Hypercapnic blood flow reactivity not increased by α-blockade or cordotomy in piglets

We tested the hypothesis that differential sympathetic innervation explains the attenuated cerebral blood flow (CBF) response to hypercapnia (hyper) in forebrain (fb) compared with brain stem in 1- to 2-wk-old piglets. In pentobarbital sodium-anesthetized piglets, CBF (microspheres) was measured during hypocapnia, normocapnia (normo), and hypercapnia [arterial CO₂ partial pressure (Pa(CO)₂) of 25, 40, and 65 mmHg, respectively] in random sequence. After pretreatment values were obtained, piglets were randomized to undergo sham treatment (n = 5), high cervical spinal cord transection (n = 6), or pharmacological α-adrenergic blockade (prazosin 1 mg/kg + yohimbine 1 mg/kg, n = 6). After each experimental treatment, CO₂ reactivity was again measured. Before experimental manipulation, hypercapnic reactivity [(CBF(hyper) - CBF(normo))/(Pa(CO₂hyper) - Pa(CO₂normo))] in brain stem was approximately three times greater than in forebrain (e.g., sham; 3.6 ± 0.8 vs. 1.2 ± 0.3 ml · min^-1 · 100 g^-1 · mmHg^-1). Hypercapnic reactivity in forebrain was not increased by cord transection (1.4 ± 0.3 vs. 1.1 ± 0.2 ml · min^-1 · 100 g^-1 mmHg^-1) or α-blockade (1.6 ± 0.6 vs. 1.2 ± 0.4 ml · min^-1 · 100 g^-1 · mmHg^-1). Likewise, hypercapnic cerebral vascular resistance (CVR) was unchanged by experimental treatment (e.g., CVR(fb); cord transection 1.1 ± 0.1 vs. 1.0 ± 0.1; α-blockade 1.1 ± 0.2 vs. 1.0 ± 0.1 mmHg · ml^-1 · min^-1 · 100 g^-1). Hypocapnic vasoconstriction, however, was attenuated by both cord transection and α- blockade in forebrain and brain stem. We conclude that physiological stimulation of the noradrenergic component of the sympathetic nervous system does not explain regional differences in CBF reactivity during hypercapnia in 1- to 2-wk-old piglets. The sympathetic nervous system, however, may participate in hypocapnic vasoconstriction.