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)

In 30 patients with congenital or acquired heart disease the haemodynamic effects of diazepam (Valium) 0.3 mg/kg were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: Heart rate (HR), arterial pressure (-Part, Psyst, Pdiast), pulmonary artery pressure (-PAP), right (-PRA) and left atrial pressure (-PLA), left ventricular pressure (PLV), left ventricular enddiastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). In comparison with a control group (n = 36) diazepam caused a decrease in arterial pressure cardiac index, stroke index, right and left atrial pressure and dp/dtmax. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect, which is of only minor importance with diazepam. These haemodynamic changes resulted in a reduction in myocardial oxygen consumption. Diazepam is a valuable drug in neuroleptanalgesia, when an increase in blood pressure can not be controlled by fentanyl or droperidol.
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PMID:[Diazepam (valium). Changes in haemodynamics, myocardial oxygen consumption and vascular tone (author's transl)]. 69 81

Defibrotide is a polydeoxyribonucleotide sodium salt with antithrombotic properties. These properties have been attributed to its profibrinolytic activity [increase of tissue plasminogen activator (t-PA) activity, concomitant decrease of that of plasminogen activator inhibitor (PAI)], but there could conceivably be other factor(s). To look for these, we studied Defibrotide in a thrombosis model (pulmonary thromboembolism in mice) in which free radicals play a pivotal role. Defibrotide was found to be active after both intravenous and oral administration. Defibrotide behaved in vitro like a scavenger of H2O2 but not of O2.- in cell-free systems. Defibrotide added in vitro to cellular systems decreased the stimulated release of beta-glucuronidase from polymorphonuclear cells (PMNs), the luminol chemiluminescence induced by oxygen species generated by stimulated PMNs and the generation of O2.- from stimulated macrophages. We think that the antithrombotic activity of Defibrotide is based on other factor(s) in addition to profibrinolytic activity, i.e., some scavenger activity and desensitization of cells involved in thrombus formation must also be taken into account.
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PMID:A novel insight into the mechanism of the antithrombotic action of defibrotide. 133 34

Ceramic pieces composed of 99.5% Al2O3, 3 to 6 mm long, were found to be a good matrix for growth of the human embryonic lung diploid fibroblast, IMR-90 cells. The tissue plasminogen activator (t-PA) was secreted in DME medium containing proteose peptone as a t-PA inducer. In addition, production of t-PA was enhanced by increasing extracellular CaCl2, from 3.6 to 5.4 mM. In order to eliminate negative feed-back control caused by t-PA produced and thus raise productivity, perfusion cultivation was performed using a ceramic-packed bed column, with a recirculating vessel. The recirculating vessel was used to mix fresh medium with spent medium, and to control dissolved oxygen concentrations in the extracellular environment by stirring. In continuous production using the packed bed column with 2 kg of ceramics (phi = H = 150 mm), increasing dilution rate to 0.5 day-1 could reduce product inhibition at 3-4 x 10(5) cells/ml. Cellular productivity of 560 IU/10(6) cells/day was obtained over 40 days and corresponded to the volumetric productivity of 183 IU/ml/day.
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PMID:Continuous production of tissue plasminogen activator (t-PA) by human embryonic lung diploid fibroblast, IMR-90 cells, using a ceramic bed reactor. 136 53

The key enzyme for fibrinolysis is plasmin, which is converted from plasminogen by plasminogen activator. Activated plasmin lyses fibrinogen and fibrin to make fibrin degradation products(FDPs) and plasmin is inactivated immediately by alpha 2 plasmin inhibitor. As FDP.D dimer is derived solely from insoluble fibrin, FDP.D dimer is thought of as an index for clot lysis. We measured plasmin-alpha 2 plasmin inhibitor complex(PIC) and FDP.D dimer plasma levels in 3 patients with acute pulmonary thromboembolism treated with recombinant tissue plasminogen activator(tPA). Fifteen million units of tPA(TD-2061) were infused in one hour on the first, second and third hospital days. PIC and FDP.D dimer before tPA infusion showed slightly elevated values as compared to normal ranges. They increased markedly after tPA infusion. These findings suggest that the fibrinolytic system is slightly activated in the acute phase of pulmonary thromboembolism and also strongly activated by tPA infusion. Increased FDP D dimer suggests that fibrin clots are dissolved by activated plasmin. Improvement of arterial oxygen tension was observed after tPA infusion. As sustained higher FDP.D dimer means the existence of fibrin clots, heparin treatment should be continued for prevention of clot formation as long as FDP.D dimer shows higher value. In conclusion, PIC and FDP.D dimer are useful indices not only to detect the activated state of the fibrinolytic system but also to know clot lysis in tPA treatment.
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PMID:[Measurements of plasmin-alpha 2 plasmin inhibitor complex and FDP.D dimer levels in the fibrinolytic therapy of acute pulmonary thromboembolism]. 138 24

