In vivo effects of hydrostatic pressure on interstitium of abdominal wall muscle.
In vivo effects of hydrostatic pressure on interstitium of abdominal wall muscle.
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体内静水压对腹壁肌肉间质的影响。
DOI：
10.1152/ajpheart.1999.276.2.h517
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Flessner,MF
中科院分区：
文献类型：
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作者：
Zakaria,ER;Lofthouse,J;Flessner,MF
从腹膜腔到周围组织的液体流失与腹膜内静水压力（Pip）直接相关。根据达西定律[Q=−KA(dPif/dx)]，组织横截面积(a)上的流体通量(Q)将随着水力导率(K)或间隙流体静水压力梯度（dPif/dx，其中距离）的增加而增加。先前，我们证明了在大鼠的前腹肌（AAM）中，dPif/dx仅增加40%，而在pip1.5和8mmhg之间，dPif/dx增加了5倍。因为它是间质体积（θif）的函数，我们假设对pip的扰动会改变pif并扩大间质，从而增加θif。为了验证这一假设，我们使用双标记定量放射自显影（QAR）测量了- 2.8至+8 mmHg范围内大鼠AAM的细胞外液体积（θec）和血管内体积（θiv）。θif通过减法（θec−θiv）得到。dPif/dx用微移管和伺服零系统测量。在Pif≤1.2 mmHg时，局部θivd值平均为0.010±0.002 ml/g， θ ifd值平均为0.19±0.01 ml/g。然而，在Pif为1.2和4.2 mmHg之间，θif增加了一倍（分别从0.20±0.00到0.39±0.01 ml/g），但不随Pif的进一步增加而增加。这种非线性的压力-体积关系并不能解释inKwith Pip的五倍增长。由于间质基质有助于间质抵抗流体流动，并且透明质酸（HA）是基质中唯一不固定在组织上的成分，我们假设间质酸的丧失是导致间质抵抗流体流动持续下降的原因。我们测定了在Pip= 0 mmHg时大鼠AAM和邻近皮下组织（SC）中的HA浓度，以及在恒定Pip= 6 mmHg时透析2小时后的HA浓度。HA含量(干重归一化)在麦从487±16减少到360±27μg / g干组织(n = 4, P < 0.05),从528±72增加到1050±136毫克/克干组织(n = 4, P > 0.001)在SC。我们认为负责的机制增加inKwith Pipinclude小间隙的扩张,间质大分子的稀释,并从麦冲刷SC的间质大分子负责流体流动阻力。
Fluid loss from the peritoneal cavity to surrounding tissue varies directly with intraperitoneal hydrostatic pressure (Pip). According to Darcy’s law [Q= −KA(dPif/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 (dPif/dx, wherexis distance). Previously, we demonstrated that in the anterior abdominal muscle (AAM) of rats, dPif/dxincreases by only 40%, whereasKrises fivefold between Pipof 1.5 and 8 mmHg. BecauseKis a function of interstitial volume (θif), we hypothesized that perturbations of Pipwould change Pifand expand the interstitium, increasing θif. To test this hypothesis, we used dual-label quantitative autoradiography (QAR) to measure extracellular fluid volume (θec) and intravascular volume (θiv) in the AAM of rats within the Piprange from −2.8 to +8 mmHg. θifwas obtained by subtraction (θec− θiv). dPif/dxwas measured with a micropipette and a servo-null system. Local θivdid not vary with Pipand averaged 0.010 ± 0.002 ml/g, and θifaveraged 0.19 ± 0.01 ml/g at Pif≤1.2 mmHg. However, θifdoubled between Pifof 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 Pif. This nonlinear pressure-volume relationship does not explain the fivefold increase inKwith Pip. 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 Pip= 0 mmHg and after 2 h of dialysis at constant Pip= 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 inKwith Pipinclude expansion of the interstitium, dilution of interstitial macromolecules, and washout from the AAM to SC of interstitial macromolecules responsible for resistance to fluid flow.