thromboxane-b2 and Blood-Loss--Surgical

The impaired hemostasis of aspirin-treated patients is an annoying problem during and after cardiopulmonary bypass. The hemostatic function of platelets comprises two mechanisms: the shear-induced and the cyclooxygenase pathways. Because the latter is inhibited in aspirin-treated patients, the hemostatic function depends mainly on the former pathway. To investigate the effect of cardiopulmonary bypass on the shear-induced pathway, a double-blind study of preoperative aspirin treatment (325 mg) and placebo was conducted in 40 patients undergoing coronary artery bypass grafting. Postoperative blood loss was higher in the aspirin-treated patients than in the placebo-treated patients (p < 0.05). The shear-induced hemostasis was monitored by the in vitro bleeding test (Thrombostat), which mimics bleeding through an injured arteriole. The shear-induced pathway of aspirin-treated platelets was not affected before cardiopulmonary bypass, but it was impaired more during the operation (p < 0.01) and remained worse afterward (p < 0.05), compared with that of placebo-treated platelets. The inhibitory effects of aspirin on thromboxane production and on collagen-induced platelet aggregation remained throughout the operation. In aspirin-treated platelets, the aggregation capacity induced by adenosine diphosphate was inhibited before the operation (p < 0.05) and showed substantial recovery during the operation (p < 0.05). These results suggest that the shear-induced pathway of aspirin-treated platelets is more vulnerable to cardiopulmonary bypass than the pathway in normal platelets and causes severe impairment of hemostasis afterward.

Topics: Adenosine Diphosphate; Aged; Aspirin; Blood Coagulation Tests; Blood Loss, Surgical; Blood Platelets; Cardiopulmonary Bypass; Coronary Artery Bypass; Double-Blind Method; Hemostasis; Humans; Middle Aged; Platelet Adhesiveness; Platelet Aggregation; Thromboxane B2

In 20 patients undergoing coronary artery bypass grafting, we studied prospectively systemic blood activation, blood loss, and the need for donor blood when using an extracorporeal circuit equipped at random with one of two different venous reservoirs. In 10 patients we used an open venous reservoir system (ORS) consisting of a hard shell venous reservoir with an integral cardiotomy filter, and in 10 patients we used a closed reservoir system consisting of a collapsible venous reservoir and separate cardiotomy reservoir. Concentrations of complement 3a, elastase, thromboxane B2, and fibrin degradation products showed a biphasic course, especially in ORS patients. During bypass, we observed a first peak of levels of complement 3a, thromboxane B2, fibrin degradation products, and elastase, which was higher in ORS patients than in patients with the closed system, because their blood continuously contacted the foreign materials of the filter and air in the open reservoir, which was avoided in the closed reservoir. Intensive blood-foreign material contact also caused the highest (p < 0.05) hemolysis in ORS patients. The larger amount of hemolytic products in ORS patients theoretically resulted in a temporary decrease in capacity of their Kupffer cells to clear endotoxin released after aortic declamping. This theory might explain the significantly (p < 0.01) higher second peak of activated products after declamping that was observed in ORS patients. Due to increased blood activation, the largest (p < 0.001) amount of shed blood loss, greatest (p < 0.05) need for colloid-crystalloid infusion, and largest (not significant) need for donor blood were found in ORS patients (0.8 +/- 0.4 versus 0.2 +/- 0.2 units of packed cells).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Blood Loss, Surgical; Blood Transfusion; Cardiopulmonary Bypass; Complement C3a; Coronary Artery Bypass; Fibrin Fibrinogen Degradation Products; Hemolysis; Humans; Middle Aged; Pancreatic Elastase; Prospective Studies; Thromboxane B2

