Experimental Study on the Biosynthesis of Fibrinogen as an Acute-Phase Protein: Influence of β-Adrenergic Blockade in Rats with Inflammation or Yoshida Sarcoma

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First, the effects of a β-adrenergic blockade on fibrinogen biosynthesis in rats with an inflammatory lesion following the injection of a toxohormone was studied. It was found 1)that the seral fibrin degradation products (FDP) level rose soon after the subcutaneous injection of turpentine or the intraperitoneal injection of a toxohormone, but that the correlation between the free fatty acids (FFA) /albumin ratio and the plasma fibrinogen was not always positive; 2) that the enhanced fibrinogen biosynthesis was suppressed significantly in rats treated with a A-blocker every 4 hours, as measured by the incorporation of ¹⁴C-leucine 12 hours after the injection of turpentine or toxohormone; 3) but that the β-blockade did not alter the incorporation of ¹⁴C-leucine into serum albumin in these experiments.
Then the effect of 5-blockade on the concentration of plasma fibrinogen in sarcoma-bearing rats was also studied. These rats were given a 5-blocker every 6 hours by stomach tube between the 5th and 8th days after the subcutaneous inoculation of Yoshida sarcoma cells.
On the 8th day, plasma fibrinogen, serum albumin and FFA were measured. The plasma fibrinogen level and the FFA/albumin ratio in these rats were reduced by the β-blocker. On the other hand,β-blockade did not interrupt the activation of fibri nolysis in rats with inflammatory disease and it enhanced the phagocytic activity of the reticuloendothelial system (RES) as measured by the carbon clearance in normal rats.
In conclusion, β-adrenergic receptors may be the m ediator, and FDP, cortisol and other products already observed may act as stimuli. In reality, a combination of various stimuli may act as stress which stimulates the β-receptors. Stress theories, such as that of Selye's, can explain an important part of the regulation of fibrinogen biosynthesis.