Propofol anesthesia enhances the pressor response to intravenous ephedrine

The induction of anesthesia with propofol is often associated with a decrease in arterial blood pressure (BP). Although vasopressors are sometimes required to reverse the propofol-induced hypotension, little is known about the effect of propofol on these drugs. We studied the effects of propofol and sevoflurane on pressor response to i.v. ephedrine. Thirty adult patients were randomly assigned to one of two groups. In the Propofol group (n = 15), patients received propofol 2.5 mg/kg i.v. for induction followed by 100 microg x kg(-1) x min(-1) i.v. for maintenance. In the Sevoflurane group (n = 15), anesthesia was induced with sevoflurane 3%-4% in oxygen and maintained with sevoflurane 2% in oxygen. All patients in both groups received ephedrine 0.1 mg/kg i.v. before and after the anesthetic induction. Ephedrine increased the heart rate significantly (P < 0.05) in awake patients in both study groups. In contrast, there was no increase in heart rate after the ephedrine administration under propofol or sevoflurane anesthesia. In awake patients, transient increases in mean BP were observed after i.v. ephedrine in both groups. In the Propofol group, 2 min after the administration of ephedrine, mean BP increased 16% +/- 10% under anesthesia but increased only 4% +/- 6% when the same patients were awake. The magnitudes of the pressor responses to ephedrine during propofol anesthesia were significantly greater (P < 0.05) than during the awake state. However, ephedrine 0.1 mg/kg i.v. showed no significant increases in BP during sevoflurane anesthesia. We conclude that propofol, not sevoflurane, anesthesia augments the pressor responses to i.v. ephedrine. IMPLICATIONS: The effect of anesthetics on vasopressor-mediated cardiovascular effects is poorly understood. We evaluated the pressor response to ephedrine during propofol or sevoflurane anesthesia. Our study suggests that anesthesia-induced hypotension may be easier to reverse with ephedrine during propofol anesthesia than during sevoflurane anesthesia.     

Oral clonidine preanesthetic medication augments the pressor responses to intravenous ephedrine in awake or anesthetized patients

To evaluate the possible interaction between clonidine and ephedrine, the authors studied hemodynamic responses to intravenous ephedrine in 80 patients who received either clonidine pre-anesthetic medication of approximately 5 micrograms.kg-1 orally (n = 40) or no medication (n = 40). The patients were studied while they were either awake (n = 40) or anesthetized with enflurane and nitrous oxide in oxygen (n = 40). Hemodynamic measurements were made at 1-min intervals for 10 min after ephedrine 0.1 mg.kg-1 was injected as a bolus. Although the responses to ephedrine were always greater in anesthetized patients, the magnitudes of mean blood pressure increases in patients who received clonidine (10 +/- 8% for awake and 27 +/- 11% for anesthetized subjects, mean +/- standard deviation [SD]) were significantly greater (P less than 0.05) than in patients not receiving clonidine (4 +/- 5% for awake and 17 +/- 11% for anesthetized subjects). The enhanced pressor responses to ephedrine observed in both awake and anesthetized patients in the presence of clonidine may be attributed to increased catecholamine storage at sympathetic nerve endings due to clonidine, enhanced sensitivity of tissue receptors to which ephedrine binds, potentiation of alpha-adrenoceptor mediated vasoconstriction of both agents, or all of these. It is concluded that oral clonidine preanesthetic medication of 5 micrograms.kg-1 does augment rather than attenuate the pressor responses to intravenous ephedrine in patients both prior to and during general anesthesia.     

Prone position results in enhanced pressor response to ephedrine compared with supine position during general anesthesia

Study ObjectiveTo elucidate and compare the pressor response to ephedrine in the prone or supine position during general anesthesia (GA).DesignProspective cohort study.SettingDepartment of General Surgery or Spine Surgery, Zhongda Hospital, Southeast University, Nanjing, China.PatientsFifty-six patients who were scheduled to undergo elective surgery in the supine or prone position (n = 28 each) and using a generic GA protocol.InterventionsDuring surgery, the patients received intravenous (IV) ephedrine when their systolic blood pressure (SBP) decreased to 90 to 110 mm Hg.MeasurementsHemodynamic changes were measured at 1-minute intervals for 10 minutes and were compared with baseline.Main ResultsForty-nine patients (23 in the prone position and 26 in the supine position) completed the study. There were no significant differences between the groups with regard to demographic characteristics, hemodynamic parameters, end-tidal concentration of sevoflurane, and dose of propofol and remifentanil (all P> .05). After the bolus injection of ephedrine, a significant increase in SBP was observed in both groups compared to baseline, but the duration and magnitude of the increase in SBP were longer and greater in the prone position than in the supine position. The magnitude of increase of the mean blood pressure was significantly greater in the prone position compared to the supine position at 2 to 7 minutes after ephedrine injection. Ephedrine could cause significant increase in diastolic blood pressure 2 minutes after IV injection, which could last until at least 9 minutes in the prone position group compared to only for 5 minutes in the supine position group (all P< .05).Conclusion:Compared to the supine position, the prone position could augment the pressor response to IV ephedrine during GA. Further studies are recommended to identify its association with other confounding factors such as surgery type or duration, patient history of cardiovascular disease, or patient hydration status.     

