• Koichi Maruyama, Shinhiro Takeda, Takashi Hongo, Noriyuki Kobayashi, Chol Kim, and Ryo Ogawa.
• Department of Anesthesiology and Intensive Care, Nippon Medical School, Tokyo, Japan.
• J Nippon Med Sch. 2004 Feb 1;71(1):44-50.

AbstractClonidine premedication prevents tourniquet pain and reduces sympathetic nerve activity. We evaluated hemodynamic changes and catecholamine release following tourniquet deflation during spinal anesthesia in patients who received oral clonidine premedication. The final analysis included 24 otherwise healthy patients undergoing lower-limb surgery randomly assigned to two groups: those receiving approximately 5 micrograms/kg of oral clonidine 1 hr before anesthesia (clonidine group, n = 12), and those receiving no premedication (control group, n = 12). After lumbar anesthesia, a tourniquet was applied for approximately 60 minutes to each patient. Electrocardiogram, arterial blood pressure, and consumption of butorphanol for tourniquet pain were monitored. Blood samples were obtained at different times to measure serum concentration of catecholamine. In the clonidine group, mean blood pressure decreased from 87 +/- 7 mmHg at baseline to 65 +/- 10 mmHg after tourniquet deflation (P < 0.05). This peak reduction of mean blood pressure in the clonidine group was significantly lower than in the control group. After receiving clonidine premedication, the plasma noradrenaline concentrations in the clonidine group were significantly lower than those in the control group. Noradrenaline concentration increased in the control group from 162.3 +/- 89.2 pg/mL before tourniquet deflation to 199.3 +/- 95.7 pg/mL afterward (P < 0.01), but there was no significant change in noradrenaline concentration after tourniquet deflation in the clonidine group. We conclude that oral clonidine premedication exacerbated the reduction in mean blood pressure following tourniquet deflation by inhibiting noradrenaline release.

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