[Alinidine in multi-vessel coronary disease: reduction of stress-induced ischemic reaction]. / Alinidine bei koronarer Mehrgefässerkrankung: Reduktion der belastungsinduzierten Ischämiereaktion.

Ten patients suffering from an angiographically documented coronary two- or three-vessel disease were examined to evaluate the effects of the specific bradycardiac agent alinidine during a bicycle stress test. Hemodynamic and electrocardiographic parameters were compared before and after an intravenous application of 30 mg of the substance. The alinidine plasma levels 30 min after the injection were 160.6 +/- 22.5 ng/ml) (mean +/- SEM). Alinidine significantly (p less than 0.05) reduced the resting levels of heart rate (8.5%), double product (10.3%), myocardial oxygen consumption (9.1%), and cardiac output (9.0%). During exercise, significantly less ST-segment depression (p less than 0.001) in the EKG was observed after alinidine application in nine out of 10 patients, and the rise of pulmonary artery pressure was significantly reduced (34.7 vs 38.1 mm Hg, mean p less than 0.05). However, alinidine had no effect on the maximum heart rate at the end of exercise. We, therefore, assume that the substance has additional anti-ischemic properties.

The effects of an infusion of prostacyclin on their endotoxin shock in rabbits.

30 rabbits received an infusion of lipopolysaccharide B (75 micrograms/kg.h) over 4 hours (groups E, EI, EA; n = 10 each). Saline was given to a control group (C; n = 8). In group EI, prostacyclin (PGI2; 500 ng/kg.min) was given simultaneously to endotoxin. Into group EA animals, aspirin (20 mg/kg) was injected before the endotoxin infusion was started. PGI2 and aspirin both improved survival of animals (6/10 each vs. 2/10 in group E). The drop of platelet counts was significantly reduced by PGI2, while leukocyte depletion was similar in all endotoxin groups. PGI2 preserved the functional capacity of platelets as indicated by collagen stimulated aggregation and thromboxane formation. PGI2 but not aspirin significantly reduced renal fibrin deposition.

Beneficial effects of prostacyclin in a rabbit endotoxin shock model.

Thirty rabbits received an infusion of lipopolysaccharide B (75 micrograms/kg.h) over 4 hours (groups E, EI, EA; n = 10 each). Saline was given to a control group (C; n = 8). In group EI, prostacyclin (PGI2; 500 ng/kg.min) was given simultaneously to endotoxin. Into group EA animals, aspirin (20 mg/kg) was injected before the endotoxin infusion was started. PGI2 and aspirin both improved survival of animals (6/10 each vs. 2/10 in group E). The drop of platelet counts was significantly reduced by PGI2, while leukocyte depletion was similar in all endotoxin groups. PGI2 preserved the functional capacity of platelets as indicated by collagen stimulated aggregation and thromboxane formation. PGI2 but not aspirin significantly reduced renal fibrin deposition.

Comparison of sympathomimetic amines with collagen, calcium ionophor and adenosine diphosphate in their effects on thromboxane formation of human platelet rich plasma.

Platelet rich plasma (PRP) was stimulated by addition of epinephrine, norepinephrine, dopamine, dobutamine, ADP, collagen or A 23187 in various concentrations. Before, during and after aggregation the levels of thromboxane B2 (TxB2) were measured by radioimmunoassay. After addition of collagen or A 23187 a strong stimulation of thromboxane synthesis was observed, beginning with the early aggregation phase. TxB2 values after complete aggregation amounted to 110-220 ng/ml and up to 500 ng/ml, respectively. After ADP, epinephrine and norepinephrine the thromboxane formation took place mainly in the late aggregation phase and reached levels of 37-51 ng TxB2/ml PRP. Dopamine and dobutamine in concentrations up to 50 microM failed to stimulate platelet's thromboxane synthesis and induced only small changes of optical density of PRP.

Effects of prostacyclin during cardiopulmonary bypass in men on plasma levels of beta-thromboglobulin, platelet factor 4, thromboxane B2, 6-keto-prostaglandin F1 alpha and heparin.

A randomized double-blind study was carried out on 40 male patients requiring aorto-coronary bypass surgery. 20 patients received a constant dose of 8 ng kg-1 min-1 of prostacyclin (PGI2), beginning two minutes before extracorporeal circulation (ECC) and ending together with ECC. Compared to the placebo-treated patient group (n = 20), PGI2-treatment significantly reduced the ECC-induced release of platelet alpha-granule proteins, beta-thromboglobulin (1178 ng/ml vs. 1926 ng/ml) and platelet factor 4 (837 ng/ml vs. 1245 ng/ml) into plasma (mean of max. values). Furthermore the decrease of platelet counts during ECC was less pronounced in PGI2-treated patients. Application of PGI2 had no effect on the increase in thromboxane B2 (TxB2) plasma levels, which amounted to 0.6 ng/ml at the end of ECC. PGI2-treatment resulted in significantly elevated plasma concentrations of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (2.1 ng/ml) throughout the infusion off prostacyclin. 6-keto-PGF1 alpha plasma levels increased up to 1.2 ng/ml in the control group patients, indicating a stimulation of endogenous PGI2 formation during ECC.

[Radiotelemetric studies on heart rates of 10 year old boys and girls during a 3000 m-run on the sports field and on the treadmill (author's transl)]. / Radiotelemetrische Untersuchungen der Herzfrequenz während eines 3000 m-Laufs auf dem Sportplatz und auf dem Laufband bei 10 jährigen Schülern und Schülerinnen.

The behaviour of heart rates of 25 untrained boys and 25 untrained girls between 9.5 and 10.5 years of age was registered telemetrically before, during and after a 3000m-run with a finish on the sportsfield and during a run over the same distance with the equivalent but constant speed on a treadmill. Additionally an exhausting spiroergometric test on a bicycle in a sitting position (method: W/kg body weight) was carried out. With a self-determined intensity the boys passed the 3000 m-distance in a shorter time than the girls. During the run the girls' heart rates remained relatively constant between 190 and 204 per min, whereas the boys' heart rates were significantly lower (about 10/min). Children with a higher relative oxygen capacity (56 ml O2/kg) run faster and revealed lower heart rates than children with less relative oxygen capacity (39.8 ml O2/kg). The same results were obtained when children with lower body weight were compared to heavier children of the same size.