Stein H J, Bauerfeind P, Hinder R A, Koerfer J, Blum A L
Department of Gastroenterology, CHUV, Lausanne, Switzerland.
J Surg Res. 1989 Jun;46(6):616-9. doi: 10.1016/0022-4804(89)90031-0.
Luminal gastric acid is essential for the formation of acute gastric mucosal lesions during ischemia. The mechanism by which luminal acid promotes gastric injury is, however, unclear. We investigated the effect of exogenous luminal acid on gastric mucosal blood flow using the radiolabeled microsphere technique. In rats with intact gastric blood supply application of exogenous luminal acid increased blood flow to the mucosa of the corpus and antrum. However, after ligation of the left gastric artery, which compromised mucosal blood flow to the corpus, application of luminal exogenous acid further decreased blood flow to the corpus. This indicates that the ability of the normal stomach to respond to luminal acidification with an increase in blood flow, which is thought to support clearance of back diffusing H+, is reversed in the ischemic stomach. The exposure to high luminal H+ concentrations may therefore promote gross injury in the ischemic stomach by further compromising nutritional mucosal blood flow.
腔内胃酸对于缺血期间急性胃黏膜损伤的形成至关重要。然而,腔内酸促进胃损伤的机制尚不清楚。我们使用放射性微球技术研究了外源性腔内酸对胃黏膜血流的影响。在胃血液供应完整的大鼠中,应用外源性腔内酸可增加胃体和胃窦黏膜的血流。然而,在结扎左胃动脉后,这损害了胃体的黏膜血流,应用腔内外源性酸进一步降低了胃体的血流。这表明,正常胃对腔内酸化作出血流增加反应(这被认为有助于清除反向扩散的H+)的能力,在缺血胃中发生了逆转。因此,暴露于高腔内H+浓度可能通过进一步损害营养性黏膜血流而促进缺血胃的严重损伤。