6-ketoprostaglandin-f1-alpha and Arteriosclerosis-Obliterans

In order to identify local changes in prostanoids in arteriosclerosis obliterans (ASO), plasma levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha(6-Keto-PGF1 alpha) in cubital venous blood (CV blood), in femoral arterial blood (FA blood) and in femoral venous blood (FV blood) of 27 patients with ASO of lower limbs and of 10 healthy controls were measured by RIA technique. The following results were obtained. 1) In the ASO patients, levels of TXB2 and the ratio between TXB2 and 6-Keto-PGF1 alpha (TXB2/6-Keto-PGF1 alpha) in FV blood of ischemic legs were elevated in comparison to those in CV blood or FA blood of the same group or those in FV blood of the controls. 2) This change was more clearly observed in the femoro-popliteal group, but in the aorto-iliac+ combined group, they were elevated not only in FV blood but also in FA blood. 3) No significant difference was observed between the Fontaine I + II group and the Fontaine III + IV group in these local changes in prostanoids. 4) The severer the angiographic manifestation between the abdominal aorta and the common femoral artery, the higher the plasma TXB2 levels in FA blood. Also, the poorer the peripheral run-off, the higher the plasma TXB2 production in the legs. These results suggest that the imbalance between TXA2 and PGI2 is obvious in ischemic legs of ASO patients, TXA2 is elevated downstream from damaged vessels, and the local plasma TXB2 levels reflect the severity of the vascular damage in ASO patients.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Arteriosclerosis Obliterans; Female; Humans; Leg; Male; Middle Aged; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Arteriosclerosis Obliterans; Blood Platelets; Cyclic AMP; Endothelium, Vascular; Epoprostenol; Humans; Pentoxifylline; Platelet Aggregation; Platelet Aggregation Inhibitors; Prostaglandins; Stimulation, Chemical; Theobromine

Erythrocytes deformability, plasma cAMP, 6-keto-PGF1 alpha, TXB2 levels and fibrinolytic activity in patients suffering from arteriosclerosis obliterans before and after Trental were studied. Trental improved the deformability of red cells and resulted in an enhancement of diminished cAMP level in plasma and increased the fibrinolytic activity. The improvement of deformability observed after Trental could depend upon the influence of a higher cAMP level in plasma on the erythrocyte membrane. The increase of cAMP level seems to be the result of the inhibiting effect of Trental on phosphodiesterase and of higher fibrinolytic activity.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Arteriosclerosis Obliterans; Cyclic AMP; Erythrocyte Deformability; Female; Fibrinolysis; Humans; Male; Middle Aged; Pentoxifylline; Rheology; Theobromine; Thromboxane B2

Current concepts of atherogenesis based on animal and human investigations indicate prostaglandins as a key factor in atherosclerotic lesions. The plasma profiles of thromboxane B2 (TXB2), 6-keto-PGF1 alpha, PGE2, PGF2 alpha, and PGA1 were investigated by means of a sensitive radioimmunoassay technique in 40 patients with arteriosclerosis obliterans and in 30 healthy control subjects. Abnormally high levels of TXB2 and PGE2 (222.97 +/- 320.86 pg/ml, mean +/- SD, vs 20 +/- 2.1 and 352.66 +/- 235.54 vs 24.4 +/- 3, p less than 0.01) were detected in arteriosclerosis obliterans patients. The ratio between TXB2 and 6-keto-PGF1 alpha was increased from 1.2 in control subjects to 6.0 in patients. In arteriosclerosis obliterans TXB2 increased in relation to clinical manifestations and to the extension of the vascular damage. In addition, TXB2 was positively related to serum triglyceride content (r = 0.562, p less than 0.05) and inversely related to platelet count (r = 0.727, p less than 0.001). The marked imbalance between the stable metabolites of thromboxane and prostacyclin in arteriosclerosis obliterans patients provides biologic evidence which fits well with the thrombogenic theory of atherosclerosis. These results further support the theory that prostaglandins may be heavily involved in atherosclerosis.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Aortography; Arteriosclerosis Obliterans; Blood Pressure; Dinoprost; Dinoprostone; Humans; Male; Middle Aged; Prostaglandins; Prostaglandins A; Prostaglandins E; Prostaglandins F; Risk; Thromboxane B2; Thromboxanes; Triglycerides

In patients with peripheral vascular disease and in healthy rabbits, infusion of PGI2 but not of 6-keto PGF1 alpha induced a rise in blood glucose level and a pathological deviation in glucose tolerance test. In experiments in vitro, the increased concentrations of glucose produced dose-dependent inhibition of PGI2 release from isolated rat aortic rings. The link between PGI2 and carbohydrate metabolism is discussed.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Animals; Aorta; Arterial Occlusive Diseases; Arteriosclerosis Obliterans; Blood Glucose; Epoprostenol; Glucose; Glucose Tolerance Test; Humans; Middle Aged; Prostaglandins; Prostaglandins F; Rabbits; Rats; Species Specificity; Thromboangiitis Obliterans

Six patients with advanced arteriosclerosis obliterans in the lower extremities were subjected to an exercise test on a tread mill with and without dipyridamole treatment. Prostacyclin (PGI2) release was measured by the concentration of its stable metabolite, 6-keto-prostaglandin F1 alpha in plasma. All the patients suffered from ischemic pain during both tests, but no changes were seen in plasma 6-keto-PGF1 alpha. Dipyridamole did not affect the physical performance. Our results suggest that atherosclerotic vessels do not increase PGI2 production in response to ischemia and that a single dose of dipyridamole does not change PGI2 production.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Arteriosclerosis Obliterans; Dipyridamole; Epoprostenol; Humans; Ischemia; Leg; Male; Middle Aged; Physical Exertion; Prostaglandins