Parks D A, Granger D N
Am J Physiol. 1986 Jun;250(6 Pt 1):G749-53. doi: 10.1152/ajpgi.1986.250.6.G749.
Two theories have been proposed to account for the mucosal injury associated with intestinal ischemia, hypoxia-countercurrent exchange, and oxygen free radicals. The countercurrent mechanism suggests that mucosal injury should occur predominately during the ischemic period, whereas the oxygen free radical hypothesis predicts that the majority of mucosal injury results from reperfusion of ischemic tissue. Histological specimens obtained during the ischemic period and following reperfusion allowed a systematic evaluation of the time course of development of mucosal lesions in a regional ischemia model. Reperfusion after 3 h of regional hypotension reduced mean mucosal thickness from 1,022.2 +/- 6.3 to 503.6 +/- 10.0 microns. The decrease in mucosal thickness was largely due to a reduction in villus height, inasmuch as the reduction in crypt depth was statistically insignificant. A significantly smaller change in mucosal thickness was observed when the bowel was subjected to 3 h ischemia without reperfusion. The mucosal injury produced by 3 h ischemia and 1 h reperfusion was more severe than that produced by 4 h ischemia without reperfusion. The results of this study suggest that most of the tissue damage produced by the widely employed regional hypotension model occurs at the time of reperfusion.
为了解释与肠道缺血、缺氧逆流交换和氧自由基相关的黏膜损伤，人们提出了两种理论。逆流机制表明，黏膜损伤应主要发生在缺血期，而氧自由基假说则预测，大多数黏膜损伤是由缺血组织的再灌注引起的。在缺血期和再灌注后获取的组织学标本，使得在区域缺血模型中对黏膜病变发展的时间进程进行系统评估成为可能。局部低血压3小时后的再灌注使平均黏膜厚度从1,022.2±6.3微米降至503.6±10.0微米。黏膜厚度的降低主要是由于绒毛高度的降低，因为隐窝深度的降低在统计学上不显著。当肠道进行3小时缺血而不进行再灌注时，观察到黏膜厚度的变化明显较小。3小时缺血加1小时再灌注所产生的黏膜损伤比4小时缺血而不进行再灌注所产生的损伤更严重。这项研究的结果表明，广泛采用的局部低血压模型所产生的大多数组织损伤发生在再灌注时。
