Platelet function (ADP-induced platelet aggregation) in 20 patients with juvenile-onset diabetes mellitus was not different from that of age- and sex-matched controls. Platelet sensitivity to exogenous PGI2 was not diminished in diabetic patients. No sex differences were detected. There was no correlation between concomitant blood glucose levels and platelet sensitivity to PGI2.

In haemodialysis an interaction between platelets and the dialysator membrane occurs, which is not prevented by heparin. This can be demonstrated by parietal depositions of platelets in the capillaries of the artificial kidney by scanning electron microscopy, as well as in a marked increase of reversible platelet microaggregates during the first phase of dialysis. Some patients are prone to develop thrombosis of the capillary kidneys in spite of a high-dose heparinization. In these cases the use of diclofenac, a cyclooxygenase inhibitor, prevents these adverse platelet reactions.

Heparin had no effect on PGI2-activity if heparin and PGI2 have been incubated-together in an ice bath for 3 minutes. But heparin was able - unlike the other Pg or GAG - to abolish PGI2-activity if it had been incubated with PGI2 in an ice bath for 15 minutes. Pg and GAG, which had been isolated from bovine aortas according to the method of Hascall, and commerically available GAG (hyaluronic acid, chondroitin-40-sulfate, chondroitin-6-sulfate and heparin) had no effect on PGI2-formation of rat aortas in short time incubation (3 min). After long time incubation (15 min) or rat aortas in heparin less PGI2 was detectable compared to a buffer incubation. These data suggest that Pg and GAG do not influence PGI2-formation of arteries. The diminished PGI2-activity after long time incubation should be due to the PGI2-degrading effect of heparin.

The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI2-release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1 alpha-levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1 alpha. Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1 alpha-level during the initial phase of hemodialysis.

PGs and GAGs have been isolated from fresh bovine aortas according to the method of Hascall and chemically characterized. These PGs and GAGs had only little effects on ADP- and collagen-induced platelet aggregation, but had very potent inhibitory action on thrombin-induced platelet aggregation and prolonged thrombin-clotting-time. Of the standard GAGs investigated hyaluronic acid, chondroitin-4-sulfate and chondroitin-6-sulfate had only little inhibitory action on thrombin-induced platelet aggregation, whereas heparin was very potent in this respect. The unsaturated disaccharides originating after degradation of GAGs with chondroitinases had no effect on platelet aggregation. No differences between PGs and GAGs in inhibiting thrombin-induced platelet aggregation could be detected.

Saphenous veins of women under chronical treatment with oral contraceptive drugs generate statistically significantly more (p < 0,01) prostacyclin (PGI2) than those of age matched controls. However, the platelet sensitivity upon exogenous synthetic PGI2 was unchanged. The platelet function (ADP-induced platelet aggregation) was slightly activated, but not to a statistically significant degree.

The synthesis of prostacyclin (PGI2), the most potent known inhibitor of platelet aggregation, varies with age. After 30 years the production decreases, but increases again in the 6th and 7th decade. Contrary to these physiological variations patients suffering from juvenile onset diabetes or peripheral angiopathy show a markedly decreased prostacyclin synthesis. Since the prostacyclin system in thought to be an important blood vessel protector, the pathological low level of PGI2-synthesis could be a key position in development or progression of vascular complications.