To assess the feasibility of manipulating human cerebrovascular resistance with adenosine, we measured cerebral blood flow (CBF) by determining the initial slope (IS) of tracer washout 20-80 s after intracarotid 133Xe injection (standard IS) during sequential 3-min intracarotid infusions of (a) saline; (b) adenosine 1.2-mg bolus followed by an infusion of 1 mg/min (bolus + infusion); (c) saline; and (d) nicardipine (0.1 mg/min). During 133Xe washout, adenosine caused a rapidly clearing compartment. Therefore, tracer washout was also analyzed 5-25 s after injection (early IS). Nicardipine (n = 8) increased both standard IS (from 39+/-12 to 53+/-16 mL 100g.min(-1); P < 0.005) and early IS (from 40+/-9 to 55+/-20 arbitrary units; P < 0.02) to a similar degree. Adenosine bolus + infusion increased early IS (from 33+/-6 to 82+/-43 arbitrary units; P < 0.02) but did not increase standard IS (from 41+/-12 to 43 +/-16 mL 100g(-1) min(-1)). Standard and early IS values were then determined before and after adenosine delivered either by infusion alone (2 mg/min for 3 min, n = 5) or bolus alone (2 mg in 1 s, n = 3). Neither standard nor early IS changed after adenosine infusion alone. Early IS increased after adenosine bolus alone. Increase in early IS, but not standard IS, suggests a transient (<30 s) increase in CBF.
Implications: Intracarotid adenosine, in the 1- to 2-mg dose range, may cause a transient, but not a sustained, increase in cerebral blood flow. Intracarotid adenosine in such a dose range does not seem to be an appropriate drug for sustained manipulation of cerebrovascular resistance.