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目的 探讨门静脉高压症鼠离体肠系膜小动脉对去甲肾上腺素反应变化的细胞内机制。方法 观察门静脉部分缩窄所致的肝前型门静脉高压症组（６７ 例）（ｐｏｒｔａｌｖｅｉｎ ｓｔｅｎｏｓｉｓ，ＰＶＳ）和手术对照组（６４ 例）（ｓｈａｍｏｐｅｒａｔｅｄ，Ｓｈａｍ）大鼠离体肠系膜小动脉对去甲肾上腺素的反应，以及Ｌ型钙离子通道阻断剂（ 硝苯吡啶）和蛋白激酶Ａ抑制剂（ＲｐｃＡＭＰＳ） 对去甲肾上腺素反应的影响。 结果 与Ｓｈａｍ 鼠〔ｐＤ２（ －ｌｏｇＥＣ５０） ＝ ６－３７±０－０５〕相比，ＰＶＳ鼠血管（ｐＤ２ ＝６－１５±０－０５） 对去甲肾上腺素反应降低（Ｐ＜０－０５） 。Ｌ型钙离子通道阻滞剂和蛋白激酶Ａ抑制剂可逆转ＰＶＳ鼠对去甲肾上腺素的低反应（硝苯吡啶：Ｓｈａｍ ５－７７ ±０－０８ ，ＰＶＳ５－７６±０－０６ ；ＲｐｃＡＭＰＳ：Ｓｈａｍ ６－３６ ±０－０５ ，ＰＶＳ６－３８±０－０８ ，Ｐ＞０－０５） 。结论 环磷酸腺苷升高，通过蛋白激酶Ａ途径抑制Ｌ型钙离子通道的钙离子内流导致门静脉高压症鼠动脉对去甲肾上腺素的低反应
Objective To investigate the intracellular mechanism of the changes of isolated mesenteric arterioles in response to norepinephrine in portal hypertensive rats. Methods The isolated portal mesenteric arterioles (PVS) and sham-operated (Sham-operated) rats were divided into two groups: Norepinephrine, and the effects of L-type calcium channel blockers (nifedipine) and protein kinase A inhibitors (rp-cAMPS) on norepinephrine responses. Results Compared with Sham mice [pD2 (-logEC50) = 6-37 ± 0-05), PVS mice (pD2 = 6-15 ± 0-05) had lower norepinephrine response (P <0-05) . L-type calcium channel blockers and protein kinase A inhibitors reversed the low response to norepinephrine in PVS mice (nifedipine: Sham 5-77 ± 0-08, PVS 5-76 ± 0-06; Rp-1 cAMPS: Sham 6-36 ± 0-05, PVS6-38 ± 0-08, P> 0-05). Conclusions Elevated cyclic AMP, inhibition of calcium influx in L-type calcium channels via protein kinase A pathway leads to low response of norepinephrine to arteries of portal hypertension rats