Reduction of cerebrovascular reactivity during hypercapnia.
The effects on cerebral blood flow of alpha- or beta-adrenergic receptor stimulation of cerebral vessels were examined in 13 unanesthetized goats before and during hypercapnia produced by inhalation of 10% CO2 in air. This procedure increased the PCO2 from 34 to 52 and was accompanied by a fall in pH from 7.39 to 7.26. Electrical stimulation of the cervical sympathetic nerve and injections of norepinephrine and tyramine into the internal maxillary artery produced reductions in cerebral blood flow that were abolished or reduced in hypercapnia. The increase in cerebral blood flow in response to beta-adrenergic stimulation with isoproterenol was also reduced. Hypercapnia caused a similar depression of the constrictor and dilatory effects of the nonadrenergic drugs vasopressin and diazoxide. The results show a decreased response of cerebral vessels to adrenergic and nonadrenergic stimuli in hypercapnia. The findings do not suggest any difference between the refractoriness of cerebral vessels in hypercapnia and that described in other vascular beds.
D000818:Animals; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004558:Electric Stimulation; D005260:Female; D006041:Goats / Q000502:physiology*; D006935:Hypercapnia / Q000503:physiopathology*; D011941:Receptors, Adrenergic / Q000502:physiology; D012016:Reference Values; D012146:Rest; D013268:Stimulation, Chemical; D013564:Sympathetic Nervous System / Q000502:physiology; D014439:Tyramine / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology
D011941:Receptors, Adrenergic; D014667:Vasopressins; D014439:Tyramine