Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental study was performed in rhesus monkeys (M. mulatta) to examine the contribution of Bunnell tendon suture to the production of postoperative tendon adhesions. It was found that Bunnell suture used with atraumatic technique caused a significant depression of in vitro tendon surface plasminogen activator activity, allowing the in vivo persistence and fibrous organization of fibrinous postoperative adhesions to sutured areas. Bunnell suture also produced coagulation necrosis of the sutured area of tendon. Collagen, which replaced the destroyed areas, was oriented randomly and frequently was continuous with surface tendon adhesions to surrounding connective tissues. Bunnell suture appears to be a cause of tendon adhesions in subhuman primates. The importance of fibrin and depressed local fibrinolysis in the relationship of tendon ischemia and adhesion formation is discussed.
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PMID:Some effects of Bunnell suture on otherwise uninjured tendons in subhuman primates. 41 Nov 89

In a randomized placebo-controlled study, seven patients with acute myocardial infarction allocated to intravenous treatment with 100 mg of recombinant tissue-type plasminogen activator (rt-PA) and seven patients allocated to placebo were studied during eight sampling periods before and after treatment. Seven patients with acute myocardial infarction treated intravenously with 1.5 million U of streptokinase were later studied during two sampling periods before and after treatment. The placebo group showed no significant deviations of endogenous factor XII-dependent fibrinolytic activity (p greater than 0.05). In the rt-PA group, this activity decreased significantly (p less than 0.001) after the infusion and remained depressed throughout the 1st 4 days. A significant decrease in activity (p less than 0.05) was also found in the streptokinase-treated patients. The depletion of factor XII-dependent fibrinolytic activity was not due to generation of inhibition or a depletion of factor XII, prekallikrein and plasminogen, but could be related to the proactivator of this system. It is concluded that rt-PA (and streptokinase) treatment in patients with acute myocardial infarction causes a prolonged depletion of factor XII-dependent fibrinolytic activity. This depression of endogenous fibrinolytic activity needs to be evaluated in relation to the enhanced risk of coronary reocclusion after thrombolytic therapy.
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PMID:Long-lasting depression of the factor XII-dependent fibrinolytic system in patients with myocardial infarction undergoing thrombolytic therapy with recombinant tissue-type plasminogen activator: a randomized placebo-controlled study. 140 37

To determine the ability of initial ST segment elevation and depression to predict infarct size limitation by thrombolytic therapy, data were analyzed in 721 patients with acute myocardial infarction who were admitted to a randomized, placebo-controlled study of intravenous recombinant tissue-type plasminogen activator. Patients with QRS duration of 120 msec or more or with previous history of myocardial infarction were excluded, leaving 322 in the treatment and 333 in the placebo group. Cumulative 72-hour release of alpha-hydroxybutyrate dehydrogenase and global ejection fraction as well as left ventricular wall motion derived from angiography were used as independent measures of infarct size. Electrocardiograms obtained at admission, 6 hours after start of therapy, and before discharge were analyzed. All ST measurements were made by hand at the J point and 60 msec after the J point. Patients with high ST segment elevation at admission (i.e., sum of ST elevation at 60 msec after the J point was 20 mm or more) had significantly larger infarction and higher hospital mortality when compared with those with lower (less than 20 mm) ST elevation. Reciprocal ST segment depression also showed a linear relation with infarct size and mortality, independent from ST elevation, both in anterior and inferior myocardial infarction. The sum of deviations measured at the J point and 60 msec after the J point differed significantly, especially in anterior myocardial infarction at admission (mean, 16 +/- 9 versus 23 +/- 11 mm). The prognostic value of one measurement was not, however, superior over the other. Treatment with recombinant tissue-type plasminogen activator was most effective in those with large ST deviations at admission, but patients with anterior infarction and smaller ST shifts also appeared to benefit from therapy. Results in individual patients were variable, and the overall correlation of initial ST shifts with enzymatic infarct size was rather low. In conclusion, the present study shows that the magnitude of initial ST elevation and also of reciprocal ST depression in the admission electrocardiogram is valuable for the management and assessment of thrombolytic therapy in patients with acute myocardial infarction.
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PMID:Significance of initial ST segment elevation and depression for the management of thrombolytic therapy in acute myocardial infarction. European Cooperative Study Group for Recombinant Tissue-Type Plasminogen Activator. 211 63

