Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations of platelet function and blood coagulation may occur with exercise or beta-adrenoceptor blockade. To determine if beta-blockade could modify exercise-induced changes in haemostatic factors we performed a double-blind study of acute strenuous exercise in normal males with and without beta-blockade. Exercise increased prostacyclin and plasminogen activator levels but there was no evidence of thrombin generation as indicated by unchanged platelet aggregation responses, beta-thromboglobulin and fibrinopeptide A levels. The only alteration in coagulation by beta-blockade was a reduction in the factor VIII:C and VIII:RAg rise after exercise and this modification may be relevant to the protective effect of these drugs in patients with coronary artery disease.
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PMID:Blood coagulation and platelet function following maximal exercise: effects of beta-adrenoceptor blockade. 614

Plasma coagulation factors were measured in twelve male insulin-dependent diabetics with no retinopathy, ten with background and ten with proliferative retinopathy and ten non-diabetics. Factor VIII pro-coagulant activities (VIII:C), ristocetin cofactor activities and factor VIII-related antigen concentrations (VIIIR:ag) were significantly related to the severity of diabetic retinopathy (P less than 0.025, trend test). The mean ratio of VIII:C/VIIIR:ag was lower in the diabetics with proliferative retinopathy than in the other groups of diabetics (P less than 0.05) or the controls (P less than 0.02). Concentrations of alpha 2 macroglobulin and alpha 1 antitrypsin were highest in diabetics with proliferative retinopathy (0.1 greater than P greater than 0.05, trend test) but mean prothrombin and activated partial thromboplastin times and mean concentrations of alpha 2 antiplasmin, plasminogen activator and antithrombin III were similar in all groups. Concentrations of the platelet-specific protein beta thromboglobulin, though higher in diabetics than controls (P less than 0.005), were not related to retinopathy. The plasma concentrations of coagulation factors did not correlate with creatinine clearance and there were no significant differences between groups in concentrations C-reactive protein; this suggests that the raised concentrations of coagulation factors in diabetics with retinopathy were not a result of associated nephropathy or an 'acute phase protein' response to diabetic tissue damage. Increased coagulation activity in diabetics may contribute to the development of retinopathy.
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PMID:Plasma haemostatic factors and diabetic retinopathy. 619 95

We confirm that basal rates of formation of plasminogen activator by cells in cultured tubule segments at stages of the cycle associated with spermiation (stages VII and VIII) are higher than those by cells in tubule segments at any other stages of the cycle of the seminiferous epithelium. We demonstrate that addition of cAMP derivatives or follicle-stimulating hormone in the presence of a phosphodiesterase inhibitor results in a large stimulation of plasminogen activator formation by tubule segments at all stages of the cycle. The greatest percentage increase (approximately 100-fold) is observed in cells in tubule segments having lowest basal rates of plasminogen activator formation (stages IX-VI). Even under stimulated conditions, however, the amounts of plasminogen activator produced by cultured tubule segments at stages VII and VIII remain greater than those produced by cultured tubule segments at other stages of the cycle, and these differences persist during organ culture for 48 h. Insulin and testosterone do not alter rates of formation of plasminogen activator. We conclude that Sertoli cells, the primary source of formation of plasminogen activator in the testis, are metabolically heterogeneous in the seminiferous tubule and that the germ cell association patterns in various stages of the cycle modulate Sertoli cell functions. We discuss the data in relation to the tissue restructuring within the seminiferous tubule which occurs during spermatogenesis and the possible role of plasminogen activator in these processes.
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PMID:Hormonal influences on formation of plasminogen activator by cultured testis tubule segments at defined stages of the cycle of the seminiferous epithelium. 631 51

The effect of DDAVP on blood coagulation factors was investigated after its intravenous infusion into normal subjects. A marked increase in factor XII was observed in addition to the expected rise of factor VIII coagulant activity (VIII:C), factor VIII related antigen (VIIIR:Ag) and plasminogen activator, DDAVP also produced a concomitant but less pronounced rise of factor VII, but there was no change in factors V, IX, X and XI.
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PMID:Effect of DDAVP on plasma level of factor XII. 640 13

