Suk-Bae Moon, et al. lets, we could demonstrate that passage was maintained at that segment (data not shown). And since the mice sur- vived after 2 to 4 weeks after bypass operation, we could assume that passage of food material was maintained. We do not have a clear explanation for this phenomenon. A previous study, which used a transection and re-anasto- mosis model in a guinea pig, demonstrated that the MMCs were unable to pass through the suture line [13]. Also, the neuronal integrity is known to be essential for the prop- agation of the MMCs [14]. Therefore, due to the disrupted neuronal integrity by the anastomosis for bypass, we might assume that the MMCs at proximal segment could not pass through the anastomosis to the distal segment. Another possible explanation is the collision of the neuro- nal signals from the proximal segment and the bypass loop at the anastomosis site, causing offset of signals nec- essary to generate MMCs. In our experiment, MMCs could be detected in sites more distal to the anastomosis, indicat- ing that a new pacemaker site for MMCs appeared (data not shown). It is known that initiation and propagation of MMCs are dependent on the intrinsic enteric nervous system; MMCs continue to occur after extrinsic denervation and are blocked by nerve conduction blocker such as tetrodotoxin [15]. After 4 weeks of total bypass, MMCs proximal to the anastomosis (channel 1) disappeared and occasional un- coordinated contractions remained, which were thought to be the result of local reflex rather than true MMCs. The only possible explanation is that intact undisturbed con- tinuity of the intestinal tract with its intact neuronal circuit is necessary for the presence of MMCs. Slow waves, which arise from the ICC, are another sig- nificant component of the intestinal motility especially in the mouse ileum [16]. In order to determine whether changes in the slow waves were present in the bypass loop, we performed conventional intracellular recordings and c-kit immunohistochemistry. Our results indicated that slow wave and ICC remained unchanged in the bypass loop (data not shown). Thus, we could conclude that the slow wave was not responsible for the development of blind loop syndrome. This study has limitations in that the experiments were conducted in ex-vivo conditions. There may be doubts on 258 the relevance of the ex-vivo motor function to the in-vivo situations. However, although some of the classic works on the gastrointestinal motility had been performed with animals in-vivo [4,5], most of the studies on mouse MMC have been performed with reproducibility in ex-vivo con- ditions [14,15]. Certainly, the intestine in our model may be autonomically denervated extrinsically, but MMC is mainly dependent on intrinsic nervous system which re- mains intact in the undisturbed bowel segment ex-vivo. Moreover, with the explosive growth in both transgenic and genomic technology, the mouse is accepted as a useful model system for investigating motility of the mammalian gastrointestinal tract [7]. Also, in each bypass model, the MMCs showed constant changes compared to the control state and therefore extrapolation from the ex-vivo results to the in-vivo situation may be reasonable. In summary, after side-to-side partial bypass anasto- mosis in mouse ileum, changes in the MMCs, especially in the direction and contractile activity within the bypass loop were noted. These changes may account for the de- velopment of stasis of luminal contents and thereby blind loop syndrome. In the total bypass model, the propagation of MMCs was maintained for a period of time. This implies the beneficial role of side-to-side anastomosis with prox- imal loop ligation or Roux-en-Y type of bypass, and should be considered when bypass surgery has to be performed. CONFLICTS OF INTEREST No potential conflict of interest relevant to this article was reported. ACKNOWLEDGMENTS This study was supported by the Grant of Clinical Research Institute, Seoul National University Hospital, Seoul, Korea (No. 04-2007-074). thesurgery.or.kr