In vivo effects of hydrostatic pressure on interstitium of abdominal wall muscle

Fluid loss from the peritoneal cavity to surrounding tissue varies directly with intraperitoneal hydrostatic pressure (P(ip)). According to Darcy's law [Q = -KA(dP(if)/dx)], fluid flux (Q) across a cross-sectional area (A) of tissue will increase with an increase in either hydraulic conductivity (K) or the interstitial fluid hydrostatic pressure gradient (dP(if)/dx, where x is distance). Previously, we demonstrated that in the anterior abdominal muscle (AAM) of rats, dP(if)/dx increases by only 40%, whereas K rises fivefold between P(ip) of 1.5 and 8 mmHg. Because K is a function of interstitial volume (θ(if)), we hypothesized that perturbations of P(ip) would change P(if) and expand the interstitium, increasing θ(if). To test this hypothesis, we used dual-label quantitative autoradiography (QAR) to measure extracellular fluid volume (θ(ec)) and intravascular volume (θ(iv)) in the AAM of rats within the P(ip) range from -2.8 to +8 mmHg. θ(if) was obtained by subtraction (θ(ec) - θ(iv)). dP(if)/dx was measured with a micropipette and a servo-null system. Local θ(iv) did not vary with P(ip) and averaged 0.010 ± 0.002 ml/g, and θ(if) averaged 0.19 ± 0.01 ml/g at P(if) ≤ 1.2 mmHg. However, θ(if) doubled between P(if) of 1.2 and 4.2 mmHg (from 0.20 ± 0.00 to 0.39 ± 0.01 ml/g, respectively) but did not increase with further increases in P(if). This nonlinear pressure-volume relationship does not explain the fivefold increase in K with P(ip). Because the interstitial matrix contributes to the interstitial resistance to fluid flow, and because hyaluronan (HA) is the only component of the matrix that is not anchored to the tissue, we hypothesized that the loss of interstitial HA was responsible for the continued decrease in interstitial resistance to fluid flow. We determined HA concentration in the rat AAM and adjacent subcutaneous tissue (SC) at P(ip) = 0 mmHg and after 2 h of dialysis at constant P(ip) = 6 mmHg. The HA content (normalized to dry weight) in the AAM was reduced from 487 ± 16 to 360 ± 27 μg/g dry tissue (n = 4, P < 0.05) and increased from 528 ± 72 to 1,050 ± 136 mg/g dry tissue (n = 4, P > 0.001) in the SC. We conclude that the mechanisms responsible for the increase in K with P(ip) include expansion of the interstitium, dilution of interstitial macromolecules, and washout from the AAM to SC of interstitial macromolecules responsible for resistance to fluid flow.