acid-phosphatase and Shock--Traumatic

The reaction of Peyer's patches to trauma manifests in: 1) vascular changes; 2) primary or stressor cells shifts recordable in traumatic shock, characterized by depletion of patch follicles by minor lymphocytes; 3) secondary changes associated with the onset of reparative processes; 4) the increased macrophagal activity detectable during the entire period of the traumatic shock and in the early post-shock period. It is suggested that changes seen may be due to endotoxin that penetrates from the intestine.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Cell Count; Lymphocytes; Lymphoid Tissue; Macrophages; Peyer's Patches; Plasma Cells; Rats; RNA; Shock, Traumatic

Topics: Acid Phosphatase; Animals; Betamethasone; Dexamethasone; Glucuronidase; Hydrocortisone; Male; Rats; Shock, Traumatic

Antishock effect of N6, O2-dibutyryl cyclic AMP (DBcAMP) Was investigated in rats subjected to Noble-Collip drum trauma and compared with effects of hydrocortisone and Trasylol. Results obtained are as follows. 1)Hydrocortisone and Trasylol administered 1 hr before initiating drumming improved the survival rate from traumatic shock with concomitant reducton of levels of acid phosphatase and beta-glucuronidase in circulating blood. DBcAMP administered i.p. immediately after trauma also improved the survival rate to the same extent as did Traylol or hydrocortisone, while no inhibitory effects were observed on acid phosphatase and beta-glucuronidase. 2)The rectal temperature fell significantly after suffering trauma, and the rats with greater fall in rectal temperature had poorer chance for survival. The fall in rectal temperature was considerably prevented by DBcAMP in a dose of 0.5 mg/100 g body weight (b.w.). 3)DBcAMP induced a rise in plasma insulin level (IRI) and insulin/glucose ratio (I/G) in shock rats, and the elevation in blood lactate/pyruvate ratio (L/P) and excess lactate otherwise observed after trauma were satisfactorily prevented by DBcAMP administration. It is concluded that the antichock effects of DBcAMP primarily resulted from improvements of the intracellular metabolism induced by its easy passage through the cell membrane and its cAMP like action, while any preventive action was not observed against elevation of lysosomal enzymes in the circulating blood.

Topics: Acid Phosphatase; Adenosine Triphosphate; Animals; Aprotinin; Body Temperature; Bucladesine; Glucuronidase; Hydrocortisone; Male; NAD; Rats; Rectum; Shock, Traumatic

Biochemical and electron microscope studies were conducted to determine the effects of traumatic shock on rabbit alveolar macrophages. Both resting and phagocytosing macrophages from the shocked animals, in comparison to comparable control macrophages, showed increased release of acid phosphatase from the cells into medium upon incubation in vitro, but decreases in the total content of acid phosphatase and beta-glucuronidase. Studies by electron microscopy showed ultrastructural alterations in macrophages from shocked animals consisting of a reduction in the number or a complete absence of lysosomes and, in some cases, increased amounts of rough endoplasmic reticulum and free ribosomes. In vitro incubation of macrophages from shocked animals with Pseudomonas aeruginosa showed that the process of bacterial ingestion was not impaired nor were the numbers of bacteria ingested decreased as compared to control macrophages. However, the ability of macrophages from shocked animals to destroy ingested bacteria appeared to be significantly altered. Extensive degradation of Pseudomonas was observed within phagocytic vacuoles of control macrophages after 15 minutes of incubation. In contrast, the majority of ingested organisms in macrophages from shocked animals showed no evidence of degradative changes.

Topics: Acid Phosphatase; Animals; Female; Glucuronidase; Lysosomes; Macrophages; Male; Phagocytosis; Pulmonary Alveoli; Rabbits; Shock, Traumatic

Plasma lysosomal enzyme levels and hepatic phagocytosis were determined following Noble-Collip drum trauma in the rat. Circulating cathepsin and acid phosphatase activity increased after sublethal trauma (300 rev), reaching maximal levels at 1-3 hr and returning to pretrauma levels at 24 hr after trauma. Hepatic phagocytosis was decreased maximally at 1 hr and recovered to control levels at 24 hr after sublethal trauma. Increasing trauma intensity (100-500 rev) resulted in a progressive failure in hepatic Kupffer cell phagocytosis and a progressive increase in plasma lysosomal enzyme levels when tested at 60-min post-trauma. A significant inverse correlation was found between the plasma lysosomal enzyme levels and Kupffer cell phagocytosis after trauma. The functional significance of the relationship between these two parameters and its importance in shock survival remain to be determined.

