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利用全细胞膜片钳技术在急性分离的胃窦平滑肌细胞上记录离子电流的方法 ,探讨外源性不饱和脂肪酸是否参与低渗牵张加强毒蕈碱电流的过程。在豚鼠胃窦平滑肌细胞上膜电位被钳制在 - 2 0 0mV等渗状态时 ,5 0 μmol/L卡巴胆碱 (carbachol,CCh)引起的毒蕈碱电流 (ICCh)作为对照 ,发现低渗牵张可以使ICCh明显增加到对照的 2 2 6 0±2 1 0 %。当用含 5 μmol花生四烯酸 (arachidacid ,AA)、亚麻酸 (linoleicacid ,LA)或亚油酸 (oleicacid,OA)细胞外液灌流时 ,ICCh分别被抑制在对照的 3 8± 0 6%、3 5 2± 0 8%和 66 6± 0 6%。在这种情况下 ,低渗牵张刺激可以使ICCh分别增加到 10 6 0± 2 5 %、173 2± 6 8%和 2 2 2 1± 11 0 %。 5 μmol/LAA抑制低渗牵张增加的毒蕈碱电流 5 1 2± 3 8% ,而在等渗状态下抑制ICCh为 96 2± 1 6%。上述结果提示 ,不饱和脂肪酸中双键数目越多 ,抑制效应越强 ;但不饱和脂肪酸不参与低渗刺激加强毒蕈碱电流的过程。
Whole cell patch clamp technique was used to record ion current on acutely isolated gastric antral smooth muscle cells and to explore whether exogenous unsaturated fatty acids participate in hypotonic stretch to enhance muscarinic currents. When the membrane potential of guinea-pig antral gastric smooth muscle cells was clamped to-200mV, muscarinic currents (ICCh) induced by 50 μmol / L carbachol (CCh) Zhang can make ICCh significantly increased to the control of 2600 ± 2110%. ICCh was inhibited by 3 8 ± 0 6% of the control when perfused with 5 μmol of arachidacid (AA), linoleic acid (LA) or oleic acid (OA) , 3 5 2 ± 0 8% and 66 6 ± 0 6% respectively. In this case, hypotonic stretch stimulation can increase ICCh to 106 ± 2 5%, 173 ± 6 8% and 2 2 1 ± 110%, respectively. 5 μmol / LAA inhibited muscarinic currents increased by 51.2 ± 38% in hypotonic stretch and 96 2 ± 16% in isotonic conditions. The above results suggest that the greater the number of double bonds in the unsaturated fatty acids, the stronger the inhibitory effect; however, the unsaturated fatty acids are not involved in the hypotonic stimulation of muscarinic currents.