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 its flow and composition. For this purpose we studied the effect of increasing net capillary filtration by venous stasis induced by multiple ligations of the jugular vein or by hypoproteinemia induced through puromycine nephrosis. A 1 mu l glass capillary was placed in the sulcus of the first maxillary molar for collection of gingival fluid (GF). Colloid osmotic pressure (COP) was determined in GF, in wick fluid from attached gingiva and buccal mucosa, and in plasma. Interstitial fluid hydrostatic pressure (P-i) was measured by micropuncture technique and the fractional removal rate of radio-labelled human serum albumin (k(Alb)) 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 from gingiva was reduced from 10.3 to 4.3 mmHg. P-i increased from 6.8 to 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 unchanged compared to the sham-operated controls. In hypoproteinemic rats 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 mmHg to 9.0 mmHg, whereas P-i in buccal mucosa showed no consistent change. The production of gingival fluid was increased about 3 times. We conclude that increased gingival fluid flow during venous stasis and hypoproteinemia is caused by increased capillary filtration, resulting in increased interstitital fluid volume and pressure.