ABSTRACT
We have explored the changes of plasma concentrations of antithrombin III and fibrinogen in patients recovering from major abdominal and cardiac surgery. In one group of patients subjected to major abdominal surgery we detected a statistically significant reduction of antithrombin III in the second and third postoperative day, followed by return to normal values in the fourth or fifth day. Fibrinogen, instead, increased to as much as 180% of the preoperative value in the first four postoperative days and reverted slowly to preoperative values between the fourth and the eighth day. In another group of patients subjected to cardiac surgery procedures utilizing the heart-lung machine, however, we found no significant reductions of antithrombin III in the early postoperative period. These results suggest the possible influence of local tissue factors affecting the plasma levels of antithrombin III differently in the two types of surgery under discussion. The patients subjected to extracorporeal circulation, on the other hand, showed a depletion of plasma fibrinogen down to less than 30 or 40% of preoperative values. This may reflect activation of coagulation processes and the considerable sequestration of fibrin at some interfaces of the heart-lung machine.
Subject(s)
Abdomen/surgery , Antithrombin III/metabolism , Cardiac Surgical Procedures , Fibrinogen/metabolism , Adult , Aged , Humans , Middle Aged , Postoperative PeriodABSTRACT
Specimens of venous tissues from a group of 25 patients with chronic uremia and 7 patients with acute renal failure generated significantly higher PGI2-like (platelet aggregation inhibiting) activity than venous tissues from 30 normal subjects. After repeated washings, when this activity could barely be detected in the controls, pronounced inhibitory activity was still evident in samples containing venous tissues from uremic patients. Both prolonged bleeding times and increased PGI2-like activity returned to normal in 4 acute uremic patients on restoration of their renal function. These findings may be relevant to the pathogenesis of bleeding in renal failure.
Subject(s)
Epoprostenol/biosynthesis , Hemorrhage/etiology , Prostaglandins/biosynthesis , Uremia/metabolism , Veins/metabolism , Acute Kidney Injury/metabolism , Adult , Arachidonic Acids/metabolism , Bleeding Time , Blood Platelets/metabolism , Female , Humans , Kidney Failure, Chronic/metabolism , Male , Middle Aged , Prostaglandin Endoperoxides/biosynthesis , Uremia/blood , Uremia/complicationsSubject(s)
Acute Kidney Injury/blood , Blood Platelets/physiopathology , Epoprostenol/blood , Kidney Failure, Chronic/blood , Prostaglandins/blood , Adolescent , Adult , Blood Coagulation Tests , Epoprostenol/biosynthesis , Female , Humans , Male , Malondialdehyde/blood , Middle Aged , Renal Dialysis , Time FactorsABSTRACT
To determine the possible role of vascular factors in the bleeding tendency of uraemic patients, three major factors of the haemostatic system normally present in vascular tissues were studied. Factor VIII-related protein (F VIII) was detected on the vascular intima of 13 patients and 10 normal subjects. Comparable values of plasminogen activator (PA) were found in tissue slices from 7 patients and 7 controls. In contrast, prostacyclin like (PGI2) activity, measured as platelet aggregation inhibitory potency, was significantly higher in specimens from 15 patients with either acute or chronic uraemia than in 10 controls. The latter abnormality, leading to impaired platelet-vessel wall interaction, might contribute to the disturbed haemostasis of uraemic patients.
Subject(s)
Blood Vessels/physiopathology , Epoprostenol/metabolism , Factor VIII/metabolism , Hemorrhage/physiopathology , Plasminogen Activators/metabolism , Prostaglandins/metabolism , Uremia/physiopathology , Adult , Aged , Blood Vessels/metabolism , Female , Hemorrhage/etiology , Hemostasis , Humans , Male , Middle Aged , Uremia/complications , Uremia/metabolismABSTRACT
Specimens of venous tissue from three normal subjects and three patients with renal failure and very prolonged bleeding-times showed prostacyclin-like activity (inhibition of platelet aggregation) during incubation at room temperature. The specimens from all three uraemic patients showed more prostacyclin-like activity than those from the controls. After repeated washings, when this activity could hardly be detected in the controls, pronounced inhibitory activity was still evident in samples containing venous tissue from the three uraemic patients. These findings may be relevant to the pathogenesis of bleeding in renal failure.
Subject(s)
Acute Kidney Injury/blood , Epoprostenol/physiology , Hemorrhage/etiology , Kidney Failure, Chronic/blood , Platelet Aggregation , Prostaglandins/physiology , Veins/metabolism , Depression, Chemical , Epoprostenol/metabolism , Female , Humans , Male , Middle Aged , Tissue ExtractsABSTRACT
Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) is a new drug shown to inhibit prostaglandin release from rat platelets. The present study indicates that ditazole, at doses similar to those inhibiting prostaglandin formation in rat, inhibits in vivo collagen--but not ADP-induced rat platelet aggregation. In addition, ditazole does not prolong the bleeding time in rats, but even tends to shorten it. This effect could be due to the inhibition of prostaglandin formation at the side of the vascular injury produced to induce bleeding.
