, i.p.) to TJ-9 (500 mg/kg/d, p.o.)-pretreated mice were markedly lower than that in endotoxin-treated mice, whereas the administration of TJ-9 significantly increased superoxide dismutase and glutathione peroxide activities in liver of endotoxin-injected mice. In the mice pretreated with a TJ-9, the levels of alpha-tocopherol and nonprotein SH in liver tissue 18 h after endotoxin injection were markedly increased as compared to those in endotoxin-treated mice. Leakages of acid phosphatase and lactate dehydrogenase isozyme in serum were markedly lower in endotoxin-TJ-9-treated mice than those in mice given endotoxin. The administration of TJ-9 clearly prevented the membrane protein damage arising from endotoxin challenge. Kampo prescription Sho-saiko-to thus appears to protect the liver plasma membrane from injury by free radicals which occur in a tissue ischemic state during endotoxemia.

Topics: Acid Phosphatase; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Membrane; Chemical and Drug Induced Liver Injury; Drugs, Chinese Herbal; Electrophoresis, Polyacrylamide Gel; Free Radical Scavengers; In Vitro Techniques; Isoenzymes; L-Lactate Dehydrogenase; Lipid Peroxides; Liver; Male; Mice; Mice, Inbred Strains; Oxygen; Shock, Septic; Sulfhydryl Compounds; Vitamin E

The influence of hydrocortisone and dopamine to the course of the organic functional changes and the activity of same lysosomal hepatic enzymes were tested in 30 dogs in endotoxic shock. A continuous lowering of the blood pressure and the central venous pressure were observed in the non-treated group. The hemodynamic impairments turned out in the treated groups in a less acute course. The coupled treatment with hydrocortisone and dopamine in the experimental endotoxic shock seems to reduce the activity of the lysosomal enzymes in the liver and in the peripheral blood.

Topics: Acid Phosphatase; Animals; Blood Pressure; Cathepsins; Central Venous Pressure; Dogs; Dopamine; Drug Therapy, Combination; Hydrocortisone; Lysosomes; Mitochondria, Liver; Shock, Septic

Topics: Acid Phosphatase; Animals; Catalase; Cholesterol; Complement System Proteins; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Free Radicals; Rats; Rats, Inbred Strains; Reference Values; Shock, Septic; Superoxide Dismutase; Vitamin E

Administration of endotoxin, a lipopolysaccharide extracted from cell walls of gram negative bacteria, elicited alterations in various metabolic parameters and in the electrocardiogram of rats. Cardiac glycogen and serum glucose were decreased, while serum pyruvate and acid phosphatase levels were increased. There was initial tachycardia followed by significant bradycardia and elevation of the ST segment in the animals with shock. Erythrocyte count, haemoglobin and haematocrit were not changed after shock. Treatment with naloxone caused significant decreases in the metabolic and electrocardiographic changes induced by endotoxin.

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Blood Cell Count; Blood Coagulation; Blood Glucose; Electrocardiography; Female; Glycogen; Hemoglobins; Male; Myocardium; Naloxone; Rats; Rats, Inbred Strains; Shock, Septic

The effects of verapamil, a calcium antagonist, on survival and on hemodynamic and metabolic parameters were studied in canines administered E. coli endotoxin. Shams, endotoxin controls, and endotoxin-shocked dogs treated with a 4-hour infusion of verapamil were studied. The animals were anesthetized, catheters and endotracheal tube were inserted, and an IV infusion was started after administration of endotoxin. All dogs were kept on a respirator for 4 hours while measurements were taken; they were then extubated and returned to their cages. Survival was considered permanent by 7 days. Eight of 13 treated dogs survived, in contrast with only one of 14 controls. Treated dogs had significantly higher cardiac index (4.64 vs 3.62 L/min/m2), pulmonary artery pressure (16 vs 13 mmHg), and left ventricular stroke work (44.3 vs 29.7 gm/m2 beat), and significantly lower heart rate and systemic vascular resistance at 4 hours. Serum glucose, acid phosphatase, pH, and Hct were also significantly improved by verapamil treatment.