辅用右美托咪定全麻诱导对麻黄碱升压效应的影响

目的观察辅用右美托咪定全麻诱导对麻黄碱升压效应的影响。方法择期行腹腔镜胆囊切除术患者44例,年龄18~65岁,随机分为生理盐水组(N组)和右美托咪定组(D组)。D组麻醉诱导前泵注右美托咪定0.8μg/kg,15min后改为0.4μg·kg-1·h-1维持,同时开始麻醉诱导和气管插管,插管后5min给予麻黄碱0.1 mg/kg。N组诱导前以同样方式泵注生理盐水,余同D组。记录泵注右美托咪定或生理盐水前(T0)、麻醉诱导前(T1)、插管即刻(T2)、插管后2min(T3)、给麻黄碱即刻(T4)及之后2min(T5)、5min(T6)、10min(T7)、15min(T8)的SBP、DBP和HR。结果与T0时比较,T2时N组SBP、DBP明显升高,HR明显增快(P0.05或P0.01),其余时点SBP、DBP均明显降低(P0.05或P0.01),T4、T7和T8时HR明显减慢(P0.05或P0.01);D组在T1~T8时的SBP、T1~T4和T8时的DBP明显降低,T1和T3~T4时的HR均明显减慢(P0.05或P0.01)。与T2时比较,T3、T4时N组SBP、DBP明显降低,HR明显减慢(P0.01);D组仅T4时SBP明显降低(P0.01)。与T4时比较,T5、T6时N组SBP明显升高(P0.05或P0.01);T5~T7时D组SBP、DBP明显升高,HR明显增快(P0.01)。与N组比较,T1~T3时D组HR明显减慢(P0.05或P0.01),T2时D组SBP、DBP明显降低(P0.01),T5~T8时SBP和DBP明显升高(P0.05或P0.01)。结论全麻麻醉诱导时辅用右美托咪定不仅可减轻气管插管反应,而且可增强麻黄碱的升压反应。     

Differential pressor response to intravenous ephedrine during recovery from deliberate hypotension

STUDY OBJECTIVE: To determine whether nitroglycerin or trimethaphan alters pressor response to intravenous (i.v.) ephedrine. DESIGN: Prospective, randomized study. SETTING: Operating room of a university hospital. PATIENTS: 60 ASA physical status I female patients scheduled for mastectomy. INTERVENTIONS: Patients were assigned to one of six groups (n = 10 in each). Group 1: nitroglycerin + normal saline (NS) i.v., Group 2: nitroglycerin + ephedrine 0.1 mg/kg i.v., Group 3: nitroglycerin + ephedrine 0.15 mg/kg i.v., Group 4: trimethaphan + NS i.v., Group 5: trimethaphan + ephedrine 0.1 mg/kg i.v., and Group 6: trimethaphan + ephedrine 0.15 mg/kg i.v. MEASUREMENTS: Hemodynamic responses to ephedrine following withdrawal of vasodilators were observed for 15 minutes. MAIN RESULTS: Ephedrine increased heart rate and mean blood pressure. After ephedrine 0.1 mg/kg i.v., the maximum pressor response in the trimethaphan group was approximately twofold that of the nitroglycerin group (p = 0.038). CONCLUSIONS: Ephedrine restored BP more easily in those patients who had received trimethaphan compared with those who had received nitroglycerin for deliberate hypotension.     

