Secondary driving forces affecting transcapillary osmotic flows in perfused heart.

We evaluated secondary hydrostatic and osmotic pressure gradients caused by an osmotic flow across the wall of rabbit heart capillaries in vitro. Tissue fluid loss after addition of 80 mM sucrose to the Ringer perfusate depressed interstitial fluid pressure (IFP) by 13.2 +/- 1.1 cmH2O, as measured with a fine intramyocardial needle. This, plus a calculated rise in capillary pressure, caused a difference of 4.3 cmH2O in transcapillary pressures which represents 1.4% of the simultaneous and opposite osmotic pressure difference. The effect of transient-induced experimental changes in interstitial effect of transient-induced experimental changes in interstitial concentration of NaCl (main resident solute) during an osmotic transient and osmotic balance experiments using opposing transcapillary flows (Jv) and a sigma sucrose = 2.9 sigma NaCl. Long-term perfusion with solutions having abnormal concentrations of NaCl did not influence Jv, whereas inclusions of sucrose as resident solute depressed Jv by 10%. Results indicate that secondary hydrostatic and osmotic forces are small relative to the main osmotic driving force. Compliance measurements and calculations suggest that cells contribute three-fourths organ water loss during an osmotic transient, thus buffering volume, pressure, and concentration changes in the interstitial spaces.