Effects of carbon dioxide on hindlimb vascular resistance in the acute spinal cat.
A cervical (C2) spinal section was carried out in anaesthetized, neuromuscularly blocked cats and the vascularly isolated hindlimbs were independently perfused at constant flow with blood taken from the abdominal aorta. One leg was denervated by sectioning the lumbar sympathetic chain. The animals were hyperventilated in 100% O2 and 5% or 10% CO2 in O2 was administered without altering the rate or tidal volume of the respirator. Increasing paCO2 (mm Hg) from 16.36 +/- 0.84 to 37.48 +/- 1.03 and to 62.23 +/- 2.23, induced a significant early vasoconstriction (P1) followed by a later more prolonged vasoconstriction (P2) in the innervated leg, while only a significant P2 response was present in the sympathetically denervated leg. A significant increase in systemic arterial pressure (SAP) was also observed with no change in heart rate (HR). After bilateral adrenalectomy increasing paCO2 from 17.16 +/- 0.66 to 37.96 +/- 1.21 and to 64.20 +/- 1.55, induced smaller but significant P1 and P2 responses in the innervated leg but only a significant P2 response was induced in the denervated leg. These results suggest that the early vasoconstriction was mainly due to activation of lumbar sympathetic neurons, while the late vasoconstriction was caused by the release of adrenal catecholamines and possibly other unidentified vasoconstrictor substances.
D000280:Administration, Inhalation; D000315:Adrenalectomy; D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology*; D002415:Cats; D003655:Decerebrate State / Q000503:physiopathology*; D006614:Hindlimb / Q000098:blood supply*; D008297:Male; D014655:Vascular Resistance / Q000187:drug effects*
D002245:Carbon Dioxide