中文摘要：

目的观察失血性休克后细胞外信号调节激酶（ERK）的活性变化及其对休克血管反应性的影响。方法采用72只健康成年sD大鼠，复制失血性休克模型，观察休克后不同时期大鼠肠系膜上动脉（SMA）血管组织中ERK活性的变化，同时测定血管反应性的变化；并观察改变ERK活性对休克血管反应性的影响。结果失血性休克后，大鼠肠系膜上动脉血管组织中ERK活性升高，在休克30min时达到最高点（为正常组的2．6倍，P〈0．01），随着休克时间的延长，ERK的活性逐渐降低，在休克后2h降低为正常对照组的56．1％（P〈0．05）；失血性休克大鼠的血管反应性变化也呈现休克早期升高、休克晚期降低的趋势。给予An出I处理可使休克2h血管组织内ERK活性升高为休克2h组的1．9倍（P〈0．01），同时休克血管反应性明显升高，而ERK的抑制剂PD98059可拮抗AngII诱导ERK活性增加和血管反应性升高的作用。结论ERK在失血性休克大鼠血管反应性调节中具有重要作用。

英文摘要：

Objective To investigate the changes of extracellular signal-regulated kinase （ERK） activity and its role in regulation of vascular reactivity following hemorrhagic shock. Methods In 72 SD rats, the hemorrhagic shock model was adopted, the activity of ERK in the superior mesenteric artery （SMA） of rats after shock was measured, and the vascular reactivity of SMA after shock was observed. The effect of altered ERK activity on the regulation of vascular reactivity of SMA after shock was investigated. Results After shock, the activity of ERK in SMA was increased about 2. 6 folds as compared to normal group （P 〈0. 01 ） , and it reached the peak at 30 min after shock. The activity of ERK 2 h after shock was reduced to 56. 1% of normal group （P 〈 0.05 ）. At the same time, the vascular reactivity of SMA was also increased at early shock and decreased at late shock. Angiotensin II （AngII） increased the activity of ERK to 1.9 folds as compared to shock 2-h group （P 〈0. 01 ）, and AngII also increased the vascular reactivity of SMA at 2 h shock. PD98059, the ERK antagonist, antagonized the effect of AngII on ERK activity and vascular reactivity of the SMA. Conclusion ERK may play an important role in the regulation of vascular reactivity after hemorrhagic shock.