Summary and conclusionsA total of 4352 patients were admitted to a prospective' randomised multicentre trial comparing the prophylactic efficacy of dextran 70 and low-dose heparin against fatal pulmonary embolism after elective operations for general, orthopaedic, urological, and gynaecological conditions. Out of 3984 patients correctly admitted, 1993 were allocated to receive dextran 70 and 1991 to receive low-dose heparin.Withdrawal of prophylaxis because of bleeding or technical difficulties occurred more often in the heparin group, but allergic reactions were more common in the dextran group. Of the 75 patients who died within 30 days after operation, 38 had been given dextran and 37 lowdose heparin. Necropsy was performed in 33 and 32 of these cases respectively. In six patients in each group pulmonary embolism was the sole or a contributory cause of death. Of these, five patients in the dextran group and two in the heparin group had received a full course of prophylaxis.There was no statistically significant difference between the two treatment groups in the incidence of fatal pulmonary embolism after a full course of prophylaxis.
Absorbable, nonwoven patches made from polyhydroxybutyrate (PHB) were implanted as transannular patches into the right ventricular outflow tract and pulmonary artery in 13 weanling sheep, the test group. Six sheep, in which a transannular Dacron patch was implanted, served as control group. The test and the control patches were harvested 3-24 months later. The results were documented macroscopically, by histological examination, and by scanning electron microscopy. The 6-keto-PGF1α activity was measured in the regenerated tissue and compared with that in the native pulmonary artery. No aneurysms were noted. Regeneration of a neointima and a neomedia, comparable to native arterial tissue, was observed in the test group. In the control group, a neointimal layer was present but no neomedia comparable to native arterial tissue. Scanning electron microscopy disclosed differences in the endothelial structure between the test and control groups. 6-keto-PGF1α activity was present in both the test and control groups. It is concluded that absorbable, nonwoven patches of PHB can be used as a scaffold for tissue regeneration in low-pressure systems. The regenerated vessel had structural and biochemical qualities in common with the native pulmonary artery.
SummaryThe background mechanism for the disappearance of intravascular fibrin from the lungs in connection with pulmonary fat embolism in the rat was studied.The reticulo-endothelial system did not appear to play an important role in the disappearance of fibrin. Premedication of the animals with trypan blue had only slight influence on this disappearance, and the capacity of RES for phagocytizing 131I-denatured albumin was not diminished.Treatment of the rats with a plasminogen activation inhibitor (EACA) resulted in a protracted presence of intravascular fibrin deposits, indicating a role of fibrinolysis in the elimination of the fibrin.In connection with experimental fat embolism induced by fracture, an increase was observed in the plasminogen activator concentration in the blood, but when the fat embolism was induced by intravenous injection of homogenized adipose tissue, this activator decreased. At an early stage following intravascular coagulation in the lungs there was an increased fibrinolytic activity in the lung. These results indicated that the disappearance of fibrin is caused by local fibrinolysis in the lung.Twenty-four hrs after the induction of the fat embolism an increase in the plasminogen activator inhibitors in the blood and a decrease in the fibrinolytic activity in the lung was observed. The significance of this inhibition of the fibrinolytic system for the understanding of the fat embolism syndrome is discussed.
SummaryThe fibrinolytic system was studied in a number of autopsy cases. It was found that in contrast to most of the other autopsy cases those persons who had died later than 1 day after trauma, especially cases of fat embolism, often showed inhibition of fibrinolysis combined with the presence of intravascular fibrin in the pulmonary vessels. The importance of this observation for the pathogenesis and diagnosis of the fat embolism syndrome is discussed.
The coronary hemodynamic effects of intracoronary administration of a fibrin(ogen)-derived pentapeptide, Ala-Arg-Pro-Ala-Lys (peptide 6A), were evaluated in open-chest anesthetized dogs. With administration of peptide 6A (2.5-30 mumol), coronary blood flow increased and coronary vascular resistance decreased promptly in a dose-related manner. Increase in coronary blood flow was independent of any change in indexes of myocardial O2 demand, indicating the peptide 6A exerts direct effects on coronary arterial tone. Systemic arterial and left ventricular end-diastolic pressures remained unchanged with smaller doses but decreased when higher doses of peptide 6A (greater than or equal to 20 mumol) were administered. Plasma concentrations of 6-ketoprostaglandin F1 alpha, stable hydrolysis product of prostacyclin, increased in coronary sinus blood samples in conjunction with increase in coronary blood flow. Administration of indomethacin (5 mg/kg iv) inhibited peptide 6A-induced release of prostacyclin and significantly attenuated the effects of peptide 6A on coronary hemodynamics. Pretreatment of animals with H2-receptor blocker cimetidine (500 mg iv) or with H1-and H2-receptor blocker diphenhydramine (50 mg iv) had no significant effects on peptide 6A-induced increase in coronary blood flow. This study suggests that this fibrin(ogen)-derived peptide has potent vasodilator effects on the coronary vascular bed of the dog, and these effects are in part mediated by stimulation of prostacyclin release.
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