Enhancement of pressor response to intravenous phenylephrine following oral clonidine medication in awake and anaesthetized patients

Clonidine, an α₂-adrenergic agonist, augments the pressor response to intravenous ephedrine. If this effect is partly due to clondine-induced potentiation of α₁-adrenoceptor-mediated vasoconstriction, it is also assumed that clonidine would enhance the pressor effect of phenylephrine as an α₁-adrenergic agonist. The authors studied haemodynamic responses to intravenous phenylephrine in 80 patients who received either preanaesthetic medication with clonidine approximately 5 μg · kg^?1 po (clonidine group, n = 40), or no medication (control group, n =40). Each group was further divided into either awake subjects (n = 20) or subjects anaesthetized with enflurane and nitrous oxide in oxygen (n = 20). Haemodynamic measurements were made at one-minute intervals for ten minutes after phenylephrine 2 μg · kg^?1 iv was injected as a bolus. The magnitudes of maximal mean blood pressure increases in the clonidine group (26 ± 7% (mean ± SD) for awake and 32 ± 15% for anaesthetized subjects) were greater (P < 0.05) than in the control group (13 ± 7% for awake and 18 ± 7% for anaesthetized subjects). However, there was no difference in the pressor effect of phenylephrine between awake and anaesthetized patients in both groups. Oral clonidine preanaesthetic medication, 5 μg · kg^?1, augments the pressor responses to phenylephrine 2 μg · kg^?1 iv in awake and anaesthetized patients. These results suggest that the enhancement of the pressor responses to phenylephrine following oral clonidine may be due to clonidine-induced potentiation of α₁-adrenoceptor-mediated vasoconstriction. This implies that restoration of blood pressure can be achieved effectively by phenylephrine in hypotensive patients with clonidine premedication.     

Effects of clonidine premedication on the pressor response to alpha- adrenergic agonists

It has been suggested that postjunctional alpha 1-adrenoceptor mediated vasoconstriction is enhanced by clonidine. We have examined in humans if the pressor responses to noradrenaline and phenylephrine are enhanced by clonidine premedication. Seventy-seven patients were allocated randomly to either clonidine (n = 38) or control (n = 39) groups. Patients in the clonidine group received approximately 5 micrograms kg-1 with famotidine 20 mg, while the control group received famotidine 20 mg alone orally, 90 min before induction of general anaesthesia with thiamylal. In all patients the lungs were ventilated mechanically via tracheal tubes and anaesthesia maintained with 1% end- tidal enflurane and 67% nitrous oxide in oxygen. When a stable haemodynamic state was obtained, either noradrenaline 0.5 microgram kg- 1 (n = 40) or phenylephrine 2 micrograms kg-1 (n = 37) was administered randomly i.v. as a bolus, while arterial pressure and heart rate were measured noninvasively at 1-min intervals for 10 min. Although noradrenaline caused significantly greater increases in mean arterial pressure (MAP) in the clonidine group (from 2 to 4 min after i.v. injection) compared with the control group, there were no significant differences in the mean maximal increment in MAP or area under the MAP curve between the two groups. However, i.v. phenylephrine produced a significantly greater increase in MAP from 2 to 7 min (P < 0.05), and greater mean maximal increase in MAP from the baseline value (21 (9) vs 14 (7) mm Hg; P < 0.05) in the clonidine than in the control group. In addition, the duration of elevated MAP in the clonidine group was significantly longer than that in the control group (7.6 (2.4) vs 5.1 (2.8) min; P < 0.01). Furthermore, the area under the curve for MAP changes after i.v. phenylephrine in the clonidine group was significantly greater than that in the control group (69.7 (64.3) vs 11.5 (64.0) mm Hg min; P < 0.01). There were no significant differences in arterial pressure or heart rate after the pressor agents between the groups. There were no significant differences between groups in the incidence of hypertension, arrhythmia or bradycardia before or after i.v. noradrenaline or phenylephrine. These results indicate that the pressor response to phenylephrine, but not to noradrenaline, is augmented in patients with clonidine premedication.      

The effects of clonidine premedication on the blood pressure and tachycardiac responses to ephedrine in elderly and young patients during propofol anesthesia

