| Abstract: | Objectives. In an attempt to develop new method of treating the end- or mid-stage pancreatic cancer, we exam-ined the effect of isr hemie re-perfusion injury plus particle embolism on the pathology and cell apoptosis of pancreat-ic cancer in Spragiue Dawely rats.Methods. 9 rr g dimethylbeneanthracine (DMBA) were implanted directly into the parenchyma of pancreatictail of Sprague-Dawely rats. After establishment of tumor, the inferior splenic artery, a main supplying vessel topancreatic tail was subjected to blockade and re-opening for 30 min separately, then embolism particles were in-fused via the artery. Mterwards, artery was ligated. Pathological changes and cell apoptosis indicators (AI) ofpancreatic cancer were observed by light microscopy and ISEL respectively 14 days after the operation.Results. The prevalence of pancreatic cancer among DMBA-implanted rats evaluated 3 months to 4 months af-ter implantation was 59%. The volumes of the tumor in positive control group (B), pancreatic ischemic group(C), pancreatic ischemic re-perfusion injury group (D) were significantly larger than pancreatic ischemicre-perfusion injury plus particle thrombus group (E) (P ＜ 0.01 ). The volumes of the tumor in groups D, E weresignificantly smalle than that in group C ( P ＜ 0.01 ) . There was a significant difference in tumor size betweengroup B and group C ( P ＜ 0. 01 ), but the difference was not significant between group D and group E ( P ＞ 0.05 ).There was a signifieant infiltration of tumor tissue in group B rats, but strong inflammatory reaction was not noted.In groups C, D, E a localized tumor growth was observed; infiltration of inflammatory cells and proliferation offibroblasts and connective fiber were obvious, and some of these fibers grew into cancer nests and separate the tu-mor. The above findings were most conspicuous in group E. There was a significant difference in AI betweengroup E (13.7 ± 1.5) and other groups (P ＜ 0. 01), with the difference being also significant between group C(4.34-2.4), D (8.5±1.1) andgroupB (1.2±0.8)(P ＜0.01), and between group C andgroup D (P ＜0.01 ) or between group D and group E ( P ＜ 0. 01 ). In the samples of group A, the apoptotic cells were not found.Conclusions. Pancreatic ischemic re-perfusion injury plus particle thrombus can cause significant infiltrationof inflammatory celts in tumor tissues thereby limiting its growth, and inducing cell apoptosis of pancreatic can-cer. This effect is ;uperior to either pancreatic ischemia alone or pancreatic ischemia plus re-perfusion injury.`` |
