Background: Cerebral blood flow (CBF) decreases over time in dogs and goats during volatile anesthesia. In the current study, we determined CBF during administration of isoflurane for 4 h in cynomolgus monkeys. In addition, we determined if nitric oxide (NO) contributes to cerebrovascular tone during isoflurane anesthesia by determining the CBF (microsphere) response to inhibition of NO synthase with N(ω)-nitro-L-arginine methyl ester (L-NAME). Methods: CBF was measured in five monkeys anesthetized with isoflurane (1.0% end-tidal). After 4 h of isoflurane (1.0% = 1 MAC), the effects of intravenous L-NAME (60 mg/kg over 10 min) followed by intravenous L-arginine (600 mg/kg over 10 min) on CBF were measured at constant cerebral perfusion pressure and arterial carbon dioxide tension. Results: CBF was unchanged over time (4 h) in cerebellum but increased by 50 ± 18% in both forebrain and hindbrain (P < 0.05). CBF decreased by 41-48% (P < 0.05) 20 min after L-NAME in forebrain, cerebellum, and hindbrain, at which time brain NO synthase activity was less than 10% of baseline. Twenty minutes after L- arginine, CBF was increased in cerebellum by 32 ± 8% and in forebrain by 41 ± 9% (P < 0.05). The cerebral metabolic rate of oxygen consumption was unaffected by time or by L-NAME or L-arginine. Conclusions: These data demonstrate that CBF increases over time during isoflurane anesthesia in primates. Tonic production of NO contributes to control of CBF in primates during isoflurane anesthesia. Increased CBF by L-arginine after L-NAME supports the hypothesis that L-NAME decreases CBF via a mechanism requiring NO synthesis.
- Anesthetics, volatile: isoflurane
- Blood vessels, vasoconstriction: N(ω)-Nitro-L-arginine methyl ester
- Brain: cerebral blood flow; cerebral metabolic rate of oxygen consumption
- Nitric oxide
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine