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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidurally administered clonidine has been reported to produce postoperative analgesia. To assess the efficacy, safety, and appropriate dose of epidural clonidine for post-cesarean section analgesia, we designed a double-blind, placebo-controlled study. Sixty women were randomly assigned to receive epidural administration of saline bolus followed by 24-h saline infusion, 400-micrograms clonidine bolus followed by 10 micrograms/h clonidine infusion, or 800-micrograms clonidine bolus followed by 20 micrograms/h clonidine infusion. Supplemental analgesia was provided with patient-controlled iv morphine. Compared to saline, both clonidine regimens produced analgesia, as measured by verbal pain scores and supplemental iv morphine use during the first 6 h after bolus injection. Time to first morphine use was similar for both clonidine groups and significantly greater than saline. However, compared to saline, only the 20 micrograms/h clonidine infusion resulted in decreased morphine usage over the entire 24-h period. Compared to saline, both clonidine doses decreased blood pressure. This decrease was greater in the 400-micrograms than in the 800-micrograms clonidine group, but no patient required treatment for hypotension. Clonidine decreased heart rate (one patient required atropine for asymptomatic bradycardia) and produced transient sedation. The 800-micrograms clonidine dose prolonged resolution of local anesthetic-induced motor blockade compared to saline. The results suggest that epidurally administered clonidine provides analgesia, as measured by decreased need for supplemental morphine, after cesarean section, but continuous infusion is required for analgesia of more than 6 h duration.
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PMID:Epidural clonidine analgesia after cesarean section. 224 Jun 74

It has been proposed that descending noradrenergic systems exercise a tonic inhibition of nociception at the spinal level. The recent finding that changes in tail skin temperature (TT) may have a strong effect on the tail-flick latency makes a reevaluation of this hypothesis necessary. The alpha-adrenoceptor agonist clonidine injected intrathecally (i.th.) in a dose of 60 micrograms increased the response temperature in the increasing hot plate test 10 min after injection, and prolonged the tail-flick latency 30-60 min after injection. A considerable part of the change in tail-flick latency was caused by a reduction in TT. The alpha 1-antagonist prazosin (30 and 60 micrograms) tended to increase the response temperature in the increasing hot plate test after 60 min, and to prolong the latency in the tail-flick test. These effects were not statistically significant. Clonidine and prazosin induced sensorimotor impairment and a reduction in body temperature after 30-60 min. The alpha 2-antagonist yohimbine had no effect in the increasing hot plate test, but reduced the tail-flick latency 10 min after drug administration. This reduction could be explained by an increase in TT. The results suggest that the reduced latency in the tail-flick test after i.th. injection of yohimbine is caused by an increase in the tail blood flow, and does not support the hypothesis of a tonic bulbospinal noradrenergic inhibition of nociception. The time course of response latencies suggests that supraspinal mechanisms may be involved in the effects of i.th. clonidine and prazosin in the tail-flick test, while there seems to be a spinally mediated antinociceptive effect of clonidine that can be demonstrated in the increasing hot plate test.
Pain 1990 Oct
PMID:The role of descending noradrenergic systems in regulation of nociception: the effects of intrathecally administered alpha-adrenoceptor antagonists and clonidine. 227 13

Clonidine and its Soviet-made analogue clopheline (10 micrograms) after epidural administration to rats equally inhibited nociceptive reactions and changes in arterial blood pressure in the somatic and visceral pain tests. In patients with obliterating atherosclerosis of the lower extremities clopheline (100 and 200 micrograms) relieved the pain syndrome and shifts of II-hydroxycorticosteroids in blood, induced bradycardia and the background arterial blood pressure-dependent antihypertensive effect.
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PMID:[An experimental and clinical study of the analgesic action of clofelin when administered epidurally]. 236 46