The dynamics of disorders in haemostasis and fibrinolysis upon continuous stress was studied in model experiments with rats exposed to emotional-pain-stress. It was shown that the plasminogen activator (PA) is released into the blood within the first few minutes of exposure to stress. Four hours after cessation of continuous stress (6 hours) the enzyme depletion and fibrinolysis depression occurred. Such stress-induced changes in the blood system function can be regarded as a risk factor in the development of thrombosis.
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PMID:Depletion of fibrinolysis activators as a result of continuous stress. 246 30

Ro 15-1788, a selective benzodiazepine (BZD) antagonist, is known to precipitate withdrawal reactions in BZD-pretreated animals. We examined whether a high dose of Ro 15-1788 can precipitate withdrawal reactions relating to behavior and changes in the stress-hormone plasma levels after acute BZD treatment in man. On two consecutive days, 15 min and 24 h respectively after a single treatment with either lormetazepam (0.06 mg/kg: LMZ group), flunitrazepam (0.03 mg/kg: FNZ group) or placebo (PLA group), 18 healthy volunteers received two injections of Ro 15-1788 (0.01 mg/kg). Behavioral responses (mood changes, anxiety), cortisol and prolactin plasma levels, and physiological parameters were examined. In all groups there were only slight changes in the circulation parameters. Minor anxiety reactions were seen after Ro 15-1788, which occurred the 1st day in the PLA group and the 2nd day in the BZD groups. Depression was noted especially in the FNZ group after both injections of Ro 15-1788. The physiological morning decrease in cortisol plasma level was influenced on the 1st day in the LMZ group (2 volunteers showed high plasma levels) and the 2nd day in the FNZ group: a slight increase of cortisol plasma level was measured after the 2nd injection of Ro 15-1788. Prolactin plasma levels arose immediately after LMZ injection and continued to increase after Ro 15-1788 injection. No increase in prolactin plasma levels was found in the other groups or in the LMZ group after the 2nd challenge by Ro 15-1788.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Benzodiazepine antagonism by RO 15-1788: psychometric, hormonal and biophysical parameters]. 290 13

After 90 min. of partial venous occlusion (40%) in dog's femoral vein plasminogen activator (t-PA) was decreased in the pre-occlusion segment and maintained in the post-occlusion segment. Prostacyclin-like activity (PLA) was maintained in the pre-, but increased in the post-occlusion segment. Treatment with heparin (loading dose-70/kg; IV perfusion-1 U/kg/min) did not affect pre-treatment pattern of t-PA or PLA in either segments. Treatment with aspirin (IV perfusion-2 mg/kg/min) promoted profound depression of PLA in both segments while t-PA remained unchanged. Treatment with lidocain (loading dose-1.5 mg/kg; IV perfusion 0.2 mg/kg/min) did not affect either PLA or t-PA in the pre-occlusion segment, but a decrease of these two activities was observed in the post-occlusion segment. We conclude that, since thrombin, prostaglandins and white blood cells were not responsible for all changes observed at t-PA and PLA vessel wall levels, it is justified, to evaluate the role of rheological factors as the probable determinant of these changes.
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PMID:Local plasminogen activator and prostacyclin-like activity after partial venous occlusion--an experimental study in the dog. 304 44

