ABSTRACT
<p><b>OBJECTIVE</b>To investigate the influence of lipopolysaccharide (LPS) and burn sera on potassium channels (Kca) in smooth muscle cells of colon of guinea pig so as to elucidate the molecular mechanism of gastrointestinal motility dysfunction after severe burns.</p><p><b>METHODS</b>Single smooth muscle cells were isolated from the taenia coli of guinea pig with enzyme digestion. The standard patch clamp technique was employed to record the single KCa channel currents of smooth muscle cell after challenged by LPS and burn serum. Data were recorded and analyzed by P clamp 6.04 software, and the probability of open (PO), mean open time (OT), mean close time (CT) and current amplitude (CA) were determined. Subsequently, LPS in the concentration of 20, 40, 60, 80 and 100 mg/L, respectively, and normal serum and burn serum in the concentration of 10% were respectively added into medium to examine the influence of the two clamps and sera on the KCa activity.</p><p><b>RESULTS</b>In hyperkalemic solution, the KCa conductance of colonic smooth muscle cells of the guinea pig was (271 +/- 7) pS, indicating it was an ionic channel with high conductivity. Subsequent to depolarization of the membrane, inner-cellular calcium level was increased, and channel PO was also increased, which could be blocked by 1 mmol/L tetraethylammonium (TEA) outside the membrane chaff. As 40 mmol/L TEA inside the membrane chaff did not show such effect, it was proved to be KCa current. The activity of the channel as determined with two kinds of clamps was increased in a dose dependent manner with LPS challenge when the concentration of calcium was 0 mol/L. The KCa activity and PO of the channel was increased obviously when the concentration of LPS was above 40 mg/L (P < 0.05 or 0.01), and it could not be reversed after irrigation with non-LPS medium. By using the two kinds of patch clamps, the KCa were activated by burn sera, but not normal sera.</p><p><b>CONCLUSION</b>Both LPS and burn sera can lead to inhibition of the gastrointestinal motility by activation of KCa channels.</p>