Plasma catecholamine levels were studied in 45 severely injured patients for 8 days after the trauma. Sixteen of the patients were classified as critically injured and 29 as seriously injured. The total plasma catecholamine values of the whole group immediately after the injury were almost twice as high as the eighth day reference values and remained significantly higher than these values for 6 hours after the trauma. On admission both the plasma adrenaline and noradrenaline levels were elevated. The plasma adrenaline levels on admission correlated with the blood volume replacement which was required within the first 6 hours. The plasma noradrenaline levels in the critically injured group were significantly higher throughout the observation period than in the seriously injured group. A corresponding difference was observed in the plasma adrenaline concentrations only during the first 12 hours. The results showed that strong stimulation of the sympathetic nervous system occurs in severely injured patients. Factors stimulating the sympathetic nervous system apparently included hypovolaemia, tissue hypoxia, acidosis and the pain produced by the trauma and therapeutic measures.
Production of various arachidonic acid metabolites from both endogenous and exogenous substrate was measured using cultures of synovial fibroblasts from healthy and rheumatic synovia. At first, the rheumatic cells showed retarded growth and an altered histological picture. Rheumatic cells produced more 6-keto-PGF1 alpha, the main metabolite of prostacyclin, and prostaglandin E2 than did normal cells, which synthesized more thromboxane B2. Later on these differences diminished or disappeared, except regarding 6-keto-PGF1 alpha. When fairly high concentrations of exogenous arachidonic acid were used, for 2-hour incubation of the cells, the production of identified metabolites, 6-keto-PGF1 alpha, PGF2 alpha, PGE2, PGD2, PGA + PGB and thromboxane B2, was slightly less in rheumatic cells. In general, the main metabolite formed was 6-keto-PGF1 alpha. Some kind of feedback mechanism between prostaglandins and cyclic nucleotides is suggested.
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