[Coagulation fibrinolysis and various diseases: pancreatitis and blood coagulation-fibrinolysis].
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Platelet count and adhesivity, availability of platelet factor 3, fibrinogen concentration and plasma antiplasmin activity were studied in 2,000 men aged 40 to 60 years. The results were estimated in comparison with the data obtained in 100 young apparently healthy subjects. Platelet count was within normal limits in 90% of the cases but with an increased prevalence of upper normal values. Platelet adhesivity to glass, expressed as adhesivity index, varied widely in both directions : a low index was found in 20.23% of the cases ; the high adhesivity index varied with age from 12.27% in subjects aged 40, to 26.5% in aged 56-60. Availability of platelet factor 3 was clearly increased in a large number of middle-aged men. Fibrinogen concentration correlated with age. Antiplasmin activity was significantly higher in the elderly subjects than in the young controls.
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BACKGROUND: Fibrinolysis has a critical role in the development of bleeding after insertion of a ventricular assist device (VAD). However, chronically, VAD-mediated fibrinolysis may also diminish thromboembolic events. Management of VADs involves fluid administration. It was hypothesized that the fluid administered could modulate fibrinolysis. METHODS: Human plasma was diluted (0% to 30%) with 0.9% NaCl, 5% albumin or Voluven (6% hydroxyethyl-starch [HES], mean molecular weight 130 kD) and exposed to tissue-type plasminogen activator (tPA). Plasma obtained from rabbits just before and after 30% dilution with PentaLyte (6% HES, 220 kD), Voluven or Hextend (6% HES, 450 kD) were exposed to tPA. Thrombelastographic clot strength and onset/rate of fibrinolysis were determined. RESULTS: In human plasma, 0.9% NaCl significantly decreased clot strength, but either prolonged or maintained the onset of fibrinolysis, with the rate of fibrinolysis significantly increased only at 30% dilution. Five percent albumin significantly decreased clot strength and did not affect the onset of fibrinolysis, but it did decrease the rate of fibrinolysis. Voluven significantly decreased clot strength to the greatest extent compared with the other fluids, and decreased the time of onset of fibrinolysis. Rabbit plasma after hemodilution demonstrated significantly decreased clot strength and decreased time of onset of fibrinolysis as compared with Voluven in human plasma. CONCLUSIONS: Compared with crystalloid or albumin, HES solutions enhance fibrinolysis by decreasing clot strength and decreasing the time of onset of fibrinolysis. Further studies are warranted to determine whether the fluid administered to patients with VADs can impact hemorrhagic and thrombotic morbidity.
Gastric intramucosal bleeding in portal hypertensive gastropathy was investigated in terms of gastric mucosal microcirculation, coagulation-fibrinolysis factors, and local fibrinolysis in patients with liver cirrhosis. The gastric mucosa was examined by endoscopy, and the patients were classified into two groups with or without bleeding. Gastric mucosal blood flow was measured simultaneously with coagulation-fibrinolysis factors or local fibrinolysis in both groups. As gastric mucosal blood flow, the gastric mucosal blood volume (IHb) and the oxygenated hemoglobin concentration (ISO2) were determined by the organ reflection spectrum method. Coagulation-fibrinolysis factors were measured in the blood. For evaluation of local fibrinolysis, gastric biopsy specimens were placed on a standard fibrin plate, and the fibrinolysis area was measured. Compared with the non-bleeding group, the bleeding group showed increased IHb and decreased ISO2 (p < 0.05), suggesting marked congestion of blood flow. Gastric intramucosal bleeding was frequently observed in patients with marked congestion of blood flow and markedly abnormal values of coagulation-fibrinolysis factors. Gastric local fibrinolysis was also significantly enhanced in the bleeding group (p < 0.05). In addition, local fibrinolysis was correlated positively with the gastric mucosal blood volume (r = 0.68, p < 0.05) and negatively with the oxygenated hemoglobin concentration (r = -0.58, p < 0.05). These results suggest the following mechanism of gastric mucosal bleeding in liver cirrhosis and portal hypertension. Congestion of gastric mucosal blood flow is present in liver cirrhosis and portal hypertension. An increase in the microvascular pressure and hypoxia cause release of tissue plasminogen activators from gastric mucosal cells and vascular endothelial cells. As a result, gastric local fibrinolysis is enhanced, causing gastric mucosal bleeding.
