acid-phosphatase and Shock

This study was designed to investigate the beneficial effect of administration of exogenous superoxide dismutase (SOD) on the inhibition of lipid peroxidation and cellular protection during superior mesenteric artery occlusion shock in rats. Wistar rats were anesthetized with sodium pentobarbital (30 mg/kg body weight), and the superior mesenteric artery occlusion shock model was induced by clamping the superior mesenteric artery for a 60-min period and then releasing the arterial clamp. The following parameters were determined: 1) average arterial blood pressure; 2) survival rate and mean survival time (MST); 3) activities of plasma lysosomal enzymes beta-glucuronidase (beta-G) and acid phosphatase (ACP); and 4) the contents of malondialdehyde (MDA) in visceral tissues. The SOD group received 15,000 U/kg body weight SOD intra-arterially 15 min before release of the clamp. The saline group received intra-arterially a corresponding volume of saline given to the SOD group. The superior mesenteric artery of rats in the control group was not clamped. In the saline group, the contents of MDA presented significant increases (P less than 0.05) in bowel and heart tissues at 1 hr after release of the clamp and showed more significant increases (P less than 0.01-0.05) in bowel, heart, liver, and lung tissues at 2 hr after release of the clamp, when compared with control values. However, the contents of MDA in bowel and heart tissues in the SOD group showed significant decreases (P less than 0.05) compared with values in the saline group and had insignificant changes (P greater than 0.05) compared with control values at 1 hr after release of the clamp. The contents of MDA in bowel, heart, and lung tissues in the SOD group were still lower than those in the saline group (P less than 0.05) at 2 hr after release of the clamp, although they were higher than those in the control group (P less than 0.05). The activities of plasma lysosomal enzymes in the SOD group were much lower than those in the saline group at 1 and 2 hr after release of the clamp. The mean survival time of shocked animals was prolonged when treated with SOD. These results suggested that administration of exogenous SOD may protect cells against lipid peroxidation injury mediated by oxygen-derived free radicals, depress the release of lysosomal enzymes, and prolong the mean survival time of shocked animals.

Topics: Acid Phosphatase; Animals; Blood Pressure; Constriction; Female; Free Radicals; Glucuronidase; Lipid Peroxidation; Lysosomes; Male; Malondialdehyde; Mesenteric Arteries; Oxygen; Rats; Rats, Inbred Strains; Shock; Superoxide Dismutase

An experimental model of haemorrhagic hypotension was standardized using rabbits to investigate the shock lung syndrome over a period of 120 minutes. Acute hypovolaemia was induced by withdrawal of blood under anaesthesia to a mean arterial pressure of 30 +/- 5 mmHg within 10 minutes. The mean leucocyte counts and the release of lysosomal enzymes (acid phosphatase and beta-glucuronidase) in the blood and in lung tissue, as well as the metabolic capacities of lung tissue in terms of protein and lipid biosynthesis, were investigated at set intervals after 30, 60, 90 and 120 minutes. The results indicate a progressive decline in leucocyte numbers over 120 minutes to about 40% of the original. An immediate granulocytopenia was observed with a relative lymphocytosis within 30 minutes. The beta-glucuronidase and acid phosphatase contents of the plasma increased with time; beta-glucuronidase activity increased progressively as leucocytes disappeared from the circulation. Concomitantly, the capacity of the lung tissue to synthesize protein and lipids was retarded with time, becoming significantly lower than baseline values after 60 minutes of hypovolaemia. The decline in leucocyte numbers in the circulation correlated well with the increase in beta-glucuronidase activity and the retarded metabolic capacity of the lung tissue.

Topics: Acid Phosphatase; Animals; Glucuronidase; Hematocrit; Leukocyte Count; Lipids; Lung; Proteins; Rabbits; Respiratory Distress Syndrome; Shock; Time Factors

In 6 dogs with superior mesenteric artery occlusion (SMAO) shock and in 6 healthy animals the total and free activity of lysosomal hydrolases (acid phosphatase, betaglucuronidase and cathepsins) in the whole homogenate, the lysosomal enriched subfraction and the supernatant of kidneys were estimated. Statistically significant differences between the two groups were not observed. These results indicate that in SMAO shock, the stability of kidney lysosomes is well preserved during observed period.