We studied the pressor and tachycardiac responses to ephedrine in elderly and young patients given either clonidine or midazolam during propofol anesthesia. In the first experiment, elderly (>60 yr) and young (20-45 yr) patients were randomly allocated to one of four groups according to age and premedicated regimens (n = 16 each; elderly-clonidine [EC], elderly-midazolam [EM], young-clonidine [YC], and young-midazolam [YM]). Under propofol anesthesia, ephedrine was injected, and hemodynamic measurements were made. In the second experiment, with clonidine premedication, elderly patients (n = 16) were given a reduced dose of propofol (EC-LP) and young patients (n = 16) were given an increased dose of propofol (YC-HP). Ephedrine was injected, and he- modynamic measurements were performed. The in-creases in mean blood pressure and heart rate were larger in the EC group than in the EM, YM, and EC-LP groups (P < 0.05). In the YC-HP group, the pressor response to ephedrine tended to be augmented as compared with the YC group but was not statistically significant. These results suggest that clonidine premedication augmented the pressor and tachycardiac responses to ephedrine, especially in elderly patients during a standard dose of propofol anesthesia, and that clonidine, age, and propofol could be involved in the augmentation of the blood pressure and tachycardiac responses to ephedrine. IMPLICATIONS: Clonidine premedication augments the pressor and tachycardiac responses to ephedrine in elderly patients during standard or large doses of propofol anesthesia but does not augment during small doses of propofol anesthesia. Clonidine, age, and propofol could be involved in the augmentation of the pressor and tachycardiac responses to ephedrine.     

Preoperative clonidine attenuates stress response during emergence from anesthesia

STUDY OBJECTIVES: To investigate whether a single preoperative IV dose of clonidine blunts the hemodynamic and hyperadrenergic responses not only to intubation, but also to extubation. DESIGN: Randomized, double-blind, placebo-controlled study. PATIENTS: 29 ASA physical status I and II patients (ages 18-65) who were scheduled for noncardiac, elective surgery. Patients were randomly assigned to either receive clonidine 3 microg/kg IV immediately before anesthesia induction or placebo. INTERVENTIONS: Insertion of a 14 G cannula in a large cubital vein for the determination of plasma catecholamines using local anesthesia. Insertion of a radial artery catheter for measuring blood pressure (BP) using local anesthesia. Transthoracic echocardiography to determine cardiac output (CO). MEASUREMENTS: Heart rate (HR), mean arterial pressure (MAP), CO, and plasma catecholamine concentrations. Measurements were performed: before induction (baseline), during intubation, 10 min after intubation, after surgery, during extubation, and 10 min after extubation. MAIN RESULTS: During intubation MAP, HR, and CO were lower in the clonidine group. Compared with baseline measurements, MAP and CO increased less in the clonidine group during intubation. During extubation, MAP was lower in the clonidine group. CO and MAP increased less as compared with baseline measurements in the clonidine group. Compared with the measurements after surgery CO less in the clonidine group during extubation (p < 0.05 for all results). CONCLUSIONS: A single preoperative IV dose of clonidine (3 microg/kg) blunts the hemodynamic responses due to extubation in noncardiac surgery of intermediate duration.     

Propofol inhibits medullary pressor mechanisms in cats

Purpose

Propofol may cause hypotension and the mechanism is complex. The present study was designed to determine the direct actions of propofol in medulla of cats.

Methods

Mean systemic arterial pressure (MSAP), heart rate (HR) and cardiac contractility (dp/dt) were compared before and after administration of propofol through the femoral vein (2, 3 or 4 mg · kg^?1), vertebral artery (1 mg · kg^?1) or the lateral cerebral ventnricle (0.5 mg · kg^?1) in eight anaesthetized cats. To study the direct effect of propofol in medulla, pressor areas of the dorsomedial medulla (DM) and rostral ventrolateral medulla (RVLM), or the depressor area of the caudal ventrolateral medulla (CVLM) were first identified with electrical stimuli and then confirmed by pressure microinjection of glutamate (Glu, 0.25M, 30 nl) via a multibarrel-micropipette in 28 cats. One hour later, propofol (0.001%, 50 nl) was microinjected at the same site. Electrical stimulation and Glu were applied again to compare changes of SAR HR and dp/dt with that of the control.

Results

Propofol dose-dependently decreased SAR HR and cardiac contractility. The percent increase of MSAP induced by Glu were reduced by propofol in DM (59 ± 3 % vs 13 ± 2 %, n = 11.P < 0.01) or in RVLM (56 ± 4 % vs 18 ± 2 %, n = 9,P < 0.01). In CVLM, propofol slightly but not significantly increased the depressor responses elicited by Glu (?27 ± 2 %vs ～-33 ± 3 %. n = 5,P > 0.05).     

Partial attenuation of the pressor response to endotracheal intubation. A comparison of the effects of intravenous clonidine and fentanyl.

In a randomized, double-blind placebo controlled study, intravenous clonidine, fentanyl and saline were compared for both their effect on the cardiovascular response to intubation, and early post-operative pain. The patients treated with fentanyl and clonidine were more sedated and the requirements for induction agents were lower compared to the control group. On intubation, both the active treatments resulted in a smaller increase in both heart rate and mean arterial pressure compared to the control group. There was no significant difference in recovery times in the three groups. Although the time to first request for analgesia was longer in the clonidine group compared to both the fentanyl and saline groups, the difference in morphine requirements between the groups was not significant. The differences between the two active treatments were not significant, and clonidine offered no additional benefits over fentanyl for this purpose.     

