Cortical nicotinamide adenine dinucleotide (NADH) kinetics in patients undergoing extracranial-intracranial bypass

Nicotinamide adenine dinucleotide (NADH) kinetics were measured in 76 cortical areas in 26 patients with transient ischemic attacks (TIAs) undergoing extracranial-intracranial bypass. Direct cortical stimulation was utilized to induce changes in surface fluorescence corresponding to a brief oxidation and reduction of mitochondrial NADH. Preoperative studies of cerebral blood flow in gray matter (CBF)g) demonstrated normal perfusion in 11 patients and ischemic changes ((CBF)g less than 43.5 ml/100 g/minute) in 15 patients. In 30 normally perfused areas within the craniotomy, the mean half-time for reduction (t1/2(red)) of cortical NAD was 21.5 +/- 2.6 seconds. In 39 ischemic areas, the mean t1/2(red) was 5.6 +/- 1.2 seconds. These rapid reduction rates were associated with supernormal overshoots of the base line indicative of a transient oxygen debt. Kinetic responses could not be elicited from 7 areas adjacent to foci of decreased attenuation on compound tomography. Bypass resulted in normalization of the t1/2(red) in 24 of 28 areas of ischemia. The dependence of NADH kinetics on blood flow through the graft was demonstrated in 15 of 19 areas of mild ischemia by the reapplication of a clip to the donor artery. It is concluded that persistent reversible abnormalities of cortical mitochondrial metabolism exit in a significant number of patients with a history of TIAs who are suitable candidates for bypass surgery. In such patients bypass may effectively augment the nutrient supply to meet the bioenergetic demands associated with increased electrophysiological activity.