Topics: Acid Phosphatase; Animals; Cathepsins; Dogs; Female; Glucuronidase; Hydrolases; Kidney; Lysosomes; Male; Mesenteric Arteries; Mesenteric Vascular Occlusion; Shock

The cause of the posttraumatic respiratory distress syndrome is not yet well known and cannot be proved with certainty. The early stage of posttraumatic lung failure has been examined both from a morphological and biochemical aspect. Lung biopsies taken during hypovolemic-traumatic shock show besides endothelial damage an accumulation of leucocytes with free granules, similar to lysosomes. Based on these results further tests have been carried out to achieve a similar reaction in the hypovolemic-traumatic shock model in the dog, enabling us to undertake more extensive examinations and to use new methods of treatment. The lung biopsies taken at the beginning and after finishing the test were observed by light-transmission and scanning electron-microscope. Similar to the results obtained from humans, we found a massive leucostasis with degranulated cells. A parallel increase of lysosomal enzyme activity and a peripheral leucocytosis was seen while after reinfusion a distinct decrease was found. The massive occurence of leucocytes in the lung may be caused either by chemotaxis or by the sieve function of the lung after peripheral leucocytes aggregation. Both could have an immunological cause, especially due to involvement of the complement system. Septic reasons in the early stage of shock can be disregarded. More likely the complex effects of the interactions complement--fibrinolysis--kallikrein system are involved. Presumably the leucocytes caused direct damage to the endothelial cells. Lysosomal enzymes as reason for producing the damage would be one possibility; an other is the recently discovered effect of oxygen radicals produced during the close contact between leucocytes and endothelium and the simultaneously activated complement system.

Topics: Acid Phosphatase; Animals; Chemotaxis; Complement Activation; Dogs; Glucuronidase; Humans; Leukocytes; Lung; Lysosomes; Respiratory Distress Syndrome; Shock

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

A 2 hr-period of regional intestinal simulated shock in cats results in small intestinal mucosal lesions and a general cardiovascular derangement, probably secondary to the release of cardiotoxic material into the intestinal venous blood. These phenomenona are accompanied by release of lysosomal and cytoplasmatic enzymes from the intestinal tissue. The effects of methylprednisolone treatment and deposition of albumin in the intestinal lumen during the regional shock period were studied. Administration of methylprednisolone early and late in the regional shock period prevented mucosal lesions and cardiovascular deterioration as well as lysosomal and cytoplasmatic enzyme release. Albumin deposition in the intestinal lumen during the regional shock period prevented lysosomal enzyme release and cardiovascular derangement and to a minor extent mucosal lesions. It is suggested that release of intestinal lysosomal enzymes is of importance for development of mucosal lesions and for production of cardiotoxic material.

Topics: Acid Phosphatase; Albumins; Alkaline Phosphatase; Animals; Cats; Glucuronidase; Intestinal Mucosa; Lysosomes; Methylprednisolone; Shock

Topics: Acid Phosphatase; Adolescent; Adult; Animals; Aprotinin; Female; Glucuronidase; Humans; Male; Middle Aged; Rats; Shock

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

Topics: Acid Phosphatase; Adrenergic alpha-Antagonists; Animals; Cell Fractionation; Cell Membrane; Cell Survival; Chlorpromazine; Glucuronidase; Hot Temperature; In Vitro Techniques; Liver; Lysosomes; Male; Methylprednisolone; Microcirculation; Phenoxybenzamine; Phentolamine; Rats; Shock; Statistics as Topic

Topics: Acid Phosphatase; Animals; Anti-Arrhythmia Agents; Aprotinin; Blood Pressure; Cats; Celiac Artery; Chymotrypsin; Enzyme Activation; Female; Hydrolases; Ligation; Lysosomes; Male; Mesenteric Arteries; Methylprednisolone; Microscopy, Electron; Pancreas; Phospholipases; Shock; Trypsin

Topics: Acid Phosphatase; Animals; Blood Cell Count; Blood Flow Velocity; Blood Platelets; Blood Pressure; Colloids; Dogs; Fibrinogen; Glucuronidase; Hematocrit; Leukocyte Count; Plasma Volume; Polystyrenes; Shock; Silicon

Topics: Acid Phosphatase; Animals; Female; Glucuronidase; Intestinal Mucosa; Kidney; Liver; Lysosomes; Organ Size; Rats; Shock; Tourniquets

Topics: Acid Phosphatase; Animals; Dogs; Ileum; Intestinal Mucosa; Intestine, Small; Mesenteric Arteries; Mesenteric Vascular Occlusion; Ribonucleases; Shock

Topics: Acid Phosphatase; Adrenal Glands; Adrenalectomy; Animals; Histocytochemistry; Immune Sera; Liver; Lysosomes; Rats; Shock; Stress, Physiological; Tourniquets

Topics: Acid Phosphatase; Animals; Glucuronidase; Hydrocortisone; Lysosomes; Male; Rats; Shock; Tourniquets

Topics: Acid Phosphatase; Alkaline Phosphatase; Anaphylaxis; Animals; Female; Histamine Release; Leucyl Aminopeptidase; Male; p-Methoxy-N-methylphenethylamine; Prednisolone; Rats; Sex Factors; Shock

Topics: Acid Phosphatase; Animals; Chlorpromazine; Endotoxins; Escherichia coli; Hydrogen-Ion Concentration; In Vitro Techniques; Liver; Lysosomes; Rats; Shock; Vitamin A

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