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WARNINGS Withdrawal: Patients should be instructed not to discontinue therapy without consulting their physician. Sudden cessation of clonidine treatment has, in some cases, resulted in symptoms such as nervousness, agitation, headache, and tremor accompanied or followed by a rapid rise in blood pressure and elevated catecholamine concentrations in the plasma. The likelihood of such reactions to discontinuation of clonidine therapy appears to be greater after administration of higher doses or continuation of concomitant beta-blocker treatment and special caution is therefore advised in these situations. Rare instances of hypertensive encephalopathy, cerebrovascular accidents and death have been reported after clonidine withdrawal. When discontinuing therapy with clonidine hydrochloride, the physician should reduce the dose gradually over 2 to 4 days to avoid withdrawal symptomatology.. An excessive rise in blood pressure following discontinuation of clonidine therapy can be reversed by ...
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Tablet. Patients who engage in potentially hazardous activities, such as operating machinery or driving, should be advised of a potential sedative effect of clonidine. Patients should be cautioned against interruption of clonidine hydrochloride therapy without a physicians advice.. Epidural Injection. Patients should be instructed about the risks of rebound hypertension and warned not to discontinue clonidine except under the supervision of a physician. Patients should notify their physician immediately if clonidine administration is inadvertently interrupted for any reason. Patients who engage in potentially hazardous activities, such as operating machinery or driving, should be advised of the potential sedative and hypotensive effects of epidural clonidine. They should also be informed that sedative effects may be increased by CNS-depressing drugs such as alcohol and barbiturates, and that hypotensive effects may be increased by opiates.. ...
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Although routine administration of pharmacologic sedation or analgesia during mechanical ventilation in preterm neonates is not recommended, its use in clinical practice remains common. Alpha-2 agonists, mainly clonidine and dexmedetomidine, are used as adjunctive (or alternative) sedative agents alongside opioids and benzodiazepines. Clonidine has not been systematically assessed for use in neonatal sedation during ventilation. To assess whether clonidine administered to term and preterm newborn infants receiving mechanical ventilation reduces morbidity and mortality rates. To compare the intervention versus placebo, no treatment, and dexmedetomidine; and to assess the safety of clonidine infusion for potential harms.To perform subgroup analyses according to gestational age; birth weight; administration method (infusion or bolus therapy); dose, duration, and route of clonidine administration; and pharmacologic sedation as a co-intervention. We used the standard search strategy of the Cochrane ...
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TY - JOUR. T1 - Inhibitory effects of clonidine on GABA-activated currents in rat DRG neurons. AU - Wang, Qin Wen. AU - Li, Qin. AU - Li, Zhi Wang. PY - 1998. Y1 - 1998. N2 - Whole-cell patch-clamp recordings were performed on neurons from freshly isolated rat dorsal root ganglion (DRG) to investigate modulatory effects of clonidine, an α2-adrenoceptor agonist, on GABA-activated currents. In the majority of the neurons examined (72/75), GABA (10-6 ~ 10-3 mol/L) induced a concentration-dependent inward current, which could be blocked by bicuculine (10-4 ~ 10-5 mol/L). In 51 out of 72 cells, pretreatment with different dosages of clonidine (10-8 ~ 10-4 mol/L) decreased the GABA (10-4 mol/L)-activated current by 8.5%, 19.0%, 33.4%, 44.4% and 40.3%, respectively, while clonidine itself only induced a slight inward current in a few cells (12/72). The inhibitory action of clonidine blockable by yohimbine (10-4 mol/L) was voltage-independent and did not change the membrane conductance during the ...
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Clonidine hydrochloride is a sympathetic inhibitor with central site of action. The antihypertensive effect in man in the supine position is associated with a decrease in cardiac output and no consistent changes in total peripheral resistance. In the standing position, however, in addition to the decrease in cardiac output, a fall in total peripheral resistance becomes evident. The fall in blood pressure results in no significant alteration in renal blood flow or glomerular filtration rate in the supine position. In the standing position a consistent decrease in renal vascular resistance is seen.. In the anesthetized dog the intravenous administration of clonidine produces a significant reduction of renal vein plasma renin activity. Similarly, in patients with essential hypertension oral administration of the drug results in a decrease in peripheral plasma renin activity.. In ambulatory essential hypertensive patients treated with clonidine alone in doses of 400 to 900 µg per day, a modest ...
