Migrating motor complex changes after side-to-side ileal bypass in mouse ileum ex-vivo: mechanism underlying the blind loop syndrome? / 대한외과학회지

PURPOSE: This study was intended to investigate the migrating motor complex (MMC) changes after ileal bypass in ex-vivo mouse models. METHODS: Partial (side-to-side) and total bypass (occlusion of proximal part of bypassed loop) were performed on ileums of female Institute of Cancer Research mice. After 2 and 4 weeks, the bypassed segments were harvested and MMCs were recorded at 4 different sites ex-vivo. Amplitude, duration, interval, direction of propagation, and the area under the curve (AUC) of MMCs were measured and compared to those of the controls. RESULTS: In control mice (n = 7), most MMCs propagated aborally (91.1%). After 2 weeks of partial bypass (n = 4), there was a significant decrease in both amplitude and AUC, and orally-propagating MMCs increased significantly (45%, P = 0.002). Bidirectional MMCs (originating in the bypassed loop and propagating in both directions) were also observed (10%). The amplitude of the MMCs remained decreased at 4 weeks after partial bypass (n = 4), and neither the AUC nor the direction of propagation showed significant changes compared to 2 weeks. Similarly, in the total bypass model, both the amplitude and AUC of the MMCs decreased significantly compared to controls. In contrast to partial bypass, 95% of the MMCs within the bypassed loop propagated aborally after 2 weeks (n = 6), which was similar to the control state. After 4 weeks (n = 5), however, MMCs either lost their temporal relationship or completely disappeared. CONCLUSION: The changes in propagation direction of the MMCs in the partially bypassed loop may contribute to stagnation of bowel contents and the development of blind loop syndrome.

Modulation of Inwardly Rectifying K+ Channel by Intracellular and Extracellular pH in Bovine Aortic Endothelial Cells

The effects of intracellular and extracellular pH on the inwardly rectifying K+ (IRK) channel of the bovine aortic endothelial cells (BAECs) were examined using whole-cell patch-clamp technique. The IRK current, efficiently blocked by Ba2+ (200microM), is the most prominent membrane current in BAECs, which mainly determines the resting membrane potential. The expression of Kir2.1 was observed in BAECs using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Intracellular alkalinization, elicited by the extracellular substitution of NaCl with NH4Cl (30 mM), significantly augmented the amplitude of IRK current. On the contrary, the amplitude of IRK current was attenuated by the Na-acetate (30 mM)-induced intracellular acidification. The changes in extracellular pH also closely modulated the amplitude of IRK current, which was decreased to 40.2+/-1.3% of control upon switching the extracellular pH to 4.0 from 7.4. The extracellular pH value for half-maximal inhibition (pK) of IRK current was 5.11. These results demonstrate that the activity of IRK channel in BAECs, probably Kir2.1, was suppressed by proton at both sides of plasma membrane.