Dysfunction of the anterior spinal arteries (ASAs) may induce paresis or paraplegia after thoracoabdominal aortic aneurysm or spine surgery. However, there have been no reports of the effects of CO2 and pH on ASAs. Information on these effects on ASAs might contribute to the perioperative management or critical care of spinal cord function. Thus, we investigated the effects of CO2 and pH on the vasomotor tone of ASAs and the third branch of the middle cerebral artery (bMCA). Prospective study of the effects of CO2 and pH on vasomotor response of porcine ASA and bMCA in vitro. University laboratories. Porcine heads and spinal cords obtained from a slaughterhouse. ASAs and bMCAs were isolated, and changes in the intraluminal region of these pressurized arteries ( approximately 80 mm Hg) were observed for 30 minutes after perfusion with a solution saturated with various concentrations of CO2 and pH. Respiratory acidosis (pH/Pco2 approximately 7.10-7.15/ approximately 60-80 mm Hg) constricted the ASAs, followed by a partial but gradual decrease in tone, whereas the bMCAs were exclusively dilated. The respiratory alkalosis (pH/Pco2 approximately 7.60/ approximately 20 mm Hg) did not influence ASA tone. Vasoconstriction of the ASAs induced by respiratory acidosis was abolished by removal of the endothelium, but not by N-nitro-L-arginine (1 microM). Respiratory acidosis dilated the ASAs in all preparations treated with ONO-3708 (1 microM), a specific thromboxane A2 receptor antagonist, and OKY-046 (1 microM), a specific thromboxane synthase inhibitor. Metabolic acidosis (pH/Pco2 approximately 7.10/ approximately 40 mm Hg) caused dilation of both bMCAs and ASAs, which was abolished by glibenclamide (1 microM). CO2-induced endothelium-dependent constriction in porcine ASAs through releasing thromboxane A2-like substance(s). Thus, hypercarbia might not be favorable for the perioperative or critical care management of spinal cord function during thoracoabdominal aortic aneurysm and spine surgery.