Topics: Acid Phosphatase; Animals; Blood Glucose; Blood Pressure; Calcium; Dogs; Escherichia coli; Heart; Heart Rate; Hemodynamics; Serum Albumin; Shock, Septic; Stroke Volume; Time Factors; Vascular Resistance; Verapamil

The ultrastructural alteration of Langerhans' islet cells as well as acinar structure in endotoxin shock was investigated in virtue of the electron histochemical procedures. One hour after administration of endotoxin, swelling and loss of cristae of the mitochondria, dilatation of the cisterna of the rough endoplasmic reticulum and swelling of the secretory granules in the B cell of Langerhans' islet cell were observed. On the contrary, the teleinsular acinar cells disclosed relatively intact ultrastructure, while the periinsular acinar cells showed in rather remarkable changes, such as the swollen mitochondria and obliteration of the rough endoplasmic reticulum. Four hours after administration of endotoxin, increase of the autophagic vacuoles in the cytoplasm of the acinar cells and in B cells of the Langerhans' islet cells were observed. Electron histochemical study disclosed the increase of rather small primary lysosomes in B cells of the Langerhans' islet cells, comparing to those of the acinar cells in normal condition. However, one hour after administration of endotoxin, acid phosphatase activity was activated and dispersed reactive substances were discernible in the cytoplasm of the B cells as well as intercellular and perivascular spaces.

Topics: Acid Phosphatase; Animals; Disease Models, Animal; Islets of Langerhans; Lysosomes; Male; Microscopy, Electron; Rats; Rats, Inbred Strains; Shock, Septic

The arachidonic acid metabolites thromboxane A2, a potent platelet aggregator, and prostacyclin, a potent vasodilator, are released early in endotoxin shock and may contribute to its pathologic sequelae. Plasma levels of thromboxane (Tx) A2 and prostacyclin were measured via radioimmunoassay of their stable metabolites immunoreactive (i) TxB2 and i6-keto-PGF1 alpha in tolerant and nontolerant rats after endotoxin. Long-Evans rats were made tolerant to endotoxin by four daily IV injections of S enteritidis (endotoxin) (0.1, 0.5, 1, and 5 mg/kg). In normal rats (N = 15) given LPS (IV, 15 mg/kg), only 11% survived at 24 h; in contrast, tolerant rats (N = 13) all survived even at a dose of 50 mg/kg. At 1 h, after endotoxin (15 mg/kg) IV, plasma i6-keto-PGF1 alpha in nontolerant rats was 1,005 +/- 149 pg/ml (N = 14) and continued to rise to 4,209 +/- 757 pg/ml (N = 5) (P less than 0.001) after 4 h. In tolerant rats, given endotoxin (15 mg/kg), plasma i6-keto-PGF1 alpha at 1 h was 800 +/- 203 pg/ml (N = 5) and was not significantly different (734 +/- 254 pg/ml) at 4 h. Plasma iTxB2 at both 1 and 4 h was significantly (P less than 0.01) lower in tolerant than nontolerant rats. Both iTxB2 and i6-keto-PGF1 alpha were significantly (P less than 0.01) lower in tolerant rats given 50 mg/kg IV endotoxin than nontolerant rats. Endotoxin-induced elevation in fibrin degradation products was significantly decreased (P less than 0.05) during endotoxin tolerance although there was no difference in the severity of thrombocytopenia. These composite observations demonstrate that endotoxin tolerance in the rat is associated with altered arachidonic acid metabolism.

Topics: Acid Phosphatase; Animals; Arachidonic Acid; Arachidonic Acids; Aspartate Aminotransferases; Blood Platelets; Disease Susceptibility; Fibrin Fibrinogen Degradation Products; Glucuronidase; Macrophages; Male; Prostaglandins F; Rats; Shock, Septic; Thrombocytopenia; Thromboxane B2

