Harris N R
Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
Am J Physiol. 1997 Dec;273(6):G1320-5. doi: 10.1152/ajpgi.1997.273.6.G1320.
Fluid filtration rate (JV/S) from rat mesenteric capillaries was measured using a modified Landis technique before and after superfusion with 100 microM NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Three groups were studied: 1) control rats, 2) rats injected with antineutrophil serum (ANS), and 3) rats injected with a monoclonal antibody (CL26) against the leukocyte adhesion molecule CD18. The relative increase in JV/S (L-NAME/ baseline) in control rats averaged 1.66 +/- 0.32 (n = 11), which was significantly higher (P < 0.05) than in ANS (0.51 +/- 0.12; n = 5)- and CL26 (0.45 +/- 0.16; n = 6)-injected rats exposed to L-NAME. The L-NAME-induced changes in JV/S in each group were due to altered permeability rather than altered pressure gradients, as determined by measurements of arteriolar hydrostatic pressure (using a servo-null apparatus) and estimates of intravascular oncotic pressure (using plasma protein concentration). These findings indicate that nitric oxide synthase inhibition increases the permeability of mesenteric capillaries to water, a response that is dependent on neutrophil adhesion.
采用改良的兰迪斯技术,在使用一氧化氮合酶抑制剂100微摩尔NG-硝基-L-精氨酸甲酯(L-NAME)进行灌流前后,测量大鼠肠系膜毛细血管的液体滤过率(JV/S)。研究了三组:1)对照大鼠,2)注射抗中性粒细胞血清(ANS)的大鼠,3)注射针对白细胞粘附分子CD18的单克隆抗体(CL26)的大鼠。对照大鼠中JV/S的相对增加(L-NAME/基线)平均为1.66±0.32(n = 11),显著高于(P < 0.05)暴露于L-NAME的注射ANS的大鼠(0.51±0.12;n = 5)和注射CL26的大鼠(0.45±0.16;n = 6)。如通过测量小动脉流体静压(使用伺服零位装置)和估算血管内胶体渗透压(使用血浆蛋白浓度)所确定的,每组中L-NAME诱导的JV/S变化是由于通透性改变而非压力梯度改变所致。这些发现表明,一氧化氮合酶抑制增加了肠系膜毛细血管对水的通透性,这种反应依赖于中性粒细胞粘附。