unlikely that the modest IABP-induced pulse pressure of only 24 ± 8 mm Hg would generate a dp/dt of 645 ± 64 mm Hg/s, particularly at the level of small cerebral arteries, and thus be enough to produce sufficient stretch to induce significant production of L-arginine in the small cerebral arteries. If the pulse pressure was not sufficient, then significant cerebral vasodilation would not be obtained to affect the SjvO 2 , and hence the IABP-induced pulsatility would be unable to ameliorate the impaired SjvO 2 . A similar study using a pulsatile system capable of producing a pulse pressure of 50 to 60 mm Hg 6 to mimic that produced by the natural heart would be needed to be able to definitely exclude or include the role played by pulsatility. The study only demonstrates that the modest IABP-induced pulsatility was not effective but by no means excludes the role pulsatility may have.3. It is widely known that during CPB the levels of circulating endogenous catecholamines including norepinephrine are increased. During systemic infusion of norepinephrine, increased electrical brain activity (consisting of increased low-voltage high-frequency waves and decreased high-voltage slow-frequency waves) suggestive of promotion of excitatory (N-methyl-D-aspartate?) receptor activation has been noted in nonischemic rabbits (unpublished observations of electroencephalograms concurrent to brain microdialysis studies), which may lead to Na + and Ca ++ influx. To maintain the normal Na + and Ca ++ transmembrane gradient, the demand for mechanisms to extrude them, which are highly oxygen consuming, will be increased. Therefore during late CPB the decreased SjvO 2 might be a manifestation of that increased oxygen extraction not counteracted by the anesthetics, pressures, or pulsatility used by the authors. The exact effect of increased circulating catecholamines during CPB on the cerebral vasculature is not known, but if it was equivalent to increased sympathetic activity, then vasoconstriction of small cerebral vessels would result with consequent decreased flow. 7 If both effects are operating, the development of decreased SjvO 2 over the first 20 minutes of perfusion and the return to normal after CPB, also in 20 or 30 minutes, are easily explainable.Norepinephrine determination with and without blockade in conjunction with metabolic studies across the brain in both groups might shed some light.
