Features of endothelial dysfunction in early diabetic nephropathy.

The release of tissue plasminogen activator (tPA) by vascular endothelial cells during exercise was studied in forty men with insulin-dependent diabetes. Three groups, matched for age and diabetes duration, were defined as: group I (n = 19), normal urinary albumin excretion (less than 30 mg/24 h); group II (n = 11), incipient diabetic nephropathy (30-300 mg albumin excreted per 24 h); and group III (n = 10), clinical diabetic nephropathy (more than 300 mg albumin excreted per 24 h). Nine non-diabetic men served as controls. The rise in tPA antigen with exercise was similar in the controls and group I but significantly smaller in groups II and III (p less than 0.01). The albumin transcapillary escape rate was significantly higher in groups II and III than in group I and normal controls (p less than 0.01). The basal plasma level of von Willebrand factor was higher in groups III (p less than 0.01) and II (difference not significant, p = 0.06) than in group I and normal controls. These findings suggest that insulin-dependent diabetic patients with only slightly raised urinary albumin excretion have general endothelial cell dysfunction or damage. It is not yet clear whether these changes are important in the pathogenesis of thrombosis and atherosclerosis in these patients.

Muscle cell leakage due to long distance training.

Abnormal myoglobinemia (above 77 microgram/l) and free hemoglobin in plasma were found in 16 runners and in nine non runners immediately following distance running. The same abnormalities were found iun six elite rowers following rowing. In parallel with the rise in myoglobin and free hemoglobin a rise was found in serum concentrations of cellular enzymes (LDH, CK, ASAT, alkaline phosphatase) and of various metabolites. We found no proteinuria nor casts in the urine. Non runners had a higher rise in serum myoglobin than runners. Competitive running caused a rise in the serum concentration of the heart specific fraction of creatine kinase in seven of the nine (healthy) elite runners. The abnormal findings are only explainable on the basis of leakage of proteins from muscle cells to the circulation in otherwise healthy, well trained persons. Myoglobinemia and a transient rhabdomyolysis is a common phenomenon in long distance running, but evidently also occurs in distance rowing. Three months of running training prevented most of the muscle damage from relaxed jogging in the nine previous non runners. Neither the observed myoglobinemia nor the hemoglobinemia resulted in any significant loss of iron in the urine.

Changes in Platelet Functions, Coagulation and Fibrinolysis in Uncomplicated Cases of Acute Myocardial Infarction.

Platelet aggregation and serotonin-release in vitro and some coagulation and fibrinolysis parameters were studied closely in 12 patients with non-complicated acute transmural myocardial infarction from the very beginning, for 3 weeks.The aggregability with ADP, epinephrine and collagen and the serotonin-release was significantly reduced the first days. Significantly increased aggregability and serotonin-release developed after a week, with peak activity on days 14-16. Most patients still exhibited increased activity at the discharge on days 21-22.Positive ethanol gelation tests developed after day 1 in most patients with a peak at day 5, contemporary with peak activities of factor VIII and negatively correlated to factor XIII activity, quantitated biologically. These values were normalized on discharge. Antithrombin III (Xa) remained unchanged, normal to slightly elevated.The fibrinolytic activity decreased after day 1 with lowest activity on day 5, contemporary with peak activity of antiplasmin. Around 50% of the patients showed decreased activity on discharge.