CONTRIBUTIONS OF ISCHEMIA AND REPERFUSION TO MUCOSAL LESION FORMATION

CONTRIBUTIONS OF ISCHEMIA AND REPERFUSION TO MUCOSAL LESION FORMATION
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DOI:
10.1152/ajpgi.1986.250.6.g749
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发表时间:
1986-06-01
影响因子:
--
通讯作者:
GRANGER, DN
GRANGER, DN
中科院分区:
其他
文献类型:
--
作者:
PARKS, DA;GRANGER, DN

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已经提出了两种理论来解释与肠缺血、缺氧逆流交换和氧自由基相关的粘膜损伤。逆流机制表明粘膜损伤应主要发生在缺血期,而氧自由基假说预测大部分粘膜损伤是由缺血组织的再灌注引起的。在缺血期间和再灌注后获得的组织学标本可以对局部缺血模型中粘膜病变发展的时间过程进行系统评估。局部低血压 3 小时后再灌注,平均粘膜厚度从 1,022.2 .+- 减少。 6.3 至 503.6.+-。 10.0微米粘膜厚度的减少主要是由于绒毛高度的减少,因为隐窝深度的减少在统计学上并不显着。当肠缺血3小时而没有再灌注时,观察到粘膜厚度的变化明显较小。缺血3小时再灌注1小时产生的粘膜损伤比缺血4小时再灌注产生的粘膜损伤更严重。这项研究的结果表明,广泛使用的局部低血压模型产生的大部分组织损伤发生在再灌注时。
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 .mu.m. 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.