6-ketoprostaglandin-f1-alpha has been researched along with Thrombophlebitis* in 6 studies
1 trial(s) available for 6-ketoprostaglandin-f1-alpha and Thrombophlebitis
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Elevated levels of 6-keto-prostaglandin-F1a from a lower extremity during external pneumatic compression.
The synthesis of either fibrinolytic serine proteases or platelet inhibitory ecosonoids by the intact endothelial cell may limit thrombus development. In a preliminary study from this laboratory, an elevation in the level of 6-Keto-prostaglandin-F1å, the stable metabolite of prostacyclin (PGI2) was demonstrated in femoral vein plasma obtained during surgical treatment from an extremity undergoing external pneumatic compression. Simultaneously, no elevations in thromboxane B2, the stable metabolite of thromboxane A2, were observed. The present study is an inclusive prospective series of 26 patients. A single pneumatic compression stocking was applied to the left limb in patients who underwent an operation under general anesthesia. Base line venous samples (3 milliliters) were obtained from the femoral vein on the experimental side and the control contralateral side, as well as from the upper limb. Additional samples were drawn at 30 and 60 minutes after the onset of compression. Nine samples per patient (234 total) were analyzed for 6-Keto-prostaglandin-F1å by competitive binding radioimmunoassay in duplicate in a single blind manner. Base line values for the upper limb, right leg and left leg were 0.08 + 0.01 nanogram per milliliter; 0.14 + 0.03 nanogram per milliliter, and 0.13 + 0.02 nanogram per milliliter, respectively (no statistical difference). By 60 minutes of compression, control samples increased to 0.40 + 0.07 nanogram per milliliter (right leg) and 0.42 + 0.08 nanogram per milliliter (upper limb) while the experimental leg increased to 0.71 + 0.13 nanogram per milliliter (p less than 0.05 versus right leg, p less than 0.005 versus upper limb). There was no statistical difference at 60 minutes between the men and women. Topics: 6-Ketoprostaglandin F1 alpha; Female; Femoral Vein; Gravity Suits; Humans; Leg; Male; Middle Aged; Prospective Studies; Thrombophlebitis | 1988 |
5 other study(ies) available for 6-ketoprostaglandin-f1-alpha and Thrombophlebitis
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Intermittent pneumatic compression in chronic venous insufficiency favorably affects fibrinolytic potential and platelet activation.
Nineteen patients with symptoms of chronic venous insufficiency (CVI) were treated with 13-week cycles of intermittent pneumatic compression (IPC) during 2 h sessions twice weekly, with most treatments at home. At study completion, quantitative subjective scores for total symptomatology were improved in 16/19 patients (84%). Enhancement of fibrinolytic potential in vivo was detected in 86% of observations on specimens from CVI patients over 2 h of IPC, with accelerated euglobulin clot lysis times (ELT) noted within 15 min of initiating compression. The enhanced fibrinolytic potential was attributed to increased urokinase plasminogen activator (u-PA), probably released from perturbed endothelial cells by IPC. Significant decreases in total t-PA antigen (mass concentration) but not t-PA activity, were produced by IPC in CVI patients only (P = 0.0001), with greater effects noted in the non-anticoagulated versus the anticoagulated cohort. Plasminogen activator inhibitor type 1 (PAI-1) levels rose rapidly after IPC only in the controls and non-anticoagulated CVI patients. PAI-1 decreased in those receiving anticoagulation. No platelet perturbation was detected during IPC by measuring levels of beta-thromboglobulin or the thromboxane A2 metabolite, 11-dehydrothromboxane B2; however, significant (P < 0.003) decreases in plasma prostacyclin (PGI2) levels (measured as the stable 6-ketoprostaglandin F-1-alpha-metabolite) were observed after 15 min of IPC in non-anticoagulated CVI patients only. There was no evidence of increased thrombin generation by IPC, determined by urinary excretion of fibrinopeptide A and prothrombin fragment 1. Concurrent anticoagulation appears to mediate more favorable biochemical alterations in CVI, although subjective improvement did not correlate with anticoagulation. The mechanism(s) by which these physiologic changes compliment the mechanical effects of IPC remain to be elucidated and will require adequately controlled and powered studies. Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; beta-Thromboglobulin; Chronic Disease; Female; Fibrinolysis; Humans; Male; Middle Aged; Platelet Activation; Pressure; Thrombophlebitis; Tissue Plasminogen Activator; Venous Insufficiency | 1996 |
Effect of policosanol on experimental thrombosis models.
Policosanol is a natural product, obtained from sugar cane wax (Saccharum officinarum L.) with which cholesterol-lowering effects have been demonstrated in experimental models, healthy volunteers and hypercholesterolemic patients. The effects of policosanol on experimental venous and arterial thrombosis in rats were investigated. Policosanol (25 mg/kg) significantly decreased the thrombus weight, in the venous thrombosis models, the protective effect persisting until 4 h after its oral administration. Policosanol (25 mg/kg single dose) was able to reduce rectal temperature variation induced by arterial thrombosis. Also at the same dose policosanol increased 6-keto-PGF1 alpha serum levels in rats. Topics: 6-Ketoprostaglandin F1 alpha; Animals; Anticholesteremic Agents; Drug Evaluation, Preclinical; Epoprostenol; Fatty Alcohols; Female; Humans; Random Allocation; Rats; Rats, Sprague-Dawley; Thrombophlebitis; Thrombosis | 1994 |
Platelet function and fibrinolytic activity in cervical spinal cord injured patients.
Topics: 6-Ketoprostaglandin F1 alpha; Adult; beta-Thromboglobulin; Blood Coagulation Tests; Catecholamines; Cyclic AMP; Female; Fibrinolysis; Hemodynamics; Humans; Incidence; Male; Platelet Aggregation; Quadriplegia; Spinal Cord Injuries; Thrombophlebitis; Thromboxane B2 | 1992 |
The changes in prostaglandins after segmental pancreatic transplantation.
Topics: 6-Ketoprostaglandin F1 alpha; Animals; Dogs; Pancreas Transplantation; Platelet Aggregation; Thrombophlebitis; Thrombosis; Thromboxane B2; Time Factors | 1991 |
Thromboxane and prostacyclin formation in patients with deep vein thrombosis.
The urinary excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha (the major urinary metabolites of thromboxane B2 and prostacyclin) was measured in ten patients with confirmed deep vein thrombosis, using specific methods based on gas chromatography - mass spectrometry with deuterium-labelled internal standards. Measurements of these major urinary metabolites makes it possible to monitor the in vivo formation of thromboxane A2 and prostacyclin. The results demonstrate an abnormally high and very variable excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha in patients with deep vein thrombosis. This indicate that both thromboxane A2 and prostacyclin are involved in the course of events associated with this disease. Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Blood Platelets; Epoprostenol; Evaluation Studies as Topic; Female; Humans; Male; Middle Aged; Thrombophlebitis; Thromboxane A2; Thromboxane B2; Thromboxanes; Time Factors | 1987 |