Changes of extracellular signal-regulated kinase activity following hemorrhagic shock and its role in regulation of vascular reactivity

Abstract

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. Key words: Hemorrhagic shock; Extracellular signal-regulated kinase; Vascular reactivity