We have studied vessel wall function in two groups of patients with chronic renal failure - 1) conservative treatment only and 2) maintenance hemodialysis. Three proteins synthesized by vascular endothelium-plasminogen activator (PA), factor VIII related antigen (VIII:RAg) and antithrombin III (ATIII) - were assayed before and after a fifteen minute period of venous occlusion. The release of PA was significantly reduced in patients on maintenance hemodialysis as compared to both undialyzed uremics and controls. Lesser amounts of VIII:RAg were also released by hemodialysis patients than by undialyzed uremics. These defects, which are suggestive of vessel wall dysfunction on maintenance hemodialysis, may contribute to the high incidence of arteriopathy and thrombotic disease observed in this group of patients.
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PMID:Impaired vessel wall response to venous occlusion in patients with chronic renal failure on maintenance hemodialysis. 644 60

The secretion of plasminogen activator (PA) has been found to be highly stage-specific during rat spermatogenesis. It is maximal in Stages VII and VIII of the cycle. At these stages, seminiferous tubules contain primitive type A1 spermatogonia, preleptotene and midpachytene primary spermatocytes, round and maturation-phase spermatids and Sertoli cells. The last cell types are the most likely sources of PA. To investigate which cell type might be involved in the regulation of PA secretion, we have sequentially isolated 1-mm segments of rat seminiferous tubules from Stages VI-IX with transillumination-assisted microdissection and measured PA secretion using 125I-labeled fibrinogen as substrate. In another experiment, spermatogenia were killed by 300 rads of x-rays and PA secretion was analyzed during the absence of desired germ cell classes. The results support the idea that upon their detachment from the basal lamina, preleptotene-stage primary spermatocytes have the major stimulatory action on the PA secretion of the seminiferous tubules. Other phenomena such as spermiation, phagocytosis of residual bodies or opening up of the Sertoli cell junctions seem to influence PA secretion to a lesser extent.
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PMID:Cellular regulation of plasminogen activator secretion during spermatogenesis. 654 Oct 63

Blood shed into a closed peritoneal cavity is incoagulable. We have investigated this poorly understood phenomenon in animal experiments. Nonthrombogenic femoral vein-peritoneal cavity shunts were established in five dogs and 10 ml/kg blood admixed with 125I-dog fibrinogen was rapidly drained into the peritoneal cavity. After 1 hr the peritoneal cavity was entered and incoagulable blood aspirated; 125I-fibrinogen Mr distribution was assessed by AGPC, demonstrating complete degradation of fibrinogen into core fragments D and E with no evidence of soluble fibrin complexes or crosslinked fibrin fragments. Peritoneal cavity clotting factors II, V, and VIII and platelets were sharply reduced compared to venous control samples. Plasminogen and antiplasmin levels in peritoneal cavity blood showed mean declines of 17% and 15%, respectively. By comparison, incubation of dog blood with 1 to 2 X 10(3) U/ml urokinase for 1 hr in vitro was insufficient to degrade 125I-dog fibrinogen to core fragments D and E, although plasminogen and antiplasmin were reduced by 66% and 100%, respectively. Pretreatment of dogs with epsilon ACA (0.13 gm/kg, N = 4) resulted in massive intraperitoneal cavity clotting, and aspirated fluid blood contained only small quantities of radiolabel. Heparin treatment (300 U/kg bolus, 150 U/kg/hr infusion; N = 4) eliminated the peritoneal cavity lytic response; analytical gel permeation chromatography consistently demonstrated intact fibrinogen only. Therefore it is apparent that blood in a closed peritoneal cavity undergoes limited clotting followed by brisk plasmin-mediated fibrinolysis as opposed to fibrinogenolysis. The closed peritoneal cavity fibrinolytic response to clotting blood represents a striking example of the efficiency of the "tissue-type" plasminogen activator.
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PMID:Peritoneal fibrinolysis: evidence for the efficiency of the tissue-type plasminogen activator. 668 80

