Purpose: This study was performed to investigate whether therapeutic hypercapnia could attenuate systemic inflammatory responses in hemorrhagic shock in rats. Methods: Male Sprague-Dawley rats were mechanically ventilated and underwent pressure-controlled (mean arterial pressure: $38{pm}1$ mmHg) hemorrhagic shock. At 10 minutes after the induction of hemorrhagic shock, the rats were divided into the normocapnia ($PaCO_2$=35-45 mmHg, n=10) and the hypercapnia ($PaCO_2$=60-70 mmHg) groups. The $PaCO_2$ concentration was adjusted by using the concentration of inhaled $CO_2$ gas. After 90 minutes of hemorrhagic shock, rats were resuscitated with shed blood for 10 minutes and were observed for 2 hours. The mean arterial pressure (MAP) and the heart rate were monitored continuously, and the results of arterial blood gas analyses, as well as the plasma concentrations of interleukin (IL)-6, IL-10, and nitrite/nitrate were compared between the normocapnia and the hypercapnia groups. Results: The MAP and the heart rate were not different between the two groups. The plasma concentration of IL-6 was significantly lower in the hypercapnia group than in the normocapnia group (p<0.05). The IL-10 concentration was not different and the IL-6 to IL-10 ratio was significantly lower in the hypercapnia group compared to the normocapnia group. The plasma nitrite/nitrate concentration of the hypercapnia group was lower than that of the normocapnia group. Conclusion: Therapeutic hypercapnia attenuates systemic inflammatory responses in hemorrhagic shock.