The effects of preanesthetic oral clonidine upon heart rate response to intravenous atropine in patients during general anesthesia]

In awake subjects the positive chronotropic effect of intravenously administered atropine 10 micrograms.kg-1 has been demonstrated to be blunted by preanesthetic medication of oral clonidine 5 micrograms.kg-1. The aim of the present study is to investigate whether general anesthesia could alter the clonidine-induced attenuation of positive chronotropic effect by atropine. Thirty-two patients were randomly assigned to one of the two groups; patients of the clonidine group received oral clonidine 5 micrograms.kg-1 (n = 12), whereas those of the control group received no clonidine. General anesthesia was induced with intravenous thiamylal 4-5 mg.kg-1, and was maintained with enflurane and nitrous oxide in oxygen after endotracheal intubation. Following the stable circulatory period of 10 min, hemodynamic measurements were made at 1 min intervals for 10 min after atropine 10 micrograms.kg-1 was administered intravenously as a bolus in both groups. A significant attenuation in heart rate response to intravenous atropine 10 micrograms.kg-1 was observed in patients receiving clonidine 5 micrograms.kg-1, as compared with that in the control group (P less than 0.01); maximal increases in heart rate were 15 +/- 8 and 22 +/- 6 beats.min-1 (mean +/- SD) in the clonidine and control groups, respectively. It is concluded that clonidine 5 micrograms.kg-1 blunts the heart rate response to intravenous atropine 10 micrograms.kg-1 in patients anesthetized with enflurane and nitrous oxide in oxygen.     

Propofol for anesthesia in a patient susceptible to malignant hyperthermia.

Propofol may be a useful anesthetic in the management of malignant hyperthermia patients. It appears not to trigger malignant hyperthermia while providing stress-free conditions. This case report, along with a small number of others, documents the safe use of propofol for this patient population.     

Intrathecal clonidine and the response to hemorrhage.

Intraspinally administered alpha 2-adrenergic agonists are being examined for postoperative analgesia, yet their effects on the hemodynamic response to acute hemorrhage have not been examined. In this study chronically prepared conscious sheep received thoracic intrathecal saline or clonidine 300 micrograms followed in 15 min by rapid removal of 1,000 ml blood. In saline-treated ewes blood pressure was maintained and heart rate steadily increased during hemorrhage of up to 700 ml blood, with further blood removal resulting in rapid decreases in both variables. In contrast, heart rate never increased and blood pressure was maintained only up to 400 ml blood loss in animals receiving intrathecal clonidine. Compared to saline controls, clonidine did not alter blood pressure or heart rate at the end of hemorrhage or during blood pressure restitution during the next hour. Clonidine inhibited the increase in plasma epinephrine at the end of hemorrhage without altering plasma norepinephrine, vasopressin, renin, or atrial natriuretic factor. Intrathecal idazoxan, a specific alpha 2-adrenergic antagonist, reversed clonidine's effect on blood pressure during hemorrhage. Intravenous DG-5128, a poorly lipid-soluble alpha 2-adrenergic antagonist, also reversed clonidine's effect and additionally completely blocked any reduction in blood pressure and heart rate during hemorrhage. These data suggest that intrathecal clonidine interferes with maintenance of blood pressure during hemorrhage, likely because of a spinal sympatholytic effect, but does not affect the ultimate decrease in blood pressure after rapid removal of 1,000 ml blood. This difference in effect during the two phases of hemorrhage can be explained by the relative importance of the sympathetic nervous system in each.     

Intravenous regional anesthesia using lidocaine and clonidine.

