Lavelle K J, Park H M, Moseman A M, Orwig C
Invest Radiol. 1980 May-Jun;15(3):267-71. doi: 10.1097/00004424-198005000-00014.
Incremental ischemic injury was induced in rabbits by transient occlusion of the renal artery. Renal localization of 99mTc-HEDP was quantitated in ischemic and normal kidneys at fixed intervals following restoration of blood flow. Creatinine clearance and microscopic evaluation of renal structure were determined concurrently with scintigraphic studies. There was a sequential reduction in creatinine clearance and an increase in tubular necrosis with prolongation of the ischemic period. 99mTc-HEDP localization in ischemic renal tissue was dependent on the degree of renal injury, ranging from twice normal with minor injury to a nine-fold increase with the most severe ischemic changes. The increased accumulation was demonstrable for longer periods with increasing ischemic injury. Considerable recovery of renal function was apparent in all groups by one week. 99mTc-HEDP may be useful in evaluation of renal failure secondary to ischemic injury.
通过短暂阻断肾动脉在兔身上诱导渐进性缺血性损伤。在恢复血流后的固定时间间隔,对缺血肾和正常肾中99mTc-HEDP的肾定位进行定量分析。同时进行肌酐清除率测定及肾脏结构的显微镜评估。随着缺血期延长,肌酐清除率呈序贯性降低,肾小管坏死增加。99mTc-HEDP在缺血肾组织中的定位取决于肾损伤程度,轻度损伤时为正常的两倍,最严重缺血改变时增加至九倍。随着缺血损伤加重,积聚增加可持续更长时间。到一周时,所有组的肾功能均有明显恢复。99mTc-HEDP可能有助于评估缺血性损伤继发的肾衰竭。