抄録
The purpose of this study was to examine input mechanism which is related to the bradycardia observed during artificial CO2 bathing in anesthesia rats. 12 male rats of the Wistar strain were used in the experiments. The rat was medicated with urethane anesthesia (1.39-1.60 g/kg). Arterial blood pressure, heart rate, tissue blood flow, pH, PaO2, PaCO2 and temperature of the immersed skin, and rectal temperature were continuously measured. Bath water exchanged for another, i. e. tap water (10-20 ppm CO2)into CO2 water (965-1400 ppm CO2) or vice versa, every about 30 min. Water temperature was controlled at 35°C. To confirm the effect of CO2 inhalation on the heart rate and blood gases during immersion, CO2-mixed gas (5% CO2, 20% O2, 75% N2) instead of fresh air was supplied into the face mask, and hemodynamic parameters and blood gases were measured. In the operation, a midline incision (about 2 cm) was made on the dorsal skin over the thoracic vertebrae (T2-T6), and the dura matter was exposed between T4 and T5 in 6 animals with above mentioned probes. No effect blood gas responses were observed in anesthetized rats during CO2-water immersion. In a mixture of 5% CO2 inhalation, HR and blood gas parameters were significantly increased on tap water and CO2-water. HR was significantly lower in CO2-water than in tap water at sham operated, but was roughly equal at spinal cord transaction. This results suggested that the expression of the bradycardia is not generated through chemoreceptors such as the carotid artery corpuscle. [Jpn J Physiol 54 Suppl:S244 (2004)]
