EFFECT OF TRIS-(HYDROXYMETHYL)-AMINOMETHANE ON EXPERIMENTAL FOCAL CEREBRAL-ISCHEMIA

Systemic and focal cerebral acidosis is considered deleterious to cell metabolism and neuronal recovery. We investigated the immediate effec t of tris-(hydroxymethyl)-aminomethane (THAM), an alkalizing agent, on focal cerebral ischemia produced by occlusion of the left middle cere bral artery (MCA) in cats with systemic acidosis. Occlusion of MCA res ulted in prompt decreases in local cerebral blood flow of the ipsilate ral marginal and ectosylvian gyri from 47.7 ml/100 g per minute in con trol to 32.3 ml/100 g per minute and 8.3 ml/100 g per minute, respecti vely. In the control group, physiological saline was infused continuou sly and the treated group received 0.3 hi THAM to normalize systemic a nd focal cerebral acidosis. There were no significant changes in the s ystemic arterial pressure, arterial PO2 and PCO2 throughout the experi ments in the two groups. Arterial pH decreased from 7.42 to 7.30 in th e control, while it remained normal during THAM treatment. Extracellul ar pH of the marginal gyrus (peri-infarct zone) decreased from 7.39 to 6.87 with 6 h ischemia in the control group. In THAM infusion, extrac ellular pH was kept between 7.26 and 7.29, which was significantly hig her than the control group. THAM significantly decreased infarct volum e and lactate and water contents of the gray matter in the marginal gy rus at 6 h after occlusion. It is concluded that THAM infusion immedia tely after ischemia onset is considered effective in improving acidosi s at the site of ischemic penumbra and consequently reduces lactate pr oduction, brain edema, and infarct volume.