THE FEASIBILITY OF INTRACAROTID ADENOSINE FOR THE MANIPULATION OF HUMAN CEREBROVASCULAR RESISTANCE

To assess the feasibility of manipulating human cerebrovascular resist ance with adenosine, we measured cerebral blood flow (CBF) by determin ing the initial slope (IS) of tracer washout 20-80 s after intracaroti d Xe-133 injection (standard IS) during sequential S-min intracarotid infusions of (a) saline; (b) adenosine 1.2-mg bolus followed by an inf usion of 1 mg/min (bolus + infusion); (c) saline; and (d) nicardipine (0.1 mg/min). During Xe-133 washout, adenosine caused a rapidly cleari ng compartment. Therefore, tracer washout was also analyzed 5-25 s aft er injection (early IS). Nicardipine (n = 8) increased both standard I S (from 39 +/- 12 to 53 +/- 16 mL . 100g(-1). min(-1); P < 0.005) and early IS (from 40 +/- 9 to 55 +/- 20 arbitrary units; P < 0.02) to a s imilar degree. Adenosine bolus + infusion increased early IS (from 33 +/- 6 to 82 +/- 43 arbitrary units; P < 0.02) but did not increase sta ndard IS (from 41 +/- 12 to 43 +/- 16 mL . 100g(-1). min(-1)). Standar d 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 bol us alone (2 mg in 1 s, n = 3). Neither standard nor early IS changed a fter adenosine infusion alone. Early IS increased after adenosine bolu s alone. Increase in early IS, but not standard IS, suggests a transie nt (<30 s) increase in CBF. Implications: Intracarotid adenosine, in t he 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 manipulat ion of cerebrovascular resistance.