An intravenous infusion of Fluosol enhanced significantly the t-PA thrombolysis of the arterio-venous shunt made by insertion of 125I-fibrin clot in rabbits. The plasma radioactivity released through thrombolysis increased in both time and dose-dependent manner after the administration of t-PA. Fluosol in combination with t-PA increased the plasma radioactivity, compared with the t-PA treatment alone at the corresponding dosage. The coronary blood flow was markedly reduced to almost zero after the thrombin injection into narrowed LCX with a clamp in open-chest dogs. An intravenous infusion of Fluosol or Pluronic F-68 solution at a dose of 15 ml/kg significantly shortened the thrombolysis time by intracoronary infusion of urokinase alone. While, little change in the QTc interval of ECG and the plasma CPK-MB activity was observed in the Fluosol group in combination with urokinase, suggesting a myocardial protective action of Fluosol possibly due to its oxygen carrying effect.
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PMID:Extended use of Fluosol emulsion in acute myocardial ischemia treatment. 139 38

The effect of intravenous recombinant human tissue-type plasminogen activator (tPA) on arterial blood gases was compared with the effect of heparin treatment in acute pulmonary thromboembolism. Fifteen patients received heparin alone (group A), 5 cases were treated with 7.7 x 10(6) I.U. of tPA (group B) and 10 cases with 15 x 10(6) I.U. of tPA (group C) combined with heparin treatment. Arterial oxygen tension before treatment was not significantly different among the three groups. PaO2 was dramatically improved on the 1st day in group C. By the 7th day, PaO2 of group B had improved to the level of group C. However, the PaO2 of group A on the 7th day was not significantly different compared to the pre-treatment value. In group C, post-treatment perfusion lung scintigrams were improved compared to the pre-treatment images, but this was not the case in group B. Treatment with tPA is more effective for acute pulmonary thromboembolism than heparin alone and a high dose of tPA (15 x 10(6) I.U.) leads to rapid improvement in arterial blood gases and lung perfusion images.
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PMID:The role of recombinant human tissue-type plasminogen activator in the treatment of acute pulmonary thromboembolism. 145 Apr 96

The subepidermal blistering skin disease bullous pemphigoid is associated with the deposition of specific autoantibodies and activated complement at the epidermal basement membrane zone of lesional skin. Subepidermal blistering is thought to depend on proteolytic enzymes, in particular on plasmin. A possible interrelation is proposed between the initiating immune reaction and the plasminogen activator system. Complement-induced chemotaxis of PMN may induce PMN infiltration. PMN-derived reactive oxygen species would interfere with the plasminogen activator inhibitors. Lysosomal elastase may degrade alpha 2-antiplasmin. At the same time, urokinase-type plasminogen activator is stimulated in tissue constituent cells and plasmin activity increases locally. The plasmin/antiplasmin equilibrium is disturbed and excess plasmin, then, may cause the degradation of extracellular proteinaceous structures of the epidermo/dermal junction. Epidermo/dermal dyshesion and subepidermal blister formation ensues. The plasminogen activator system is seen as a part within the wide array of effector systems that may be operative upon stimulation by an initial immunological event.
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PMID:Complement and plasminogen: pathways in inflammation. 152 63