To evaluate the extent of shed blood activation in two autotransfusion systems and the effect of circulating blood activation upon autotransfusion, we performed a prospective study in 18 patients undergoing internal mammary artery bypass operation and a control group of 10 patients. The autotransfusion systems were from Sorin (n = 9) consisting of a hard shell reservoir with a filter having a small contact area (0.32 m2), and from Dideco (n = 9) consisting of a hard shell reservoir with a filter having a larger contact area (4.64 m2). We found high concentrations of thromboxane, fibrinogen degradation products, complement split product C3a, and elastase in the shed blood and, with the exception of C3a, in the circulating blood of autotransfused patients. There was no such activation in control patients. The degree of the systemic inflammatory reaction was determined by the type of autotransfusion system and by the amount of infused shed blood. The Dideco system provoked more inflammatory response than did the Sorin. This was reflected by the larger shed blood loss during autotransfusion in the Dideco patients than in Sorin patients, resulting in infusion of more shed blood (means, 737 mL versus 566 mL; not significant). After autotransfusion, Dideco patients shed significantly more blood than did Sorin or control patients (p < 0.05). Dideco patients also needed more colloid/crystalloid solution per 24 hours than Sorin patients (p < 0.05). This became clinically relevant only after infusion of more than 800 mL of shed blood (p < 0.001): hemodilution indicated the need for packed cells in 4 Dideco patients and in 1 Sorin patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Blood Loss, Surgical; Blood Transfusion; Blood Transfusion, Autologous; Complement C3a; Coronary Artery Bypass; Crystalloid Solutions; Female; Fibrin Fibrinogen Degradation Products; Hemodynamics; Hemostasis; Humans; Isotonic Solutions; Male; Middle Aged; Pancreatic Elastase; Plasma Substitutes; Prospective Studies; Thromboxane B2

The interest in autologous red blood cell salvage is increasing rapidly, but it is well known that platelets and white cells are activated during cell washing. Therefore, we aimed to determine whether or not eicosanoids transfused together with the salvaged blood are responsible for nonhemolytic immunological transfusion reactions.. In 11 patients who underwent radical prostatectomy we studied the release of eicosanoids, prostaglandin E(2) (PGE(2)) and thromboxane B(2) (TxB(2)), in association with reinfusion of intraoperatively salvaged blood. Blood samples were taken before operation, on days 1 and 3 after operation and before and after cell washing.. There was a twofold increase in PGE(2) and a twentyfold increase in TxB(2) in the unwashed salvaged blood. Washing caused a reduction in eicosanoid plasma levels of up to 95%, but a significantly lower level in relation to its corresponding preoperative value was only found for PGE(2). After transfusion of an average of 420 ml RBC sediment from washed blood, the patients' plasma concentrations of PGE(2) and TxB(2) on the 1st and 3rd postoperative day did not significantly differ compared to baseline values.. Our data support the notion that RBC sediment from 'salvaged' and washed autologous blood contains increased amounts of PGE(2) and TxB(2). It remains, however, questionable if these passively infused eicosanoids become biologically active. According to our study, the PGE(2) and TxB(2) transfused are apparently not responsible for nonhemolytic immunological transfusion reactions.

Topics: Aged; Blood Loss, Surgical; Blood Transfusion, Autologous; Dinoprostone; Eicosanoids; Humans; Male; Middle Aged; Prostatectomy; Thromboxane B2

This animal study was designed to compare a collagen coated heparin bonded vascular graft (CHG) versus a collagen coated vascular graft (CG) regarding intraoperative blood loss and healing process. 24 polyester vascular grafts (12 CHG and 12 CG) of 6 mm in diameter and 5 mm in length were implanted between the common iliac and external iliac artery in 12 adult dogs. The grafts were explanted between the first and the sixth months which followed the implantations. The healing process was observed by gross examination, microscopic and scanning electron microscopic examination. Prostaglandin PGE2, TXB2, 6 keto PGF1 alpha and PGF2 alpha were measured by radioimmunologic assay from samples retrieved from the medium part of the graft. During implantation, there was no notable difference in blood loss through the graft. At the time of explantation, 20 grafts were patent (10 CHG, 10 CG). In both grafts, the healing process developed progressively between 2 and 6 months and 90% of the internal surface of the grafts were covered with endothelial like cells. At 6 months, the internal layer was thinner in heparinized graft. PGI2 secretion was found with the two types of grafts. In conclusion, the present study showed no difference in the blood loss or healing characteristic of CHG and CG except for a potentially thinner internal layer with CHG. Comparative studies in humans are necessary to evaluate the potential benefit of heparin bonded graft in clinical practice.

Topics: 6-Ketoprostaglandin F1 alpha; Anastomosis, Surgical; Animals; Blood Loss, Surgical; Blood Vessel Prosthesis; Collagen; Dinoprost; Dinoprostone; Dogs; Epoprostenol; Graft Occlusion, Vascular; Heparin; Iliac Artery; Microscopy, Electron, Scanning; Polyesters; Radioimmunoassay; Thrombosis; Thromboxane B2; Vascular Patency