Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma polymorphonuclear leukocyte elastase (PMNE) activity is known to increase during cardiopulmonary bypass (CPB), and is considered to mediate pulmonary tissue damage causing postoperative respiratory failure. We made a clinical study in order to clarify the effects of ulinastatin (Miraclid), a proteolytic enzyme inhibitor, on plasma PMNE activity and respiratory function. Twenty adult patients undergoing coronary artery bypass grafting were divided into 2 groups; 10 to group U and 10 to group C. The patients in group U received 500 U/kg body weight of ulinastatin intravenously before and after CPB, and the patients in group C not receiving the dose served as controls. Arterial blood samples were obtained before the operation, 1 hour after CPB, 3 hours, 1 day and 4 days after the operation. The leukocyte count was significantly lower in group U 1 hour after CPB and 3 hours after the operation compared to group C (p less than 0.01). The plasma PMNE activity rose rapidly after starting CPB and the peak level appeared 1 hour after CPB; 1165 +/- 560 micrograms/l in group U and 1981 +/- 562 micrograms/l in group C (p less than 0.02). There was a significant correlation between the leukocyte reduction and the rate of increase of beta-glucuronidase activity were diminished in group U compared to preoperative values (p less than 0.05). The recovery of the oxygenation index (PaO2/F1O2), which was used for evaluation of the respiratory function, was worse in group C (p less than 0.01). These results suggest that the administration of ulinastatin in patients undergoing CPB is useful for the prevention of the deleterious effects of PMNE on the lung.
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PMID:[Effects of ulinastatin on plasma polymorphonuclear leukocyte elastase activity and respiratory function in patients undergoing cardiopulmonary bypass]. 237 94

The use of prostaglandins is currently undergoing clinical trials in respiratory failure accompanying sepsis. The effect of prostaglandin E1 (PGE1) and prostacyclin (PGI2) infusion on endotoxin-induced lung injury, with attention to interstitial fluid flux (QL), pulmonary vascular pressure (Ppa), leukocytes, platelets, and release of the lysosomal enzyme beta-glucuronidase, was investigated. A chronic lung lymph fistula model in sheep was used. Seven sheep alternately received Escherichia coli endotoxin and endotoxin plus PGE at a dosage of 1 microgram/kg/min. Six sheep received PGI2 (0.2 microgram/kg/min) instead of PGE1. Both PGE1 and PGI2 decreased the pulmonary hypertension and the interstitial edema produced by endotoxin primarily through their vasodilatory properties. Prostacyclin seemed to have an additional membrane-stabilizing effect. A rebound increase in QL, Ppa, and platelets occurred when PGE1 or PGI2 infusion was discontinued.
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PMID:Prostaglandin infusion and endotoxin-induced lung injury. 703 77