We have examined the effects of extradural clonidine 150 micrograms or morphine 4 mg on postoperative pain, stress responses, cardiopulmonary function and motor and sensory block in a double-blind, randomized study in 20 patients undergoing hysterectomy with general anaesthesia. Observations were made for 6 h after each patient's first request for analgesia. Clonidine provided greater pain relief than morphine only for the first 2 h of observation (P less than 0.001). Plasma cortisol concentrations decreased to a greater extent (P less than 0.05) with morphine, while plasma glucose concentration increased by a similar extent in both groups. After clonidine, mean arterial pressure decreased from 100 (SEM 3) mm Hg to 70 (3) mm Hg (P less than 0.05), but there was no change after morphine. There were no significant changes in heart rate, pulmonary function (FEV1), motor function or sensory analgesia to touch, temperature and pinprick in both groups. Additional systemic opioids were required by five and six patients in the clonidine and morphine groups, respectively.
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PMID:Comparison of the effects of extradural clonidine with those of morphine on postoperative pain, stress responses, cardiopulmonary function and motor and sensory block. 251 58

Dose-response curves for clonidine-produced analgesia in rats were constructed using the tail-flick and formalin tests. Subsequently, the relative role of alpha 1 and alpha 2 receptors in clonidine analgesia in each of these tests was determined using systemic administration of vehicle controls, tolazoline, yohimbine and prazosin prior to injection of an ED50 dose of clonidine. Clonidine was found to be significantly more potent in the formalin test than in the tail-flick test. Furthermore, clonidine analgesia in the tail-flick test was completely antagonized by tolazoline and yohimbine, but not by prazosin, whereas clonidine was antagonized by tolazoline and prazosin, but not by yohimbine in the formalin test. The implications of these findings with regard to the contributions of different alpha-receptor subtypes to clonidine-produced analgesia in different pain tests are discussed.
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PMID:Different alpha-receptor subtypes are involved in clonidine-produced analgesia in different pain tests. 253 53

Experimental data and anecdotal clinical observations have shown that clonidine, an alpha 2-agonist, has a marked analgesic effect. We investigated clonidine-induced analgesia in response to nociceptive stimuli. On 2 different days 7 normal volunteers received either placebo or clonidine (200 micrograms) orally according to a cross-over, double-blind, randomized, placebo-controlled design. Analgesia was assessed by measurement of the subjective (VAS) and objective (R III reflex) pain thresholds. A close correlation was observed between subjective and objective pain thresholds (r = 0.88, y = 0.2 + 1.2 x). Clonidine increased the objective threshold by 21% (+6.2 mA, SEM 2.4) and the subjective threshold by 10% (+2.4 mA, SEM 1.3). Drug effect was rapid (peak between 90 and 120 min) and overall analgesia lasted up to 4 hours. Side effects were a moderate fall in blood pressure, sedation and dryness of the mouth. A single oral dose of clonidine induces significant analgesia. These results suggest that clonidine is potentially a worthwhile drug for pain treatment which deserves further clinical investigation.
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PMID:[Analgesic effects of an oral dose of clonidine]. 261 77

The effects of intrathecal clonidine on spinal fentanyl analgesia were studied by the hot-plate test (52.0 degrees C) in rats. Clonidine (5 micrograms) and/or fentanyl (5 micrograms) were administered alone or combined in volume of 10 microliters through a chronically-implanted polyethylene catheter (PE-10) whose tip was near the lumbar enlargement of the spinal cord. Injections were done repeatedly every two or three days to determine the time course of thermal analgesia. Results were as follows; 1) Intrathecal clonidine (n = 5) produced no thermal analgesia. 2) Intrathecal fentanyl (n = 10) produced a profound thermal analgesia which was attenuated markedly by the repeated injections in six rats before the 9th injection. 3) Two out of six fentanyl tolerated rats responded with remarkable increases in thermal thresholds following the intrathecal clonidine with fentanyl. 4) Rats which were administered with both clonidine and fentanyl from the 1st injection (n = 9) responded with a extended prolongation of the escape latency, compared with the rats which received fentanyl only. In this group, the tolerance developed in only three animals by the 9th injection. In conclusion, combined intrathecal administration of clonidine with fentanyl potentiated the analgesic effect of fentanyl and then definitely suppressed the tolerance formation even if a small dose of clonidine which produces no analgesic effect was used. These results suggest that intrathecal or epidural administration of clonidine with narcotics might be useful in managing intractable pain.
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PMID:[Intrathecal clonidine--how does it work in spinal fentanyl analgesia in rats?]. 272 14

