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Effects of CO2 to modulate the norepinephrine constrictor response in isolated perfused rabbit carotid artery.

It has been suggested that large cerebral arteries contribute to cerebral vascular resistance and thus participate actively in the regulation of cerebral blood flow (CBF) during changes in arterial carbon dioxide tension (PCO2). In order to test this hypothesis, 3-cm segments of carotid artery from adult male rabbits were studied. The segments were mounted in a chamber with constant surrounding pressure and temperature and perfused at constant pressure. Inflow pressure, outflow pressure, and outflow rate were measured and values of resistance (R) were calculated before (C) and after stimulation with two sequential norepinephrine concentrations: 4 X 10(-6) M (NE1), 1 X 10(-5) M (NE2). During each sequence, the PCO2 of the surrounding and perfusion media were held equal and constant at one of four levels. The following mean R values were obtained: (table; see text) Symbols (*) represent significance (p less than 0.05) between the indicated R and the corresponding normocapnic (PCO2 = 35 mm Hg) R. Hypercapnia (PCO2 = 61 mm Hg) enhanced the response to both NE1 and NE2. Moderate hypocapnia (PCO2 = 27 mm Hg) had no effect. These studies support the claim that large cerebral arteries contribute to CBF regulation during PCO2 changes. However, the effect of large cerebral arteries may not be significant during PCO2 variations of less than 20 mm Hg.