OBJECTIVE: To evaluate the impact of energy and access methods on extrahepatic tumor spreading and the ablation zone in an ex vivo subcapsular tumor mimic model with a risk of extrahepatic tumor spreading. MATERIALS AND METHODS: Forty-two tumor-mimics were created in bovine liver blocks by injecting a mixture of iodine contrast material just below the liver capsule. Radiofrequency (RF) ablations were performed using an electrode placed parallel or perpendicular to hepatic surface through the tumor mimic with low- and high-power protocols (groups 1 and 2, respectively). Computed tomography (CT) scans were performed before and after ablation. The presence of contrast leak on the hepatic surface on CT, size of ablation zone, and timing of the first roll-off and popping sound were compared between the groups. RESULTS: With parallel access, one contrast leak in group 1 (1/10, 10%) and nine in group 2 (9/10, 90%) (p < 0.001) were identified on post-ablation CT. With perpendicular access, six contrast leaks were identified in each group (6/11, 54.5%). The first roll-off and popping sound were significantly delayed in group 1 irrespective of the access method (p = 0.002). No statistical difference in the size of the ablation zone of the liver specimen was observed between the two groups (p = 0.247). CONCLUSION: Low-power RF ablation with parallel access is proposed to be effective and safe from extrahepatic tumor spreading in RF ablation of a solid hepatic tumor in the subcapsular location. Perpendicular placement of an electrode to the capsule is associated with a risk of extrahepatic tumor spreading regardless of the power applied.
Animals ; Catheter Ablation ; Electrodes ; Iodine ; Liver ; Liver Neoplasms, Experimental ; Methods ; Neoplasm Seeding

Telmisartan is an angiotensin-II receptor blocker and acts as a selective modulator of peroxisome proliferator-activated receptor gamma (PPARγ). Several studies have demonstrated that telmisartan ameliorates depression and memory dysfunction and reduces brain inflammation. We hypothesized that the beneficial effects of telmisartan on brain could be due to modulation of the blood-brain barrier (BBB) function. Here, we examined the effect of telmisartan on tumor necrosis factor alpha (TNF-α)-induced expression of intercellular adhesion molecule 1 (ICAM-1) which plays an important role in leukocyte transcytosis through the BBB. Telmisartan blocked TNF-α-induced ICAM-1 expression and leukocyte adhesion in U87MG human glioma cells but showed no effect on human brain microvascular endothelial cells. In U87MG cells, a PPAR antagonist, GW9662 did not block the effect of telmisartan on ICAM1 expression but rather potentiated. Moreover, GW9662 caused no change in TNF-α-induced ICAM-1 expression, suggesting no implication of PPARγ in the telmisartan effect. Further studies showed that telmisartan blocked TNF-α-induced activation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), p38, and nuclear factorkappa B (NF-κB). In contrast, inhibitors of JNK, ERK1/2 and NF-κB but not p38, blocked ICAM-1 expression induced by TNF-α.Thus, our findings suggest that the beneficial effect of telmisartan is likely due to the reduction of astrocytic ICAM1 expression and leukocytes adhesion to astrocytes, and that this response was mediated by the inhibition of JNK/ERK1/2/NF-κB activation and in the PPAR-independent manner. In conclusion, this study enhances our understanding of the mechanism by which telmisartan exerts the beneficial brain function.