Search

AbstractIn 36 patients with meningococcal infection a close association between the laboratory evidence of disseminated intravascular coagulation (DIC) and unfavourable prognostic factors was established. Patients with platelet count <100 000μl, Normotest <50 and plasma fibrinogen concentration <100 mgdl had a serious prognosis. No significant differences could be established between patients with infection from serogroup A and B meningococci for either laboratory evidence of DIC or prognostic factors.

Conflicting reports have been published concerning the spontaneous release of prostacyclin (PGI2) from endothelial cells and vascular tissue in vitro. In this study the effect of using various incubation medias on the release of PGI2 and 6-keto-PGF1α from primary cultures of confluent endothelial cell monolayers (ECM), grown from human umbilical cord veins, was examined. The incubations were carried out for 5 min at 22 °C on a rocker platform. The release of these compounds differed substantially with the various incubation media. Hypotonic and thrombin-containing media produced the greatest release. The 51Cr release from prelabeled ECM was also assayed. A high correlation existed between PGI2, 6-keto-PGF1α and 51Cr occurring in the various media. Since 51Cr release is considered to be a marker of cell membrane damage, the study indicates that under in vitro conditions the amount of PGI2 released is related to the degree of cell injury.

Unsaturated fatty acids (FA) were bound to human albumin in a molar ratio of 2 and were then added to platelet-rich plasma (PRP), increasing the total FA concentration by 1 mM. Separate FA and FA paired with di-homo-γ-linolenic acid (DHLA) and arachidon-ic acid (AA), respectively, were incubated with PRP for 5 and 90 min, and platelet aggregation and platelet factor 3 (PF3) activity were measured. DHLA inhibited adenosine-diphos-phate- and collagen-induced platelet aggregation after 5 min, an effect which was enhanced after 90 min. The effects of AA, which stimulated platelet aggregation and increased PF3 activity, were partially counteracted by DHLA after 90 min. When linoleic acid and AA were incubated with PRP in equimolar concentrations for 90 min, an inhibition of collagen-induced platelet aggregation was observed which was not observed after incubation with these FA separately. This study indicates that exogenous albumin-bound AA and DHLA may be used directly by the platelet cyclo-oxygenase pathway before significant incorporation into the platelet phosphoüpids has occurred.

The effects of estradiol and progesterone added to the growth medium of human umbilical vein endothelial cells for 72 h on the formation and release of prostacyclin were investigated. The influence on collagen-induced platelet aggregation and on the platelet formation of thromboxane A2 following aggregation, of the growth medium collected before and after thrombin stimulation of the endothelial cells, was studied simultaneously. Under basal conditions, endothelial cells grown with progesterone released significantly less prostacyclin into the growth medium than did controls (p < 0.05). Following thrombin stimulation, endothelial cells grown with estradiol (p < 0.05) or a combination of estradiol and progesterone (p < 0.01) contained significantly less prostacyclin than controls. No significant effects on the platelet aggregation or platelet thromboxane formation could be found. This study indicates a lowering effect of both female sex hormones on the endothelial cell prostacyclin formation and release. This may be of significance for the increased risk of vascular disease in pregnant women and oral contraceptive users, but can hardly explain the consequences of the hormonal loss occurring at the menopause.