Effects of Intraluminal Irradiation with Holmium-166 for TIPS Stenosis (32P) (8) or 166Ho (9), for an arterial stent during or after angioplasty could significantly reduce the arterial myointi- mal hyperplasia and as a result, increase the original luminal patency. Our experimental study, based on the similar proliferating processes between neointimal hyperplasia and PIH, showed that the intraluminal irradia- tion using 30 Gy 166Ho during TIPS procedures significantly reduced PIH in a swine model. The standard local radiation dosages for inhibiting the proliferative process in various settings have not been established. In a previous experimental study with the various activity levels (0.15 23 Ci) of 32P, the dose- related effects of the radiation source showed differential response to the doses of continuous irradiation (the intermediate activity level showed a more severe neointi- mal response and greater luminal narrowing than that in the nonradioactive stents), that is, a non-linear relation, and this suggested a complex biological interaction of endovascular radiation and vascular repair after stent placement (10). Furthermore, the excess dosage of irradia- tion is assumed to lead to adverse effects such as extensive parenchymal injury as well as aggravation of thrombosis by the increased fibrin deposits (14). In this experiment, an absorbed radiation dose at the luminal surface of 30 Gy with 4.5 minutes of dwell time was used, and this radiation dose was thought to be a clinically applicable maximum therapeutic dosage for vascular irradiation therapy (15, 16). This dosage was higher than the common dosage (less than 20 Gy) used in neointimal hyperplasia (7, 9, 11). Consequently, the use of this protocol did not induce the radiation-associated changes such as endothelial prolifera- tion or atypical fibroblasts in the vascular structures in any cases, indicating there was acceptable tissue compatibility to a high dosage of 166Ho. An ideal isotope for brachytherapy should have a high specific activity with short range for avoiding unnecessary irradiation to the adjacent normal tissue, and also achiev- ing a uniform dose distribution over the treated area is a must. To date, 32P has been the most frequently used radionuclide due to its relatively short half-time of 14.3 days, its limited range of 3 4 mm in tissue and no gamma radiation (8, 11). In comparison with 32P, the 166Ho used in this trial is another beta emitter with a specific activity of 7.4 GBq mg 1, a short physical half-life of 26.8 hours and a short (1 2 mm) range of the absorbed -particles distrib- ution. These data suggest that 166Ho is superior to 32P from the view of both the physical half-life and the activity range. A few recent studies (9, 16, 17) that were performed in vitro or in vivo with using 166Ho as the radiation source supported this suggestion. Joh et al. (16) showed the 166Ho administered through a balloon Korean J Radiol 8(2), April 2007 angiocatheter in a tissue equivalent solid water phantom delivered an adequate dose within a clinically allowable dwell time, and so this avoided unnecessary irradiation of the normal tissue. Hong et al. (17) demonstrated that 166Ho- DTPA in vivo showed simple radiolabelling, high radiochemical stability (> 98%) and rapid urinary excretion. Kim et al. (9) delivered 20 Gy of 166Ho in a porcine coronary stent restenosis model and the irradiated group demonstrated a significantly decreased stenosing area compared to the control group. Pig is highly useful as an animal model for evaluating new techniques related to human TIPS, and pigs have been used in the previous related studies (18 20). Further, the liver vascular anatomy of pig is similar with human. Also, PIH in a swine model demonstrated remarkable similarities in the histologic components and development sites to that of human. On the other hand, to mimic the human hemodynamic situations and to create the chronic portal hypertension in animal models, various embolic agents such as gelatin foam, polyvinyl alcohol, stainless steel coils and ethiodized oil have been applied (18, 20, 21). Unfortunately, chronic portal hypertension was success- fully created in a dog model only, not in a swine model, in which the increased portal pressure was transient and not prolonged (20, 21). In our study, the portal hypertension was artificially induced via intraportal injection of a NBCA and lipiodol mixture (1:3); this is one of the most common embolic materials used in other various procedures, includ- ing treating vascular malformations and prior to lobectomy (22, 23), and administering this material was done in a single session. Our previous pilot study that used two pigs was performed to evaluate the portal pressure after NBCA embolization, and the results showed that the portal hypertension was maintained for two weeks. Despite of the small number of subjects as a limitation, from the results of this pilot study, we can propose the possibility of NBCA embolization for creating stable portal hyperten- sion in a swine model. Based on the pilot study, all the animals of this experiment were assumed to maintain increased peripheral portal venous pressure, and this resulted in preferential blood flow into the TIPS tract rather than into hepatic sinusoids, at least for two weeks. The follow-up period in this study was determined as two weeks because the pig model provided a highly accelerated rate of shunt stenosis within two to four weeks after TIPS creation when compared to human (shunt stenosis developed two weeks later in human) according to Kichikawa et al. (18) and Lessie et al. (11). In our study, the more rapid development of PIH in the control group (within 2 weeks) may be due to that anticoagulation therapy wasn’t given, the stent characteristics and the 133