Mourelle M, Vilaseca J, Guarner F, Salas A, Malagelada J R
Digestive System Research Unit, Hospital General Vall d'Hebron, Barcelona, Spain.
Am J Physiol. 1996 Mar;270(3 Pt 1):G425-30. doi: 10.1152/ajpgi.1996.270.3.G425.
The contribution of nitric oxide (NO) to the altered colonic contractility of acute colitis was investigated in the 2,4,6-trinitroben-zenesulfonic acid model. NO synthase was measured in colonic tissue; the effects of NO synthase inhibition on colonic contractility were studied in vitro and in vivo. Inducible NO synthase was not detected in normal colons, whereas inflamed colons showed high activity. Acute inflammation was associated with enlarged colonic perimeter. NO synthase inhibitors or selective inhibitors of the inducible enzyme prevented colonic dilatation. In vitro, contractile responses to KCl were lower in muscle from colitic than control rats. After NO synthase inhibition, however, no difference was observed between colitic and control muscle contractility. In vivo, intracolonic pressure was lower in colitic than in control rats. Selective inhibition of inducible NO synthase increased intracolonic pressure in colitic but not in control rats. In conclusion, NO generation by inducible enzymes impairs smooth muscle contractility in colitis and may be involved in the pathogenesis of toxic dilatation of the colon.
在2,4,6-三硝基苯磺酸模型中，研究了一氧化氮（NO）对急性结肠炎时结肠收缩性改变的作用。检测结肠组织中的一氧化氮合酶；在体外和体内研究一氧化氮合酶抑制对结肠收缩性的影响。在正常结肠中未检测到诱导型一氧化氮合酶，而炎症结肠显示出高活性。急性炎症与结肠周长增大有关。一氧化氮合酶抑制剂或诱导型酶的选择性抑制剂可防止结肠扩张。在体外，与对照大鼠相比，结肠炎大鼠肌肉对氯化钾的收缩反应较低。然而，在一氧化氮合酶抑制后，结肠炎和对照肌肉收缩性之间未观察到差异。在体内，结肠炎大鼠的结肠内压低于对照大鼠。选择性抑制诱导型一氧化氮合酶可增加结肠炎大鼠而非对照大鼠的结肠内压。总之，诱导型酶产生的NO损害结肠炎时的平滑肌收缩性，可能参与结肠中毒性扩张的发病机制。
