AIM To investigate the protective effects and mechanism of Diltiazem (Dil) on liver, pancreas and smallintestine in hemorrhagic-shock canine.METHODS The canines were bled to a mean arterial pressure (MAP) of 5.33kPa-6.67kPa for 30min toestablish the shock model. During the shock state, the dogs received either water-soluble calcium blocker Dilor saline solution. The MAP was kept at this level for 90min, then the total blood which was bled previouslywas reperfused. The total observation time of the experiment was 240min.RESULTS Dil could significantly increase MAP from 150min to 240min (P<0.01) and the activity ofsuperoxide dismutase (SOD) of pancreas tissue (P<0.01), and it could also decrease the content ofmalondialdehyde (MDA) in liver, pancreas and small intestine tissues (P< 0.01) and the activity of SOD ofthe liver and small intestinal tissues (P<0.01) in the canines. Electron microscopic data indicated that theultrastructures of liver, pancreas and small intestine tissues were normal in Dil group.CONCLUSION Dil can protect the structure and function of the liver, pancreas and small intestinal inhemorrhagic-shock canine.

Objective:　To study the mechanism of macrophage injury after trauma-hemorrhagic shock.　　Methods:　Wistar male rats underwent trauma (closed bone fracture) and hemorrhage (mean arterial blood pressure of 35 mm Hg±5 mm Hg for 60 minutes, following fluid resuscitation). Rats without trauma, hemorrhage or fluid resuscitation served as controls. Peritoneal macrophages were harvested at 6 hours and 1, 2, 3, 7 days after traumatic hemorrhagic shock to determine the effects of pertussis toxin (PTX, as a specific inhibitor to Giα) and cholera toxin (CTX, as a stimulant to Gsα) on macrophage-Ia expression and TNF-α production and levels of Giα and Gsα. 　　Results:　The macrophages from the injured rats revealed a significant decrease of Ia positive number and TNF-α release in response to LPS. With pretreatment with PTX 10-100 ng/ml Ia positive cells and LPS-induced TNFα production in both control and impaired macrophages populations were dose-dependently increased. Both macrophages populations were not responding to CTX treatment (10-100 ng/ml). Western blot analyses showed that the levels of Giα protein expression increased as much as 116.5%-148.8% of the control level from 6 hours through 7 days after traumatic hemorrhage. The levels of Gsα protein expression were reduced at 6 hours and decreased to the lowest degree; 36% of the control at day 1, began to return at day 2 and returned to the normal level at day 7, following traumatic hemorrhagic shock.　　Conclusions:　PTX-sensitive G-protein may participate in the modulation of macrophage-Ia expression and TNF-α release following traumatic hemorrhagic shock. Analyses of the alteration of Giα and Gsα protein expressions further supports the concept that G-protein is involved in trauma-induced macrophage signal transduction pathways.