Fig. 2. IP triggers the systemic elevation of agmatine and L-arginine level in rats. (A) The level of agmatine in the rat brain was significantly increased in the IP group during MCAO and at the early reperfusion time. The highest peak was noted in the IP group at 2 hr after injury. The level of agmatine was gradually reduced in the IP group at 23 hr of reperfusion. However, in the EC group, the agmatine level was gradually in the brain at 23 hr of reperfusion. (B) Three days before severe MCAO, experimental animals were subjected to 10-min MCAO. The level of agmatine was significantly increased in the ipsilateral and contralateral hemisphere after 10-min IP compared to normal control (NC). The level of agmatine was still intensified about 3.5 folds at 3 days after IP compared to the normal level of agmatine, but there was no significant difference between ipsilateral and contralateral hemisphere. (C) On the other hand, the level of agmatine in liver was significantly reversed after IP. 30 mins after IP, the level of agmatine was significantly reduced about 20% compared with NC. (D) The level of agmatine precursor, L-arginine, in the liver was significantly suppressed after IP compared with NC. (E) Simultaneously, the level of agmatine in plasma and brain was significantly increased at 30 mins after IP. The ratio of agmatine in the plasma was markedly increased about ten-fold at 30 min after IP (**p<0.05 vs. EC; ***p<0.01 vs. EC).
© Exp Neurobiol