Dual lumen silicon rubber right atrial catheters were implanted into the jugular of 8 rabbits and tunneled subcutaneously to exit sites between the ears. Using a miniaturized tubing-pump system, blood flow rates of 25 ml/min could be achieved for up to 3 1/2 hours without sign of hemolysis in an extracorporeal blood circuit. Seven catheters functioned an average of 75 +/- SE 19 days (range 24-117). One catheter remains functional after 176 days. Infection and thrombosis were the main reasons for failure. 20 plasmaphoresis experiments were carried out in four heparinized rabbits (blood flow rates 15 ml/min, plasmaflux 1.5-2.0 ml/min) using polypropylene minifilters (average pore size, 0.55 micron) with the plasma recirculated back into the animal. No hemolysis was detectable throughout the 4 hr experiment. Plasma proteins with a MW of 69 X 10(3) to 3 X 10(6) (Albumin, LDH, SGOT, SGPT, CPK, fibrinogen, LDL) showed a sieving coefficient close to 1.0. The good filtration performance and the absence of side effects make this system a possible use for plasmaphoresis in neonates.

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PubMedDate not supplied

[Experimental plasmin arthritis].

It is known, that plasmin is capable of specifically activating the complement factors C1 q and C3. In addition plasmin can activate procollagenase to collagenase. Since both mechanisms could possibly play a decisive role in the pathogenesis of rheumatoid arthritis, we have carried out animal experiments to investigate the primary role of plasmin in the development of arthritis. Twenty-two rabbits were subjected to intraarticular injection with an equal dose of plasmin on days 1, 4, and 8. An aspirate was taken on day 9 for a white cell count and a histological investigation of the synovial tissue. Already after a single dose of 0.25 CU plasmin an inflammatory reaction was clearly observed. Increasing amounts of plasmin (2.5 and 12.5 CU) caused an increased inflammatory response. On the basis of these results, it is discussed whether the observed arthritic reaction after plasmin injection is caused by complement activation. Possible analogies with rheumatoid arthritis are discussed.

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