Acidosis is the most dangerous complication of subarachnoid hemorrhage (SAH). Although the carotid bodies (CBs) network is essential for pH regulation, neither binuclear neurons (BNN) nor their functions have been mentioned so far in the literature. The aim of this study was to investigate the crucial roles of mononuclear (MNN) or BNN in CBs on acidosis following SAH. Twenty-five hybrid rabbits were used. Five rabbits were used as a control group, six for sham, and the remaining 14 rabbits were used as the study group by injection of 1 mL of autologous arterial blood into the cisterna magna to produce SAH. Normal and degenerated MNN/BNN densities of CBs were counted by stereological methods. The mean blood pH values were: 7.362 +/- 0.041 in the control group; 7.324 +/- 0.064 in sham, 7.272 +/- 0.062 in the SAH group. The degenerated MNN and BNN values were 5 +/- 1/mm(3) and 9 +/- 3/mm(3) in the control group; 15 +/- 5/mm(3) and 22 +/- 6/mm(3) in sham, 965 +/- 113/mm(3) and 1532 +/- 176/mm(3) in the SAH group. Mean pH values were under 7.212 +/- 0.130 in animals with prominent degenerated BNN. The differences between MNN/pH changes were significant between the SAH and control groups (P < 0.005); whereas BNN/pH values were significant between the SAH and sham groups (pH < 0.005), SAH and control (P < 0.0001). BNN degeneration could result in more severe acidosis than MNN following SAH which has not been described so far.