Relationship between lysophospholipid accumulation and plasma membrane injury during total in vitro ischemia in dog heart.
Relationship between lysophospholipid accumulation and plasma membrane injury during total in vitro ischemia in dog heart.
复制标题
狗心脏体外完全缺血时溶血磷脂积累与质膜损伤的关系。
DOI：
10.1016/s0022-2828(84)80625-2
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发表时间：
1984
影响因子：
5
通讯作者：
Jennings,RB
中科院分区：
文献类型：
--
作者：
Steenbergen,C;Jennings,RB
本文用离体犬心脏全缺血模型研究了缺血时组织磷脂组成的变化与质膜破坏之间的关系。已知该制剂与膜损伤的迹象相关，并且是定量缺血中磷脂变化的理想制剂，因为组织的重量不受缺血持续时间的影响，并且因为没有侧支流来去除磷脂降解的终产物。每克组织的磷脂磷酸盐的测量证实，在包括24小时缺血后采集的样品在内的所有样品中，磷脂及其降解产物的回收基本上是完全的。结果表明，溶血磷脂在缺血组织中逐渐积累，24小时后，它们占总组织磷脂的12%。在150分钟总缺血心肌的超微结构检测质膜的不连续性，而在相同的条件下，溶血磷脂含量不到总组织磷脂的1%。磷脂降解不受钙的利用率，因为溶脂的生产率并没有提高心肌组织在培养基中含有1.25毫米钙孵育，尽管超微结构的证据先行质膜破坏。这些数据表明，溶血磷脂积累在缺血心肌侧支血流或炎性细胞浸润的情况下，但溶血磷脂积累发生缓慢，并没有出现质膜碎片的主导机制。
The relationship between alterations in tissue phospholipid composition and disruption of the plasma membrane during ischemia in dog heart was examined using a homogeneousin vitromodel of total ischemia. This preparation was known to be associated with signs of membrane damage and was ideal for quantitation of phospholipid changes in ischemia because the weight of the tissue is unaffected by the duration of ischemia and because there is no collateral flow to remove the endproducts of phospholipid degradation. Measurements of phospholipid phosphate per gram of tissue confirmed that recovery of phospholipids and their degradation products was essentially complete in all samples including a sample taken after 24 h ischemia. The results showed that lysophospholipids gradually accumulated in the ischemic tissue; after 24 hin vitroischemia, they comprised 12% of the total tissue phospholipids. Discontinuities of the plasma membrane were detected ultrastructurally in myocardium subjected to 150 min total ischemia, while under the same conditions, the lysophospholipid content amounted to less than 1% of the total tissue phospholipids. Phospholipid degradation was not limited by calcium availability since the rate of lysolipid production was not enhanced by incubation of myocardial tissue in a medium containing 1.25 mmcalcium despite ultrastructural evidence of antecedent plasma membrane disruption. These data indicate that lysophospholipids accumulate in ischemic myocardium in the absence of collateral flow or inflammatory cell infiltration but that lysophospholipid accumulation occurs slowly and does not appear to be the dominant mechanism of plasma membrane fragmentation.