The level of plasminogen activators was measured in 12 volunteers at rest and after maximum exercise. Two formulations of a beta-blocker "propranolol," or placebo, were given (oral dose, 10 mg) 2 h before exercise commenced. At weekly intervals over 21 d, randomized double-blind, cross-over trials were conducted. Two hours after drug/placebo administration, subjects exercised to maximal capacity using an incremental exercise protocol on a bicycle ergometer. Before and 2 h after drug/placebo administration and immediately after maximum exercise, heart rate, blood pressure, and oxygen consumption were measured, venous blood was removed, and plasma separated for the measurement of plasminogen activators using the fibrin plate method. Duplicate portions of plasma were taken: portion 1 for determination of total plasminogen activators activity, by the addition of dextran sulphate and flufenamic acid; portion 2 to assay extrinsic plasminogen activator, intrinsic plasminogen activator being blocked by the addition of C1-inactivator. Resting and postmaximum exercise heart rates showed significant decreases (P less than 0.05), with a nonsignificant difference in the resting level of extrinsic and intrinsic activators when the subjects were premedicated with either of the two formulations. Total and extrinsic activities, but not intrinsic activity, were significantly increased (P less than 0.05) to maximum exercise when subjects were given placebo. However, premedication with the drug formulations 1 and 2 significantly decreased (P less than 0.05) the normal total and extrinsic activities response to maximum exercise, with no effect on the intrinsic activity. It is suggested that the resting level of activators activity may not be affected by premedication with propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extrinsic plasminogen activator response to exercise after a single dose of propranolol. 154 27

The role of tissue-type plasminogen activator (t-PA) was investigated in the gastric ulcer formation induced by microvascular derangement. The rat stomach was exposed and repeated electrical stimuli (irritation) were applied on the small arterial wall close to the lesser curvature to induce mucosal ischemia followed by hyperemia. The t-PA activity in the regional blood of the stomach was significantly elevated as early as 5 min after the irritation. Immunohistochemical study using anti-t-PA monoclonal antibody revealed that t-PA was detectable in the endothelial cells of capillaries and collecting venules, suggesting the involvement of endothelium-mediated fibrinolytic activity in the irritation-induced ulcer formation. Pretreatment of SOD or allopurinol significantly attenuated the irritation-induced t-PA activation, suggesting that the t-PA activity was modulated by xanthine oxidase-associated superoxide anions. CV-6209, a selective antagonist of platelet-activating factor (PAF), also prevented the activation of t-PA as well as ulcer formation, providing a concept that PAF may be associated with the local fibrinolytic activation which may cause hemorrhagic changes in the gastric mucosal microvasculature. The present study supports the hypothesis that increased t-PA activity may reflect the microvascular endothelial damages caused by vasomotor derangement and suggests that oxygen-derived free radicals may participate in the regulation of endothelium-derived fibrinolytic activities in the mucosal microvasculature.
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PMID:Involvement of superoxide anion and platelet-activating factor in increased tissue-type plasminogen activator during rat gastric microvascular damages. 165 Sep 66

The preovulatory surge of gonadotropins causes resumption of oocyte meiosis, rupture of follicle wall and release of a fertilizable ovum, and luteinization. In the present lecture, current studies of the biochemical mechanism of follicle rupture are discussed. Over the past decade the cyclooxygenase pathway of arachidonic acid metabolism, namely prostaglandins (PGs), has received considerable attention in ovulation studies. We studied the changes in ovarian levels of eicosanoids during ovulation and the effects of indomethacin or lipoxygenase inhibitors on ovulation and ovarian eicosanoids in PMSG/hCG primed immature rats. Our data demonstrate that lipoxygenase products, especially 15-hydroxyeicosatetraenoic acid (HETE), is more essential for the ovulatory process than PGs. Ovarian steroidogenesis shifts from estradiol to progesterone after LH surge. It is not yet clarified how progesterone participates in the ovulatory process. We studied the effects of epostane and RU486 on ovulation rate, ovarian levels of steroids and eicosanoids, ovarian 3 beta-HSD activity, and ovarian proteolytic enzymes (collagenase, plasminogen activator and kallikrein) activities in the rats. The results show that progesterone plays an important role in the initial 4 hours of the ovulatory process by regulating proteolytic enzyme activities, and that an autocrine regulation may take place in progesterone production during ovulation. Morphological studies have demonstrated dilation and increased permeability of follicle vasculature during ovulation. We investigated the relation between ovarian blood volume and progesterone, and the role of active oxygen in ovarian vascular permeability by using SM-SOD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Control mechanism of ovarian function]. 165 26


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