EFFECT OF VENOUS STASIS AND HYPOPROTEINEMIA IN GINGIVAL FLUID FORMATION IN RATS

Experiments were performed to provide information on the mechanisms of the formation of gingival fluid in rats and on the determinants of it s flow and composition. For this purpose we studied the effect of incr easing net capillary filtration by venous stasis induced by multiple l igations of the jugular vein or by hypoproteinemia induced through pur omycine nephrosis. A 1 mu l glass capillary was placed in the sulcus o f the first maxillary molar for collection of gingival fluid (GF). Col loid osmotic pressure (COP) was determined in GF, in wick fluid from a ttached gingiva and buccal mucosa, and in plasma. Interstitial fluid h ydrostatic pressure (P-i) was measured by micropuncture technique and the fractional removal rate of radio-labelled human serum albumin (k(A lb)) was recorded in attached gingiva and buccal mucosa. During venous stasis the gingival fluid flow increased from 1.7 mu l/h to 3.8 mu l/ h, whereas COPGF fell from 14.1 mmHg to 8.8 mmHg. COP in wick fluid fr om gingiva was reduced from 10.3 to 4.3 mmHg. P-i increased from 6.8 t o 13.1 mmHg, and k(Alb) in sham-operated controls increased from 0.068 to 0.189 h(-1). In buccal mucosa COPi was significantly decreased to 7.1 mmHg in rats with venous stasis, whereas P-i and k(Alb) remained u nchanged compared to the sham-operated controls. In hypoproteinemic ra ts COPGF was 5.0 mmHg and COPp was reduced from 18.9 to 8.0 mmHg. COPi declined from 8.9 mmHg to 2.4 mmHg in gingiva and from 8.1 mmHg to 2. 7 mmHg in buccal mucosa. P-i in attached gingiva increased from 6.1 mm Hg to 9.0 mmHg, whereas P-i in buccal mucosa showed no consistent chan ge. The production of gingival fluid was increased about 3 times. We c onclude that increased gingival fluid flow during venous stasis and hy poproteinemia is caused by increased capillary filtration, resulting i n increased interstitital fluid volume and pressure.