This study was designed to evaluate hypoxemia and platelet aggregation in man following intravenous administration of clonidine. With Institutional approval and following informed consent, 20 patients (ASA I-II) without spontaneous or drug-induced coagulation disorder undergoing elective total hip replacement were studied. They were randomly divided into two groups. Group A (n = 10) received an IV loading dose of 4 micrograms/kg of clonidine in 30 minutes followed by an infusion of 1 microgram/kg/h till the end of the procedure. Group B (n = 10) received saline. Platelet aggregation was assessed before infusion and at the end of both the loading dose and the infusion. PaO2 was measured before anesthesia (FIO2 = 0.21), before femoral cementation (FIO2 = 0.40), 2 min. after prosthesis implantation (FIO2 = 1), before the end of the procedure (FIO2 = 0.40) and in the recovery room (spontaneous breathing with FIO2 = 0.21). Plasma clonidine levels were assessed at the end of both the loading dose and ...
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Background. Stress and exposure to drug-related cues (environmental stimuli previously associated with drug availability) are considered factors that increase the risk of relapse to heroin and/or cocaine use. The two factors may act through different neural mechanisms. Alpha-2 adrenergic agonists, such as clonidine, have been shown to block stress-induced relapse, but not cue-induced relapse, to heroin and cocaine self-administration in rodents. The ability of clonidine to attenuate stress- or cue-induced heroin and cocaine craving in drug abusers has not been tested. It is important to determine, in humans, whether clonidine blocks the acute effects of only one putative class of relapse precipitants, or whether its effects are more general.. Scientific goal. To compare the ability of clonidine to reduce stress-induced and cue-induced cocaine and heroin craving in drug abusers.. Participant population. A total of up to 160 drug abusers using cocaine, heroin, or both will be enrolled. Target ...
Background. Though buprenorphine effectively treats opioid dependence, some abstinent patients relapse to maladaptive use of opioids during treatment. Relapse may be triggered by stress. Rodent studies have demonstrated that stress can induce relapse to heroin and cocaine use (Erb, et al., 1996; Shaham, et al., 1996; Shaham and Stewart, 1995). In a rodent model, stress-induced relapse to heroin and cocaine seeking is blocked by the alpha-2 adrenergic agonist clonidine. In this study, clonidine will be compared to placebo in preventing relapse to opioid abuse in opioid maintained patients who have achieved abstinence while on buprenorphine and contingency management.. Scientific goals. To determine whether clonidine, given to abstinent patients maintained on buprenorphine, prevents relapse to opioid use more effectively than placebo.. Participant population. 300 opioid-dependent outpatients (120 evaluable). Target enrollment will include 40 persent women and 60 percent minorities (mostly ...
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BACKGROUND: Clonidine is an alpha(2) adrenoreceptor and imidazoline receptor agonist, which has analgesic, sedative, and minimum alveolar anesthetic concentration-sparing effects. It has been used orally, IV, and epidurally. In spinal surgery, there is a reluctance to use local anesthetic-based epidural analgesia postoperatively because of fears of masking important signs of nerve root or spinal cord injury. METHODS: We randomized 66 patients undergoing uncomplicated decompressive spinal surgery to receive an epidural infusion of either clonidine (Group C) or saline placebo (Group P) postoperatively. Morphine consumption by patient-controlled analgesia device was recorded for 36 h. RESULTS: Morphine consumption was significantly lower in Group C. The mean consumption at 36 h was 35 mg (95% confidence interval 21-50 mg) in Group C, compared with 61 mg (95% confidence interval 48-74 mg) in the control group. Nausea was significantly reduced in Group C (6.5%), when compared with placebo (38.2%). CONCLUSION
Clonidine functions as a sympatholytic by stimulating presynaptic α2-receptors leading to decreased release of norepinephrine at both central and peripheral adrenergic terminals. In addition to its influence on the autonomic nervous system, it is well established that clonidine is an effective analgesic, and this is also attributable to its α2-agonist activity.. Remember that a tremendous amount of modulation of incoming pain signals occurs in the dorsal horn of the spinal cord prior to being sent to higher centers in the CNS. Messages are either strengthened or attenuated by release of various neurotransmitters by primary afferent Aδ or C fibers, interneurons, and descending bulbospinal fibers. Nociceptive stimuli will promote release of excitatory transmitters from primary afferents in the dorsal horn. To compensate, there is simultaneous release of norepinephrine from descending inhibitory bulbospinal neurons, which binds to α2-receptors in the dorsal horn to diminish afferent pain ...
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