Hypercapnia and stimulation of the substantia innominata increase rat frontal cortical blood flow by different cholinergic mechanisms.
This study was designed to further investigate in the rat how the cerebrovascular response to excitation of the projections from the substantia innominata (SI) to the frontal cerebral cortex was mediated. Local cortical blood flow (CoBF) (by helium clearance) and tissue gas partial pressures (pO2, pCO2) (indices of energy metabolic activity) were measured in the frontal cortex in unanesthetized adult Fischer rats in response to electrical stimulation of the SI and, for comparison, in hypercapnic conditions. SI stimulation and hypercapnia increased CoBF to a similar extent (+92% and +106%, respectively). Differences between the changes in tissue gas partial pressures under hypercapnia and SI stimulation suggest that different patterns of flow-metabolism coupling prevail in the mechanisms underlying the two cerebrovascular responses. Cortical pCO2 increased under hypercapnia, but decreased during SI stimulation, indicating that a 'vascular' mechanism (i.e. independent of energy metabolism activation) is at least partly responsible for the flow increase in the latter condition. However, cortical pO2 rose more under hypercapnia than during SI stimulation, suggesting that oxygen consumption, and hence energy metabolism, was increased in the latter case. The ability of the acetylcholine esterase inhibitor physostigmine and the muscarinic receptor antagonist scopolamine to modulate the responses was quantified. In both experimental conditions, CoBF changes were potentiated by 0.15 mg/kg/h physostigmine (by factors of about 2). In contrast, 1 mg/kg scopolamine reduced by 65% the frontal CoBF response elicited by SI stimulation but was without effect on the response to hypercapnia. Thus, although a cholinergic mechanism may be implicated in both responses, activation of muscarinic receptors appears to occur when the stimulation originates from the SI but not from the hypercapnia.
Laboratoire de Physiologie et Physiopathologie Cérébrovasculare, Faculté de Médecine Villemin, Paris, France.
F
F
Dauphin
P
P
Lacombe
R
R
Sercombe
E
E
Hamel
J
J
Seylaz
D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002540:Cerebral Cortex / Q000098:blood supply*; D002560:Cerebrovascular Circulation / Q000502:physiology; D004558:Electric Stimulation; D004562:Electrocardiography; D004734:Energy Metabolism / Q000187:drug effects; D006935:Hypercapnia / Q000503:physiopathology*; D008297:Male; D013058:Mass Spectrometry; D010101:Oxygen Consumption / Q000187:drug effects; D010275:Parasympathetic Nervous System / Q000502:physiology*; D010830:Physostigmine / Q000494:pharmacology; D051381:Rats; D011916:Rats, Inbred F344; D012601:Scopolamine / Q000494:pharmacology; D013377:Substantia Innominata / Q000502:physiology*
D002245:Carbon Dioxide; D010830:Physostigmine; D012601:Scopolamine