Interstitial fluid pressure in rat skin becomes more negative in the initial phase of carrageenan-induced edema.
Increased negativity of the interstitial fluid pressure (P(i)) in the skin is a major driving force to create the initial edema in burn injury and, to a smaller degree, in the edemas formed in the initial phase of the chemical irritation induced by xylene and the anaphylactic reaction induced by dextran. The phenomenon of increased negativity of P(i) is the basis for stating that the connective tissues become 'active' in fluid exchange since the increased negativity of P(i) will be a major driving pressure for transcapillary fluid flux under these circumstances. The present study was performed to investigate if increased negativity of P(i) contributes to formation of the inflammatory edema induced by carrageenan in the rat paw skin, since carrageenan inflammation involves mechanisms principally different from burn injury, xylene and dextran anaphylaxis. Control P(i) averaged -0.42 mmHg +/- 0.12 (SE). Injection of normal saline increased P(i) by 1.4 mmHg in 6-10 min. In animals with intact circulation P(i) decreased to -4.75 +/- 0.60 mmHg in the same time period following subdermal injection of carrageenan and later returned to control values by 21-30 min. To prevent the edema formation which will increase P(i) and potentially lead to underestimation of an increased negativity in P(i), measurements were also performed after circulatory arrest when there will be no transcapillary fluid flux in response to the inflammatory agent. In this group P(i) fell to -4.10 +/- 0.71 mmHg (11-20 min) and remained at -2.75 to -4.10 mmHg throughout the observation period. Premedication with aprotinin (protease inhibitor), indomethacin (prostaglandin inhibitor) and 1,2 benzopyrone did not change the increased negativity in P(i) induced by carrageenan. In conclusion, the increased negativity of P(i) contributes to the formation of edema also in carrageenan-induced inflammation and is an effect of carrageenan which has previously not been described.
Department of Physiology, University of Bergen, Norway.
S A
SA
Rodt
R K
RK
Reed
D000818:Animals; D002351:Carrageenan; D004487:Edema / Q000139:chemically induced / Q000503:physiopathology*; D005110:Extracellular Space / Q000502:physiology*; D005260:Female; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000503:physiopathology*
D002351:Carrageenan