Deamino-8-D-argenine vasopressin (DDAVP) was given by intravenous infusion to normal subjects, haemophiliacs and patients with von Willebrand's disease (vWd) and the factor VIII and plasminogen activator response was studied. In normal subjects and most patients with mild haemophilia and mild (intermediate) von Willebrand's disease there was an increase in plasminogen activator and all factor VIII related activities. In patients with mild vWd the prolonged bleeding time was shortened by DDAVP despite only a modest rise in factor VIII related Ristocetin cofactor activity (VIIIR:RiCoF). Sub-groups of patients have been characterized in whom atypical responses was observed. In two brothers with clinically severe haemophilia, but with 5--6 u/dl procoagulant factor VIII (VIIIC), there was an increase in VIIIC but no rise of the corresponding antigen, suggesting increased release of an antigenically abnormal poorly functioning molecule. A patient with intermediate vWd was studied in whom neither DDAVP, adrenaline infusion, nor venous occlusion resulted in an increase in either plasminogen activator or factor VIII related antigen (VIIRAg), although there was a significant increase in VIIIC. In a further patient with severe vWd, DDAVP failed to elicit any plasminogen activator or VIII response. The results obtained from these two patients suggested that in some individuals the presumed endothelial cell abnormality in vWd may be more extensive than a defect in VIIIRAg synthesis. Sub-groups of patients have been identified for whom treatment with factor VIII concentrates would be more appropriate than DDAVP prior to minor surgery.
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PMID:Factor VII and fibrinolytic response to deamino-8-D-argenine vasopressin in normal subjects and dissociate response in some patients with haemophilia and von Willebrand's disease. 677 73

Peritoneal fluid does not clot spontaneously on collection, due to a lack of prothrombin activation, consequent upon a virtual absence of factors V and VIII. Factor VIII related antigen is present in peritoneal fluid in only very small amounts, suggesting that this factor is excluded from the peritoneal cavity, probably by virtue of its size. Slight thrombin activity is demonstrated by the presence of fibrin monomers in the fluid. That peritoneal fluid also contains fibrinolytic activity is shown by high levels of plasminogen and plasmin-antiplasmin complexes, though no plasminogen activator could be detected. No differences were found in clotting and fibrinolytic activities, between fluid taken from these patients with, and those without, laparoscopic evidence of pelvic endometriosis.
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PMID:Clotting and fibrinolytic activities in peritoneal fluid. 677 52

We prospectively studied the hemostatic system of ten persons bitten by the Eastern diamondback rattlesnake (Crotalus adamanteus) during 1978-1980. Blood was drawn when the patients arrived in the emergency room and every 6 hr thereafter. All envenomated victims developed incoagulable blood (defined by a thrombin time greater than or equal to 120 sec, normal less than 20 sec). Platelet counts and plasma levels of antithrombin III and factors II and VIII were not drastically altered, which distinguished this disorder from classic disseminated intravascular coagulation. Fibrinogen levels were markedly decreased (mean coagulable level of 0 mg/dl and antigenic levels of 99 mg/dl). Plasminogen levels were 20% of normal, alpha-2-plasminogen inhibitor was 17% of normal, and plasminogen activator was 20 times normal. Levels of fibrin degradation products peaked at a mean of 7,680 micrograms/ml. The magnitude and duration of the coagulopathy were proportional to the clinical severity of envenomation. Treatment with antivenin blunted the coagulopathy. Because venom from the Eastern diamondback rattlesnake does not directly activate plasminogen, we conclude that coagulopathy following envenomation by that reptile appears to be due to partial proteolysis of fibrinogen with secondary activation of plasminogen by released plasminogen activator, probably of endothelial origin.
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PMID:Mechanism of defibrination in humans after envenomation by the Eastern diamondback rattlesnake. 685 33


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