Atropine does not attenuate cerebral vasodilatation during hypercapnia.

To study the contribution of cholinergic nerves to cerebral vasodilation during hypercapnia, we blocked muscarinic cholinergic receptors with atropine. We used two new approaches. First, total and regional cerebral blood flow (CBF) were measured with microspheres. Second, efficacy and specificity of muscarinic blockade by atropine were examined using the cranial window method. In anesthetized cats we measured CBF with 15-micrometers microspheres six times during each experiment: during normocapnia (PCO2 = 32-34 Torr), moderate hypercapnia (PCO2 = 48-50 Torr), and severe hypercapnia (PCO2 = 61-64 Torr), before and after intravenous administration of vehicle or atropine (0.5 mg/kg). Hypercapnia produced graded increases in blood flow in all areas of the brain. Atropine did not attenuate increases in CBF during hypercapnia. We examined efficacy and specificity of muscarinic blockade by atropine using the cranial window method. Acetylcholine (10(-7) and 10(-6) M) and adenosine (10(-7) and 10(-5) M), dissolved in artificial cerebrospinal fluid, dilated pial arteries in a dose-dependent fashion. Intravenous administration of atropine attenuated vasodilation produced by acetylcholine but did not affect the response to adenosine. Thus atropine, at a dose that effectively blocked muscarinic receptors, did not attenuate the increase in CBF during hypercapnia. The study suggests that cholinergic nerves are not involved in steady-state cerebral vasodilatation during hypercapnia.