From systematic studies of both the activation and the inhibition of fibrinolysis in human blood vessels, data which provided insight into the fibrinolysis antagonism along and across the human vessel wall were obtained. The capacity for fibrinolysis initiated by plasminogen activator in sections of human arteries and veins as demonstrated by the fibrin slide technique differed greatly along and across the vessel walls. Inhibition of plasmin fibrinolysis in these blood vessels as detected by the fibrin slide sandwich technique was present at sites of low fibrinolytic activity, while inhibition was absent in areas showing strong fibrinolysis. Fibrinolysis was related to endothelial cells, while inhibition of fibrinolysis was brought about by smooth muscle cells. The results indicate that differences in endothelial fibrinolysis may be the result of differences in inhibition of fibrinolysis caused by variations in the number of smooth muscle cells present locally. A systemic decrease in endothelial fibrinolysis observed in endotoxin shock, hyaline membrane disease and a Waterhouse-Friderichsen syndrome appeared to be associated with a systemic increase in inhibition of fibrinolysis not related to smooth muscle cells.
BACKGROUND: During surgery, the balance between thrombosis and fibrinolysis is altered. Methods reported to increase fibrinolysis, such as compression devices, may reduce venous thrombosis. However, there are no prospective studies comparing methods and the effect on fibrinolysis. MATERIALS AND METHODS: In a prospective study, general surgical patients were randomized to either sequential compression devices (Group 1) or subcutaneous heparin (Group 2), and fibrinolysis factors were measured in order to determine the effect on the fibrinolysis system. Blood samples were drawn at a similar time of the day with the tourniquet off. Specifically, t-PA antigen, plasminogen activator inhibitor-1 (PAI-1), and D-dimer were measured preoperatively (preop) and on Postoperative Days (POD) 1 and 7 by the ELISA method. Fibrinolysis factors were reported as the mean +/- SD and as percentage change from preoperative values. Noninvasive vascular studies were performed preop, and on POD 1, 7, and 30, by an examination of the infrainguinal venous system and external iliac veins in bilateral lower extremities. Nonambulatory patients were excluded from the study and DVT prophylaxis methods were initiated at surgery and used through POD 2. RESULTS: For the 136 patients in the study, there were no differences in clinical characteristics such as age, surgical time (all > 60 min), anesthesia type (general or spinal), type of surgical procedure, or other risk factors for DVT. Two DVTs occurred at POD 1 and 30 (both Group 2), and one pulmonary embolism in each group (POD 7 for Group 1; POD 1 for Group 2). For subjects without thrombosis, D-dimer changes were parallel for both groups, increasing through POD 7. Similarly, t-PA antigen levels rose from baseline on POD 1 in both groups, with a return toward baseline by POD 7. The PAI-1 levels increased on POD 1 in both groups, but severalfold more in Group 1 (compression devices). The elevation in PAI-1 decreased by 50% in Group 1 by POD 7, while values returned to normal in Group 2. These changes were not significant using the Mann-Whitney test. Only three patients had thrombotic episodes so that data on changes in fibrinolysis factors are difficult to compare with the larger group. CONCLUSIONS: This is the first report of a prospective, randomized comparison of fibrinolysis factors using sequential compression devices in comparison to low dose unfractionated heparin in general surgical patients, and comparing postoperative values to preop. Both groups showed an enhanced fibrinolysis by elevation in t-PA antigen and D-dimer on POD 1, as expected when fibrinolysis occurs. While PAI-1 and t-PA work in parallel, the marked elevation of PAI-1 on POD 1 (although only slightly above reference values) and continuing into POD 7 for subjects using compression devices requires further inquiry. The elevation of PAI-1 in the face of elevated t-PA and D-dimer has been reported, but the comparison between patients using sequential compression devices and mini-dose heparin has not been reported. The reason for the elevation requires additional study into other influences on the synthesis, secretion, and/or function of PAI-1 that do not affect t-PA.
BACKGROUND: Patients with an acute myocardial infarction require a rapid response to their symptoms and the earlier fibrinolysis is given (where indicated), the better the outcome. AIMS: The aim of this study is to compare 'door to needle times' for fibrinolysis in Acute Myocardial Infarction (AMI) in three phases of one year each, at Letterkenny General Hospital. METHODS: In the PREINTERVENTION year all fibrinolysis was performed in the Coronary Care Unit (CCU). In the INTERVENTION year Emergency Department (ED) fast track fibrinolysis was introduced and in the POST INTERVENTION year most fibrinolysis was performed on fast track in the ED. RESULTS: The time saved by the introduction of ED fibrinolysis was significant, 41 minutes on average per patient. Elderly, female patients were more likely to bypass ED fast track fibrinolysis and to be brought to CCU for fibrinolysis, with attendant delays. This has educational implications in relation to the variation in clinical presentation of AMI with age and sex. CONCLUSION: The ED fast track fibrinolysis system is recommended as an effective, safe, achievable and worthwhile intervention towards improving 'door to needle times' for fibrinolysis in AMI.