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The patients were divided by chance into 2 groups: the first one (15 persons) was given a natrium salt of prostacyclin (Epoprostenol Wellcome or Chinoin) in a dose of 5 mg/kg/min. intravenously by an infusion pump in 5 infusions; the control group (15 persons) received instead of prostacyclin a placebo (0.1 M glycine buffer of pH 10.5). Besides all the patients were given Doxium or Calcium dobesilate, Rutinoscorbin, Vitamin C, and Polopyrin S (Soluble Aspirin). Immediately after the completion of the treatment the authors did not find any essential differences between the examined groups. In prolonged observations however one demonstrated a significantly smaller frequency of the development of neovascularization in the eyes of persons treated by prostacyclin in comparison with the control group.

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Kallikrein (Padutin-Depot) was administered to 20 patients with obliterative atherosclerosis of the lower limbs of the II degree (19 patients) and IV degree (1 patient). The drug was given in the daily dose of 40 U i.m. for 28 days. An effect of kallikrein on the distance in intermittent claudication, rate of pain relieve after walking the maximal distance, blood flow in the lower limbs, and on the index of circulating aggregates have been determined. Clinical improvement has been noted after a 4-week therapy with kallikrein. The drug in a single dose of 40 U activates plasma fibrinolytic system for 5 hours and decreases the number of circulating aggregates (2-5 h). The authors explain kallikrein action as the release of endogenous bradykinin, which subsequently releases two epithelial mediators, i.e. PFG1 and EDRF.

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Prostacyclin (PGI2) connects all the pharmacologic properties of drugs being used till now in sudden deafness. 30 patients with sensori-neural sudden deafness were treated by prostacyclin and placebo in the double-blind test situation. In therapeutic group of 15 patients were 87% of complete recovery, but in placebo only 6%.

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In a pilot study the therapeutic effect of 2 x 500 mg etofibrate (Lipo Merz retard) on lipids and lipoproteins, fibrinolytic activity and clinical parameters was studied for four weeks in hyperlipidemic patients suffering from arteriosclerosis obliterans (Fontaine stage II/III). The study parameters were evaluated prior to and after the four weeks of treatment. Administration of etofibrate resulted in a significant decrease in serum cholesterol and triglyceride levels, the decrease in LDL-/HDL-cholesterol-ratio due mainly to an elevation of the HDL-cholesterol fraction, an increase in plasma fibrinolytic activity, an increased peripheral blood flow in the ischemic leg, and an increase in the pain-free walking distance. Thus, etofibrate applied twice daily might be recommended for the treatment of hyperlipidemic patients with signs of arteriosclerosis obliterans, Fontaine stage II/III.

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Thirty patients with acute ischaemic stroke were allocated randomly into a group treated with prostacyclin and a group receiving placebo. The treatment was started 24 to 72 hours after the onset of stroke. Prostacyclin sodium (Wellcome, U.K. or Chinoin, HPR) or its solvent (glycine buffer) were administered intravenously once daily during 2 weeks in 6-hour infusions. Prostacyclin was infused at rates of 2.5-5.0 ng/kg/min. Statistically significant improvement appeared from the second day on in the prostacyclin group, and only from the eighth day on in the placebo group. However, the final improvement was not statistically different between these groups.

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A double-blind study on prostacyclin (5 ng/kg/min infused i.v. for 5 hrs per day during 6 consecutive days) for the treatment of peptic gastric ulcers was carried out in thirty patients (15 prostacyclin, 15 placebo). Gastroscopy and its scoring was performed 1-2 days before the treatment, as well as a day and a week after the course of treatment was completed. Basal acid output (BAO) and pentagastrin stimulated release of gastric acid (maximum acid output MAO; peak acid output PAO) were measured before the treatment, during the third infusion, and one day after all the infusions had been completed. At the same time the basal release of bicarbonate into gastric juice was determined. Prostacyclin significantly accelerated healing of the ulcers at the end point of the study. Simultaneously, in the prostacyclin-treated patients an increase in bicarbonate release into gastric juice was noted, although the acidity of gastric juice was not changed. Our study shows a cytoprotective action of prostacyclin on a damaged human gastric mucosa.

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Blood plasma of patients with arteriosclerosis obliterans and diabetes showed a higher antioxidant potency as compared with plasma of healthy volunteers. Serum copper level in those patients was also elevated, but on the contrary to healthy subjects no correlation between serum copper level and plasma antioxidant potency was found. Similar changes were observed in rabbits fed four weeks with atherogenic diet. Administration of vitamin E increased plasma antioxidant potency, however, only in the patients suffering from arteriosclerosis obliterans with high regime of dosage of vitamin E (3 X 200 mg daily p.o.). N-ethylmaldimide-stimulated (malondialdehyde (MDA)) generation by washed platelets was suppressed by addition of homologous plasma to washed platelet preparation. Preincubation of rat aortic tissue with plasma from healthy volunteers resulted in an increase in PGI2-biosynthesis b 75%. We were not able to demonstrate the antioxidant activity of aortic endothelial cell homogenates. We conclude that antioxidant properties of plasma may play an important role in protection of serum lipids against autooxidation. Antioxidant ability of plasma is not exclusively correlated with plasma copper or ceruloplasmin level.

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Twenty-one patients with arteriosclerosis obliterans of lower extremities were treated with beta-pyridylcarbinol (Ronicol) for five weeks. The long-term therapy with beta-pyridylcarbinol did not influence platelet aggregability. Activation of the fibrinolytic system was observed. This fibrinolytic effect of Ronicol was abolished in patients treated with aspirin. In most cases a slight clinical improvement was seen, manifested by elongation of pain-free walking distance and increased blood flow in affected limbs. It is concluded that the therapeutic effect of Ronicol in humans may be partly mediated by the release of endogenous prostacyclin.

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Infusion of PGI2 at a dose of 5 or 10 ng/kg/min during 72 hours into patients with peripheral vascular disease was followed by increased susceptibility of platelets to proaggregatory action of ADP and collagen but not that of arachidonate. The above effects were observed 24 hours after termination of infusion of PGI2. A tendency to an increased formation of TXA2 in PRP aggregated by arachidonate was also noticed. Infusion of PGI2 at a dose of 2 mg/kg/min during 72 hours into the patients caused the decreased platelet aggregability to ADP and arachidonate but not to collagen, and a decreased tendency to production of TXA2 in PRP aggregated by arachidonate. The existence of a "rebound effect" in platelets after a long term PGI2 therapy is suggested.

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In patients with peripheral vascular disease and in healthy rabbits, infusion of PGI2 but not of 6-keto PGF1 alpha induced a rise in blood glucose level and a pathological deviation in glucose tolerance test. In experiments in vitro, the increased concentrations of glucose produced dose-dependent inhibition of PGI2 release from isolated rat aortic rings. The link between PGI2 and carbohydrate metabolism is discussed.

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