[Role of arterial myo-endothelial gap junction on the vascular contractile reactivity following hemorrhagic shock in rats].

OBJECTIVE

To observe the role of arterial myo-endothelial gap junction (MEGJ) on endothelium-dependent and independent vascular contractile reactivity following hemorrhagic shock in rats.

METHODS

Fifty-six SD rats were randomly divided into noradrenaline (NE) group and myricetin group. NE group was further divided into 5 subgroups: normal control group, 0, 0.5, 1 and 2 hours after hemorrhagic shock groups. Myricetin group was further divided into 7 subgroups: normal control group, 0, 0.5, 1, 2, 3 and 4 hours after hemorrhagic shock groups. Superior messenteric artery (SMA) was used to compare the changes in vascular responsing to NE or myricetin with or without 18alpha-glycyrrhetinic acid (18alpha-GA).

RESULTS

Compared with normal control group, the reactivity of SMA rings to NE was significantly increased at 0 and 0.5 hour after shock and then decreased at 1 hour and 2 hours after shock. 18alpha-GA had no effect on SMA constriction induced by NE. The reactivity of SMA rings to myricetin was increased at 0, 0.5, 1 hour and 2 hours after shock, and it reached the peak at 2 hours, then it significantly decreased at 3 hours and 4 hours after shock. 18alpha-GA antagonized SMA constriction induced by myricetin. The antagonizing effect on myricetin in shock 1, 2 and 3 hours groups was more obvious than that in the other groups.

CONCLUSIONS

At the early stage after hemorrhagic shock, the endothelium-dependent and independent vascular contractile response show a compensatory increase. The endothelium-independent contractile response is significantly decreased at 1 hour and 2 hours after shock, and the endothelium-dependent contractile response is significantly decreased at 3 hours and 4 hours after shock. MEGJ plays an important role in endothelium-dependent vascular contractile reactivity following hemorrhagic shock.