Essential fatty acid deficient (EFAD) rats are significantly more resistant to the lethal effects of S. enteritidis endotoxin (20 mg/kg, IV) than normal control rats. Compared to endotoxin-treated normal rats, EFAD rats also manifested less severe alterations of hepatic and lysosomal integrity and became less hypoglycemic. Administration of the ethyl ester of the essential fatty acid, arachidonic acid (100 mp, IP) two days prior to challenge with S. enteritidis endotoxin (20 mg/kg) in EFAD rats restored their sensitivity to endotoxin, as denoted by a 100% mortality compared to a 24% mortality (P less than 0.01) in EFAD rats. Treatment of EFAD rats with the fatty acid docosahexaenoic acid, a non-prostaglandin and thromboxane precursor, (100 mg, IP) produced significantly less (less than 0.01) mortality than ethyl-arachidonate-treated groups (ie, 40% vs 100%). The arachidonate metabolite, thromboxane B2 (TxB2), increased from nondetectable plasma levels (less than 200 pg/ml) to 2285 +/- 449 pg/ml (N = 10) at 30 min and remained elevated for 180 minutes after endotoxin administration in nondeficient rats. However, plasma TxB2 was not detectable in endotoxin-treated EFAD rats and was only slightly elevated in groups supplemented with docosahexaenoic acid (273 +/- 104 pg/ml, N = 6) after 30 minutes. In ethyl arachidonate (100 mg, IP) supplemented EFAD rats, plasma TxB2 rose to 873 +/- 204 pg/ml (N = 8), 30 min after endotoxin. Pretreatment of the ethyl-arachidonate-supplemented EFAD group with a specific thromboxane synthetase inhibitor, 7-(1-imidazolyl)-heptanoic acid (30 mg/kg, IV), significantly reduced mortality 100% to 50% (P less than 0.05) from endotoxic shock. These observations suggest a deleterious role for arachidonic acid and its conversion to TxA2 in the pathogenesis of endotoxic shock.

Topics: Acid Phosphatase; Animals; Arachidonic Acid; Arachidonic Acids; Blood Glucose; Disease Models, Animal; Fatty Acids, Essential; Female; Fibrin Fibrinogen Degradation Products; Male; Muridae; Pregnancy; Shock, Septic; Thromboxane B2

Lysosomal enzymes are released in the blood stream in various types of shock. The role of the released enzymes in the development of irreversible shock is still controversial. The present study was undertaken to determine the effect of the administration of lysosomal enzymes in normal rats and rats treated with endotoxin. Lysosomal enzymes were prepared from the isologous liver. They were given either intravenously or intraperitoneally to normal rats. No hemodynamic effect was observed. They were also given to the rats that received the lethal dose of endotoxin. No hemodynamic effect was found in this group. The survival time and the time course of the blood pressure to death did not change. The lysosomal enzyme preparation was given to the rats that received various dosages of endotoxin of less than LD190. The mortality rate of the rats that received endotoxin was not modified by the administration of the lysosomal enzyme preparation. These results indicate that lysosomal enzymes released into the blood in endotoxin shock may not contribute significantly to the irreversibility of shock.

Topics: Acid Phosphatase; Animals; Blood Pressure; Cell Extracts; Escherichia coli; Glucuronidase; Liver; Lysosomes; Rats; Shock, Septic

The efficacy of corticosteroid therapy in the treatment of shock remains controversial. In order to evaluate this question, the following controlled experimental study was undertaken. There were 44 puppies (2-6 kg) used to examine the effects of methylprednisolone (30 mg/kg) in both hemorrhagic and live Escherichia coli septic shock. In order to isolate the effects of steroid treatment, no volume or antibiotic therapy was given. Arterial, venous, and pulmonary artery catheterization allowed continuous hemodynamic and metabolic monitoring. One control group received steroid treatment and was not subjected to shock. Septic shock was achieved by a rapid bolus infusion of 10(9) live E. coli organisms. Hemorrhagic shock was produced by bleeding the puppy an average of 43% of his blood volume. Four septic and four hemorrhagic shock groups received either no treatment, steroids at the time of shock, or steroids 30 min before or after shock. Cardiac outputs of less than 50% of control values and significant lactic acidosis were documented in all of the shock animals. The septic groups showed more profound alterations in these parameters and a decreased overall survival. No statistically significant differences could be found, however, in the hemodynamic, metabolic or survival figures among the different septic shock groups, or among the various hemorrhagic shock animals. The anticipated preservation of cardiac output and decrease in leakage of lysosomal acid phosphatase were not seen with any treatment schedule. The theoretical benefits of corticosteroid treatment in shock could not be documented in these two models of severe septic and hemorrhagic shock in puppies.

