In hypovolemic shock, multiple organ failure is caused by translocation of endotoxins and microorganisms from the ischemic gut mucosa. Therefore, much attention has been paid to the gut mucosa oxygenation in shock resuscitation. The current guidelines on cardiopulmonary resuscitation restrain the use of sodium bicarbonate due to paradoxical intracellular acidosis. Because THAM, CO2-consuming agent, does not produce CO2 and induce intracellular acidosis, THAM has been known as a effective buffering agent. This study was purposed to investigate the effect of THAM and sodium bicarbonate on the gut mucosa oxygenation in cats which were in hemorrhagic shock and resuscitation.

18 anesthetized cats were subjected to hemorrhage to decrease the mean arterial blood pressure to 35-45 mmHg and this blood pressure was maintained for 120 minutes. After 90minutes, we infused 1.945% hypertonic saline, 2.8% sodium bicarbonate and 0.3M THAM as same volume and osmolality. Mean arterial pressure(MAP), mesenteric arterial-venous pH differences[pH(a-v)], mesenteric venous oxygen tension(PvO2), mesenteric arterial-venous carbon dioxide tension differences[P(v-a)CO2], mesenteric arterial-venous lactate differences[Lactate(v-a)] were measured 1, 5, 15, 30 minutes after drug infusion and 30, 60 minutes after reperfusion.

There were no statistical significances in MAP, pH(a-v), PvO2, Lactate(v-a) among the three groups. There were significant differences in P(v-a)CO2 and ETCO2 between sodium bicarbonate group and THAM group.

This study suggest that THAM and sodium bicarbonate do not have significant effects on the tissue oxygenation and hemodynamic improvement in hypovolemic shock. We suppose that THAM does not produce carbon dioxide but may correct intracellular acidosis.