Topics: Acid Phosphatase; Animals; Cathepsins; Kupffer Cells; Lysosomes; Male; Phagocytosis; Rats; Shock, Traumatic; Time Factors

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Blood Vessels; Dogs; Glycogen; Histocytochemistry; Myocardium; Shock, Traumatic; Succinate Dehydrogenase

The authors studied the activity of acid phosphatase (AP), lactic dehydrogenase (LDH), aspartic and alanine-aminotranspherases (AST and ALT) in the serum of rats with intact and removed adrenal glands after a severe multifocal trauma induced according to Noble-Collip (300 rpt of the drum with the rotation speed of 37 rpt/min). Adrenalectomy showed practically no influence on the dynamics of the LDH and AP activity. An increase in the activity of the AST and especially of the ALT in the serum of adrenalectomized rats after the trauma was considerably less than in the animals with the intact adrenal glands.

Topics: Acid Phosphatase; Adrenal Glands; Animals; Aspartate Aminotransferases; L-Lactate Dehydrogenase; Male; Rats; Shock, Traumatic

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Cholinesterases; Dogs; Female; Intestinal Absorption; Liver; Male; Oxygen; Shock, Traumatic; Time Factors

Topics: Acid Phosphatase; Adolescent; Adrenal Glands; Adult; Aged; Alkaline Phosphatase; Burns; Child; Histocytochemistry; Humans; Hyperplasia; Hypothalamus; Methods; Neurosecretion; Pituitary Gland; Shock, Traumatic; Time Factors

Topics: Acid Phosphatase; Animals; Biopsy; Charcoal; Female; Histocytochemistry; Injections, Intravenous; Liver; Male; Mononuclear Phagocyte System; Rabbits; Shock, Traumatic; Time Factors; Tourniquets

Topics: Acid Phosphatase; Adolescent; Adrenal Gland Diseases; Adrenal Glands; Adult; Aged; Alkaline Phosphatase; Burns; Cholesterol; Emaciation; Humans; Lipid Metabolism; Middle Aged; Shock, Traumatic; Succinate Dehydrogenase; Time Factors; Toxemia

Topics: Acid Phosphatase; Animals; Brain Stem; Cerebral Cortex; Rats; Shock, Traumatic

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

Topics: Acid Phosphatase; Alkaline Phosphatase; Aminopeptidases; Burns; Dihydrolipoamide Dehydrogenase; Glucosidases; Histocytochemistry; Kidney; Rats; Research; Shock, Traumatic

Topics: Acid Phosphatase; Glucuronidase; Histocytochemistry; Kupffer Cells; Liver; Mononuclear Phagocyte System; Oxygen; Phagocytosis; Research; Shock, Traumatic; Spleen

Fatal shock was produced in animals by drum trauma, temporary occlusion of the superior mesenteric artery, and bacterial endotoxin. Measurements were made of release of beta glucuronidase and cathepsins from the large granule fractions of livers, and of levels of circulating beta glucuronidase and acid phosphatase in these animals. Experiments were also carried out with animals rendered tolerant by previous exposure to sublethal amounts of trauma or by pretreatment with cortisone. The results show that release of beta glucuronidase and cathepsins from the large granule fraction of liver was increased during traumatic and endotoxin shock in the rat. Similarly, circulating levels of acid phosphatase and beta glucuronidase were increased during traumatic shock in rats and rabbits, and during endotoxin shock in rats. The data also indicate that tolerance to traumatic injury, induced by prior conditioning, prevented the increase in levels of circulating acid phosphatase normally observed after stress, and may have been associated with an increased stability of hepatic lysosomal particles. In addition, cortisone, which appears to "stabilize" hepatic lysosomes in vivo, also reduced the increase in plasma acid phosphatase brought about by endotoxin and trauma. From the foregoing observations, it is suggested that: (a) Disruption of lysosomes and release of their contained enzymes in free, active form may occur in liver and intestine of shocked animals. (b) The activation of lysosomal hydrolases within cells and their release into the circulation may play an important role in exacerbating tissue injury and accelerating the development of irreversibility during shock. (c) The increased stability of lysosomes of tolerant and of cortisone-treated animals may constitute an important component of the resistance of these animals to shock.

Topics: Acid Phosphatase; Animals; Blood; Cathepsins; Cytoplasm; Endotoxemia; Endotoxins; Glucuronidase; Hydrolases; Liver; Lysosomes; Peptide Hydrolases; Rabbits; Rats; Shock; Shock, Traumatic