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首页> 外文期刊>American Journal of Physiology >Cytochalasin D induces edema formation and lowering of interstitial fluid pressure in rat dermis.
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Cytochalasin D induces edema formation and lowering of interstitial fluid pressure in rat dermis.

机译：细胞松弛素D诱导大鼠真皮中水肿的形成和间质液压力的降低。

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The increased capillary fluid filtration required to create a rapid edema formation in acute inflammation can be generated by lowering the interstitial fluid pressure (P(IF)). The lowering of P(IF) appears to involve dynamic beta(1)-integrin-mediated interactions between dermal cells and extracellular matrix fibers. The present study specifically investigates the role of the cell cytoskeleton, i.e., the contractile apparatus of cells, in controlling P(IF) in rat skin as the integrins are linked to both the cytoskeleton and the extracellular matrix. P(IF) was measured using a micropuncture technique in the dorsal skin of the hind paw at a depth of 0.2--0.5 mm and following the induction of circulatory arrest with the intravenous injection of KCl in pentobarbital anesthesia. This procedure prevented the transcapillary flux of fluid and protein leading to edema formation in acute inflammation, which in turn can increase the P(IF) and therefore potentially mask a decrease of P(IF). Control P(IF) (n = 42) averaged -0.8 +/- 0.5 (means +/- SD) mmHg. In the first group of experiments, subdermal injection of 2 microl cytochalasin D, a microfilament-disrupting drug, lowered P(IF) to an average of -2.8 +/- 0.7 mmHg within 40 min postinjection (P < 0.05 compared with control). Subdermal injection of vehicle (10% DMSO in PBS or PBS alone) did not change the P(IF) (P > 0.05). Lowering of the P(IF) was not observed after the injection of colchicine or nocodazole, which specifically disrupts microtubuli in cultured cells. In the second group of experiments, 2 microl of cytochalasin D injected subdermally into rats with intact circulation increased the total tissue water (TTW) and albumin extravasation rate (E(ALB)) by 0.7 +/- 0.2 and 0.4 +/- 0.3 ml/g dry wt, respectively (P < 0.05 compared with vehicle). Nocodazole and colchicine did not significantly alter the TTW or E(ALB) compared with the vehicle (P > 0.05). Taken together, these findings strongly suggest that the connective tissue cells can participate in control ofP(IF) via the actin filament system. In addition, the observation that subdermal injection of cytochalasin D lowered P(IF) indicates that a dynamic assembly and disassembly of actin filaments also occurs in the cells of dermal tissues in vivo.
机译：可通过降低组织液压力（P（IF））来产生在急性炎症中快速形成水肿所需的增加的毛细管液过滤。 P（IF）的降低似乎涉及真皮细胞和细胞外基质纤维之间的动态β（1）-整合素介导的相互作用。由于整联蛋白与细胞骨架和细胞外基质都相关，因此本研究专门研究了细胞骨架，即细胞的收缩装置在控制大鼠皮肤中的P（IF）中的作用。使用微穿刺技术在后爪背皮肤深度0.2--0.5 mm并在戊巴比妥麻醉中静脉内注射KCl诱导循环停止后测量P（IF）。该程序防止了在急性炎症中导致水肿形成的液体和蛋白质的毛细血管通量，这反过来又可以增加P（IF），因此有可能掩盖P（IF）的降低。对照P（IF）（n = 42）平均为-0.8 +/- 0.5（平均值+/- SD）mmHg。在第一组实验中，皮下注射2微升细胞松弛素D（一种破坏微丝的药物）在注射后40分钟内将P（IF）降低至平均-2.8 +/- 0.7 mmHg（与对照组相比，P <0.05）。皮下注射媒介物（仅含PBS或PBS的10％DMSO）不会改变P（IF）（P> 0.05）。注射秋水仙碱或诺考达唑后未观察到P（IF）的降低，这会特别破坏培养细胞中的微管。在第二组实验中，将2微升细胞松弛素D皮下注射到完整循环的大鼠中，使总组织水（TTW）和白蛋白渗出率（E（ALB））增加0.7 +/- 0.2和0.4 +/- 0.3 ml / g干重（与溶媒相比，P <0.05）。与载体相比，诺考达唑和秋水仙碱没有显着改变TTW或E（ALB）（P> 0.05）。综上所述，这些发现强烈表明结缔组织细胞可以通过肌动蛋白丝系统参与P（IF）的控制。另外，皮下松弛素D的皮下注射降低了P（IF）的观察结果表明肌动蛋白丝的动态组装和拆卸在体内真皮组织的细胞中也发生。

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