Clonidine was administered by epidural injections with per os relay and long term therapeutic follow-up to 38 patients with deafferentation neurological sequellar pain either fully or partly intractable to classical pain treatments. In such types of pain, this technique provides hypoalgesia which can be enhanced by the administration of serotoninergic anti-depressants or low dose tricyclics. However, side effects may occur. After some time, a tolerance develops with a lesser antalgic efficiency, as well as rare cases of withdrawal syndromes when the treatment is suddenly discontinued.
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PMID:[Thoracolumbar or sacral epidural administration of clonidine in deafferentation pain: possibilities, limits and long-term follow-up]. 275 Oct 43

Epidurally administered clonidine has been reported to produce postoperative analgesia. To assess the efficacy, safety, and appropriate dose of epidural clonidine for postoperative analgesia, clonidine (range, 100-900 micrograms in 100-micrograms increments) was injected in 22 patients following abdominal surgery or total knee arthroplasty (TKA). Clonidine produced analgesia, as measured by change in verbal pain scores and supplemental iv morphine usage. The largest doses examined (700-900 micrograms) produced complete pain relief for 5.0 +/- 0.8 h (mean +/- SEM; range 2-11 h), without other sensory or motor blockade. Clonidine also produced dose dependent decreases in blood pressure, being less following small (100-300 micrograms) and large (700-900 micrograms) doses than following intermediate (400-600 micrograms) doses. Six patients required iv ephedrine for treatment of blood pressure decrease of greater than 30%. Clonidine decreased heart rate 10-30% and produced transient sedation. Oxyhemoglobin saturation, serum glucose, and arterial blood gas tensions were not altered by clonidine, whereas there was a small (28%) dose-independent decrease in serum cortisol following clonidine injection. Clonidine was absorbed in a dose-dependent manner into the systemic circulation, with plasma concentrations 0.1-3.3 ng/ml 1 h following injection. These results suggest that hemodynamic depression and short-lasting analgesia may limit the usefulness of bolus epidural clonidine analgesia in the postoperative setting.
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PMID:Epidural clonidine analgesia following surgery: phase I. 281 56

Intrathecally administered clonidine has been reported to produce analgesia in cancer patients tolerant to intrathecal opiates. To assess the efficacy, safety, and appropriate dose of epidurally administered clonidine for the treatment of cancer pain, clonidine (range, 100-900 micrograms in 100-micrograms increments) was injected in nine patients with severe, intractable cancer pain. Clonidine produced analgesia, as measured by change in verbal pain scores, lasting more than 6 h. Clonidine also decreased blood pressure, although this effect was well tolerated and no patient met criteria for receiving iv ephedrine (greater than 30% decrease in mean arterial pressure not responsive to 500 ml iv crystalloid infusion). Clonidine decreased heart rate 10-30% and produced transient sedation. Serum glucose and cortisol and oxyhemoglobin saturation were not altered by clonidine. Clonidine was absorbed in a dose-dependent manner into the systemic circulation, although absorption and elimination kinetics were highly variable. Following study seven patients received epidural clonidine/morphine infusions at home for periods of up to 5 months with sustained analgesia. These results suggest that epidurally administered clonidine may offer effective analgesia in patients with severe, intractable cancer pain.
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PMID:Epidural clonidine analgesia for intractable cancer pain: phase I. 281 57


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