Despite successful thrombolysis of occluded prosthetic grafts, rethrombosis remains a problem. We investigated the efficacy of aspirin in maintaining patency of polytetrafluoroethylene grafts (3 mm X 3.5 cm) in canine femoral arteries after thrombolytic therapy. After induction of thrombosis, either tissue-type plasminogen activator (t-PA) or urokinase (UK) was infused just proximal to the thrombus (4000 U/min) until complete thrombolysis was achieved. Five of the 10 UK-treated dogs and five of the 10 t-PA-treated dogs received aspirin immediately after recanalization, and aspirin was continued (325 mg/day) for 4 weeks or until occlusion occurred. A systemic aspirin effect was confirmed by marked depression of serum thromboxane B2 and absent platelet aggregation. Only two of the 10 grafts in the aspirin-free group remained patent for 4 weeks. The remaining eight grafts had all reoccluded by 2 weeks. None of the 10 grafts in the aspirin-treated group reoccluded during the 4 weeks. This significantly improved patency (p less than .001) in the aspirin-treated group was observed equally in grafts treated with t-PA or UK. Thus aspirin is a potent agent in preventing rethrombosis after thrombolytic recanalization of prosthetic grafts.
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PMID:Beneficial effect of aspirin in maintaining the patency of small-caliber prosthetic grafts after thrombolysis with urokinase or tissue-type plasminogen activator. 309 Dec 89

Among 29 patients recovering from a first-time acute myocardial infarction (AMI) 9 patients suffered reinfarction during a four year follow-up period. The 9 reinfarction patients were found to belong to a subgroup of 17 patients with a selective depression to near zero of euglobulin t-PA activity. None of the group of 12 patients with marked t-PA activity suffered a relapse. Euglobulin fibrinolytic activity as usually assayed did not distinguish between groups with or without relapse.
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PMID:A selective depression of tissue plasminogen activator (t-PA) activity in euglobulins characterises a risk group among survivors of acute myocardial infarction. 311 Sep 93

Sepsis due to impaired host defence mechanisms is one of the most frequent causes of death in severely burned patients. However, it is not precisely known to what extent syntheses and release of suppressive mediators of the burned tissue affect the cellular and humoral immune responses. In this study a decreased production of plasminogen activator by macrophages is demonstrated after incubation with skin components, indicating a decreased macrophage helper function for T-B cell cooperation. An additional effect of the skin fraction is a considerable increase in mitogenic activity as measured in the antibody-forming cell test. This enhancement of macrophage-T-B cell cooperation is concentration dependent and lower in the burned skin fraction as compared to the unburned control. A known skin-derived cytokine with mitogenic properties is epidermal cell-derived thymocyte activating factor (ETAF) exhibiting interleukin-1 (I1-1) like activity including mitogenic enhancement of murine thymocyte stimulation by phytohaemagglutinin. Burned and control skin fraction as tested in a thymocyte assay did not show interleukin-1-like activity. The experiments suggest the presence of a skin-derived growth factor which is not interleukin-1 but which stimulates T-B cell cooperation when there is depression of macrophage function. Further purification is required in order to assess the clinical relevance of the factor in burned patients.
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PMID:Changes in the cellular immune response by a subfraction of burned murine skin. 348

Administration of the synthetic estrogen diethylstilbestrol (DES) lowers the systemic resistance of mice to challenge with either tumor cells or the facultative intracellular parasite Listeria monocytogenes. To assess the potential role of impaired mononuclear phagocyte system (MPS) function in this depression of host resistance, we addressed the question of systemic perturbations of the MPS induced by administration of DES. A panel of objective quantitative markers which have been previously shown to identify and characterize macrophages in the several stages of development of activation was employed. DES perturbed the resident population of peritoneal macrophages by increasing their number approximately twofold and by enhancing their competence for phagocytosis, cytostasis of tumor cells, and secretion of plasminogen activator. When we examined the competence of the MPS in DES-treated mice to respond to challenge with activating stimuli, we found that DES systemically suppressed the development of macrophages, in response to either pyran copolymer or BCG, to develop tumoricidal function and to gain competence for secretion of reactive oxygen intermediates such as H2O2. Since these data suggested that DES inhibited the development of macrophages from a precursor stage (i.e., responsive macrophages) to activated macrophages in vivo, we tested this possibility directly by applying known activating signals in vitro to responsive macrophages. Responsive macrophages from DES-treated mice did not become activated in response to the application of two known potent activating signals (i.e., MAF + LPS). Taken together, the data indicate that DES systemically perturbs the MPS and does so by enhancing development of the early stages of maturation and suppressing subsequent development.
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PMID:Functions of mononuclear phagocytes in mice exposed to diethylstilbestrol: a model of aberrant macrophage development. 380 3


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