BACKGROUND: Clonidine has been added to local anesthetic regimens for various peripheral nerve blocks, resulting in prolonged anesthesia and analgesia. The authors postulated that using clonidine as a component of intravenous regional anesthesia (IVRA) would enhance postoperative analgesia. METHODS: Forty-five patients undergoing ambulatory hand surgery received IVRA with lidocaine, 0.5%, and were assigned randomly and blindly to three groups. The control group received intravenous saline, the intravenous clonidine group received 1 microg/kg clonidine intravenously, and the IVRA clonidine group received 1 microg/kg clonidine as part of the IVRA solution. After their operations, the patients' pain and sedation scores and analgesic use were recorded. RESULTS: Patients in the IVRA clonidine group had a significantly longer period of subjective comfort when they required no analgesics (median [range]) for 460 min (215-1,440 min), compared with 115 min (14-390 min) for the control group and 125 min (17-295 min) for the intravenous clonidine group (P<0.0001). The patients who received IVRA with clonidine reported significantly lower pain scores 1 and 2 h after tourniquet deflation compared with the other groups, and they required no fentanyl in the postanesthesia care unit. They also required fewer analgesic tablets (325 mg acetaminophen with 30 mg codeine) in the first 24 h (2+/-1, mean +/- SD) compared with the other two groups, 5+/-1 tablets (control) and 4+/-2 tablets (intravenous clonidine) (P<0.0001). No significant postoperative sedation, hypotension, or bradycardia developed in any of the patients. CONCLUSION: The addition of 1 microg/kg clonidine to lidocaine, 0.5%, for IVRA in patients undergoing ambulatory hand surgery improves postoperative analgesia without causing significant side effects during the first postoperative day.     

Propofol-nitrous oxide anesthesia enhances the heart rate response to intravenous isoproterenol infusion

Heart rate (HR) response to IV atropine is attenuated during propofol-nitrous oxide (N(2)O) anesthesia. We studied the effects of propofol-N(2)O anesthesia on isoproterenol-induced HR changes. The control group (n = 15) received no propofol and no N(2)O. Patients in the propofol-N(2)O group (n = 21) received IV propofol 2.5 mg/kg over 1 min followed by a continuous infusion of propofol 10 mg x kg(-1) x h(-1). After tracheal intubation, anesthesia was maintained with propofol 5 mg. kg(-1) x h(-1) and 67% N(2)O in oxygen. All patients in both groups received IV isoproterenol at incremental infusion rates (2.5, 5, 7.5, 10, 12.5, 15, and 17.5 ng x kg(-1) x min(-1) for 2 min at each dose) until HR increased more than 20 bpm from baseline values. At the end of each infusion period, hemodynamic data were collected. The HR response to isoproterenol 7.5 ng. kg(-1) x min(-1) was increased more in the propofol group than in the control group (20 +/- 5 versus 14 +/- 4 bpm; P < 0.05). During the isoproterenol infusion at 10 ng. kg(-1) x min(-1), HR increased by more than 20 bpm in all patients in the propofol group but in only 31% of patients in the control group (P < 0.0001). These results suggest that continuous isoproterenol infusion might be useful when a large dose of atropine is ineffective in restoring normal HR during propofol-N(2)O anesthesia. IMPLICATIONS: We demonstrated that the heart rate response to IV isoproterenol infusion is enhanced during propofol-nitrous oxide anesthesia. This suggests that continuous isoproterenol infusion may be useful when a large dose of atropine is ineffective for restoration of normal heart rate in patients receiving propofol-nitrous oxide anesthesia.     

Adding clonidine to lidocaine for intravenous regional anesthesia prevents tourniquet pain.

Tourniquet pain often complicates the use of the pneumatic tourniquet during surgical procedures performed under IV regional anesthesia. Clonidine-containing local anesthetic solutions have better analgesic properties than plain solutions when used for spinal, epidural, or peripheral blocks. We tested the hypothesis that the addition of clonidine may improve the quality of IV regional anesthesia, especially tourniquet tolerance. Forty patients were allocated randomly in a double-blinded, randomized study to receive 40 mL of 0.5% lidocaine and either 1 mL of isotonic saline or clonidine (150 microg). A double-cuffed tourniquet was kept inflated until patients complained of pain, leading to release of the distal cuff. Pain at the tourniquet site, at the surgical site, and in the distal part of the arm was rated on a visual analog scale (VAS) and a verbal rating scale (VRS) every 15 min during tourniquet placement and every 15 min for 1 h after tourniquet deflation. Motor blockade, sedation, arterial pressure, and heart rate were also recorded. VAS and VRS scores were significantly lower in the clonidine group 30 and 45 min after tourniquet inflation. The tolerance for the distal tourniquet was also significantly longer in the clonidine group (median [range]: 22 [10-40] vs 10 [5-20] min; P < 0.05); motor blockade was comparable between the two groups. Pain was not different in the two groups after tourniquet release. The clonidine group experienced a higher degree of sedation. We conclude that clonidine improves tourniquet tolerance when added to a local anesthetic solution. IMPLICATIONS: A 150-microg dose of clonidine added to lidocaine improved tourniquet tolerance during IV regional anesthesia.