Does clonidine bolus alter jugular bulb oxygen saturation and carbon dioxide reactivity during desflurane anesthesia?
Clonidine supplementation during desflurane anesthesia causes cerebral artery constriction but preserves carbon dioxide reactivity.
Background: The -agonist clonidine is an adjunct in general anesthesia. Clonidine constricts cerebral arteries and decreases cerebral blood flow (CBF), but does not alter cerebral metabolic rate (CMR). Thus cerebral ischemia is possible due to CBF/CMR imbalance. This study was designed to prove the effects of clonidine bolus up on CBF and reactivity in desflurane anesthesia. Methods: Thirty patients were divided into a clonidine group (n = 15) and a control group (n = 15). Anesthesia was induced with thiopental and pancuronium, and maintained with 50% / Desflurane. The jugular bulb was cannulated to measure jugular bulb oxygen saturation (). MAP and were measured after induction, after clonidine (/kg) or normal saline administration and during hyperventilation. Results: After clonidine administration, MAP decreased from 95.7 9.8 mmHg to 81.1 6.3 mmHg and was 79.9 5.0 mmHg during hyperventilation. In the control group, the corresponding MAP values 95.7 9.8 mmHg, 81.1 6.3 mmHg and 79.9 5.0 mmHg. After clonidine administration, was decreased from 84.7 3.7% to 81.1 5.2%, and was 71.5 8.4% during hyperventilation (P = 0.003, P = 0.000) and in control group, there were 95.7 9.8%, 81.1 6.3% and 79.9 5.0%, respectively. reactivity was expressed as a change of per unit change of , 1.15 1.19%/mmHg versus 1.43 0.98%/mmHg (P = 0.49). Conclusions: During desflurane anesthesia, clonidine-induced constriction of the cerebral arteries was demonstrated but reactivity was well preserved.
In et al. (2003) studied this question.