Topics: Acid Phosphatase; Animals; Disease Models, Animal; Dogs; Escherichia coli; Fatty Acids, Nonesterified; Glucose; Hemodynamics; Lactates; Methylprednisolone; Methylprednisolone Hemisuccinate; Shock, Hemorrhagic; Shock, Septic; Triglycerides

During endotoxemia, there is a significant increase in arachidonic acid-derived metabolites. To test the hypothesis that one or more of these metabolites play a significant role in the pathogenesis of endotoxic shock we investigated the therapeutic efficacy of varying doses of ibuprofen, a cyclooxygenase inhibitor, on the pathophysiologic sequelae of endotoxic shock in the Long-Evans rat, induced by S. enteritidis endotoxin (20 mg/kg). Pretreatment with ibuprofen (1-3.75 mg/kg) produced an optimal survival rate of 80% compared to only 11% in the vehicle-treated group. Doses of 0.1, 0.5 and 30 mg/kg of ibuprofen also significantly (P < .05) improved survival over nontreated shocked controls. Plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha(PGF1 alpha) levels rose from < 200 pg/ml to 2207 +/- 282 (N = 16) and 840 +/- 59 (N = 8), respectively, within 30 min after injection. The rise in plasma thromboxane B2 and 6-keto-PGF1 alpha levels was reduced with ibuprofen (3.75 and 30 mg/kg) to < 200 pg/ml. Ibuprofen (3.75 and 30 mg/kg) reduced thrombin-induced in vitro platelet thromboxane B2 synthesis by 95 and 99%, respectively. The severity of coagulopathies as reflected by elevations in serum fibrogen/fibrin degradation products and lysosomal integrity were likewise significantly reduced (40%) with ibuprofen (3.75 mg/kg) pretreatment. These results are consistent with the hypothesis that arachidonic acid metabolites play a significant early role in the pathogenesis of endotoxic shock. Our observations suggest potential benefits from agents which inhibit fatty acid cyclooxygenase.

Topics: Acid Phosphatase; Animals; Fibrin Fibrinogen Degradation Products; Glucuronidase; Ibuprofen; Lysosomes; Male; Prostaglandins F; Rats; Shock, Septic; Thromboxane B2

Lysosomal disruption with release of lysosomal enzymes has been described in shock. Our study was designed to demonstrate the release of lysosomal enzymes in the liver and lung in addition to determining circulating serum lysosomal enzyme values. Terapeutic means of reducing or inhibiting lysosomal disruption were also investigated. Five groups of baboons were investigated: Group A: (control group) - no endotoxin or treatment administered. Group B: (endotoxin only) - liver and lung tissues showed an increase in free lysosomal enzymes, and a similar increase in curculating serum lysosomal enzymes was demonstrated. Group C: (chloroguine treatment (lysosomal stabiliser) following endotoxin administration) - the liver and lung tissues showed a smaller increase in free lysosomal enzymes and a corresponding lesser increase in circulating serum lysosomal enzymes was demonstrated. Group D: (dexamethasone treatment (lysosomal membrane stabiliser) following endotoxin administration) - the rise in lysosomal tissue and serum enzyme values was less than that in group B. Group E: (combination of chloroquine and dexamethasone treatment following endotoxin administration) - the rise in lysosomal tissue and serum values was less than that demonstrated in group B. The survival of the animals in the various groups correlated well with the lysosomal enzyme tissue and serum values, as did the monitored haemodynamic, hoematological and other parameters.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Blood Coagulation Tests; Blood Platelets; Blood Pressure; Body Temperature; Chloroquine; Dexamethasone; Female; Fibrinogen; Liver; Lung; Lysosomes; Male; Papio; Pulmonary Artery; Shock, Septic; Vascular Resistance

Topics: Acid Phosphatase; Animals; Calcium; Drug Evaluation; Endotoxins; Escherichia coli; Kidney; Liver; Lysosomes; Male; Methylprednisolone; Mitochondria; Mitochondria, Liver; Oxygen Consumption; Rats; Shock, Septic

The effect of corticosteroids on cellular resistance in shock was studied by serial measurement of the serum concentration of the lysosomal enzyme acid phosphatase in untreated and steroid dogs subjected to hemorrhagic, endotoxin and cardiogenic shock. In each shock category, elevation in serum acid phosphatase was significantly less in steroid treated dogs as compared to untreated animals at corresponding time intervals. This difference was most apparent in endotoxin shock, next in hemorrhagic shock and least in cardiogenic shock. Steroid treatment also reduced the serum lactate increment in hemorrhagic and cardiogenic shock and delayed or reduced the onset and severity of the occurring acidosis, an apparent reflection of the ability of steroids to promote increased tissue perfusion. In addition, steroid treatment increased or prolonged survival in all three shock groups. By showing that glucocorticoids affect a reduction in the release of the lysosomal enzyme acid phosphatase during shock, the study offers direct evidence that steroids enhance cellular resistance to shock stress in the dog. Whether this salutary effect is due solely to the ability of steroids to stabilize cellular membranes or is in part secondary to promoting improved tissue hemodynamics could not be established. The interpretation and clinical application of these results must take into account the possibility of a species specific response.

Topics: Acid Phosphatase; Acidosis; Animals; Blood Transfusion, Autologous; Cell Membrane Permeability; Coronary Vessels; Endotoxins; Hemoglobinometry; Lactates; Ligation; Lysosomes; Methylprednisolone; Pyruvates; Shock, Cardiogenic; Shock, Hemorrhagic; Shock, Septic; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Disease Models, Animal; Hypoxia; Lysosomes; Male; Microelectrodes; Mitochondria, Liver; Muscles; Oxygen; Proteins; Rats; Shock, Hemorrhagic; Shock, Septic; Spectrophotometry

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Cell Survival; Cysteine; Glucuronidase; Kupffer Cells; Lactates; Lead Poisoning; Liver; Male; Methylprednisolone; Phagocytosis; Pyruvates; Rats; Salmonella enteritidis; Shock, Septic; Sulfobromophthalein

Topics: Acid Phosphatase; Animals; Colorimetry; Dogs; Lymph; Lysosomes; Methylprednisolone; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Shock, Septic; Thoracic Duct

Topics: Acid Phosphatase; Acidosis; Adenosine Triphosphatases; Animals; Calcium; Escherichia coli; Hydrogen-Ion Concentration; Lysosomes; Male; Mitochondria, Liver; Oxidoreductases; Potassium; Rats; Shock, Septic; Sodium; Succinates

Topics: Acid Phosphatase; Adenosine Triphosphatases; Animals; Hypoxia; Liver; Lysosomes; Male; Microscopy, Electron; Mitochondria, Liver; Oxygen Consumption; Rats; Shock, Hemorrhagic; Shock, Septic; Time Factors

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Blood Glucose; Dextrans; Endotoxins; Glucuronidase; L-Lactate Dehydrogenase; Liver; Lysosomes; Palmitic Acids; Rats; Rats, Inbred Strains; Salmonella; Shock, Septic; Sulfobromophthalein

Topics: Acid Phosphatase; Animals; Biological Assay; Endotoxins; Freezing; Glucuronidase; Hydrogen-Ion Concentration; Iron; Lipopolysaccharides; Liver; Liver Extracts; Lysosomes; Macrophages; Male; Mononuclear Phagocyte System; Rats; Salmonella; Shock, Septic; Time Factors; Vibration

Topics: Acid Phosphatase; Animals; Dogs; Escherichia coli Infections; Glucuronidase; Histocytochemistry; Liver; Lysosomes; Microscopy, Electron; Shock, Septic

Topics: Acid Phosphatase; Animals; Depression, Chemical; Dogs; Escherichia coli; Glucuronidase; Lipopolysaccharides; Lysosomes; Polysaccharides, Bacterial; RNA, Transfer; Shock, Septic

Topics: Acid Phosphatase; Acid-Base Equilibrium; Animals; Blood Pressure; Carbon Dioxide; Dogs; Drainage; Glucuronidase; Hydrogen-Ion Concentration; Lactates; Lysosomes; Oxygen; Oxygen Consumption; Respiration; Shock, Hemorrhagic; Shock, Septic; Splenectomy; Thoracic Duct

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Antibodies; Aspartate Aminotransferases; Blood Coagulation; Blood Platelets; Blood Pressure; Dogs; Endotoxins; Escherichia coli; Fibrinogen; Hematocrit; Hemodynamics; Immune Tolerance; L-Lactate Dehydrogenase; Lactates; Leukocyte Count; Metabolism; Prothrombin Time; Pyruvates; Shock, Septic

Topics: Acid Phosphatase; Animals; Antibodies; Antibody Formation; Antigen-Antibody Reactions; DNA; Glucuronidase; Haplorhini; Hemagglutination Inhibition Tests; Hemagglutination Tests; Lactates; Nucleotides; Shock, Hemorrhagic; Shock, Septic

Topics: Acid Phosphatase; Alanine Transaminase; Animals; Aspartate Aminotransferases; Dogs; Endotoxins; Escherichia coli; Female; Heparin; Lactates; Male; Prothrombin Time; Pyruvates; Shock, Septic

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