Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relatively few clinically significant drug interactions with anaesthetics have been documented in the literature. The following should be stressed since these interactions are not readily predictable or are potentially fatal. Pethidine should never be administered to patients who have received monamine oxidase inhibiting drugs within the last fortnight, since a fatal hyperpyrexia and/or hypertension may result. Thiopentone induction seems to make the heart more susceptible to arrhythmias caused by adrenergic drugs, and may cause severe arterial hypotension in patients treated with diazoxide. Midazolam orally should possibly be avoided as premedication in patients treated with erythromycin since anaesthetic concentrations of midazolam may result. Patients for whom bupivacaine analgesia is planned could preferentially be premedicated with other drugs than diazepam, which causes the serum level of bupivacaine to increase. Bradycardia and hypotension not attributable to sympathetic blockade have been reported following bupivacaine extradurally in verapamil-treated patients. Sulfonamides and the ester group of local anaesthetics, such as prilocaine in combination, may result in severe methaemoglobinaemia in infants. Epinephrine added to local anaesthetics may cause local vasodilation if administered to patients concurrently being treated with cyclic antidepressants, and the combination imposes the risk of severe hypertension and arrhythmias.
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PMID:Drug interactions with intravenous and local anaesthetics. 814 Aug 67

Adrenal medullary chromaffin cells produce high levels of endogenous opioid peptides. Recent data suggest that transplantation injected locally into the spinal subarachnoid space reduced intractable malignant pain. In order to determine the feasibility, the efficacy and the risks of using adrenal medullary tissue for control of irreducible pain, we have developed a transplantation protocol on cancer pain patients selected when they required chronic intrathecal injection of morphine and progressively increasing doses to maintain the level of analgesic effects. At the present time, our clinical trial involves 8 patients. We report here our initial results (mean follow-up: 5 months). The various data collected before and after the intrathecal administration of chromaffin cells included: 1) Pain evaluation over time, with concomitant narcotic intake, 2) CSF sampling through an implanted access port to determine the following biological parameters: biochemical assay for opioid peptides, cell count and phenotyping of lymphocytes, 3) peripheral blood samples for lymphocyte typing. The results confirm the efficacy of adrenal medullary transplantation into spinal CSF for controlling irreducible cancer pain. Complementary intrathecal and oral morphine were totally stopped in 2 cases and stabilized in 5 others. It seems essential to have an important volume of grafted tissue to achieve analgesia with high levels of metenkephalin in CSF. A progressive decrease in metenkephalin release was observed from 2 to 4 months after the transplantation. Two patients with a long-term follow-up (8 and 12 months) needed another intrathecal chromaffin cell graft.
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PMID:Transplantation of human chromaffin cells for control of intractable cancer pain. 874 93

Epinephrine is often given with epidurally administered drugs to prolong and enhance analgesia, which is partly attributed to alpha-adrenergic processes. This investigation evaluates the effect of epinephrine on the distribution of epidurally administered [3H]-clonidine hydrochloride (clonidine HCl) in serum and in the central nervous system. After placing a lumbar epidural catheter via a laminectomy, rabbits were randomly assigned to receive 20 microCi of clonidine HCl with epinephrine (1:200,000) (n = 5) or without (control; n = 5) for 90 min. During the administration, which included bolus and slow infusion, blood samples were collected at 15-min intervals. At the end of the administration, rabbits were perfused with normal saline, leading to exsanguination. Brain and spinal cord tissues were excised for radiometric analysis. In both groups, the concentration of clonidine HCl was greatest in the lumbar cord. Epinephrine further enhanced accumulation of clonidine HCl into the lumbar cord but did not alter the concentration of clonidine HCl in serum, brain, cervical cord, and thoracic cord. We conclude that lumbar administration of epidural clonidine HCl leads to increased concentrations in the lumbar cord, which is further enhanced by epinephrine. The increased spinal cord accumulation of clonidine may be another mechanism by which epinephrine improves epidural analgesia.
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PMID:Epinephrine increases spinal cord concentrations of [3H]-clonidine hydrochloride in rabbits after epidural infusion. 958 15

Epidural analgesia and spinal analgesia are the most effective techniques for relieving labour pain. Basically, local anaesthetics (i.e. bupivacaine) and opioids (i.e. fentanyl or sufentanil), especially when combined, produce excellent analgesia with minimal motor blockade. However, none of these agents is devoid of side-effects and analgesia remains sometimes imperfect, suggesting that new drugs would be welcome. Adrenalin and clonidine act on a2-adrenoceptors in the spinal cord and both have been found to improve analgesia. These two drugs have already been used in many patients and studies because the absence of neurotoxicity has been well documented. Clonidine looks more attractive, although sedation and hypotension limit its use. Other analgesic drugs are promising alternatives but are still at an experimental or very early clinical stage. Neostigmine and ketamine (without preservative) are not neurotoxic while midazolam neurotoxicity is still controversial. Intravenous remifentanil might prove useful when neuraxial analgesia is contraindicated.
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PMID:Promising non-narcotic analgesic techniques for labour. 1002 28

Several authors have found that pre-incisional injection of local anaesthetics reduces postoperative pain. In the present double-blind study, comprising 126 inpatients aged 6-42 (mean 19) years, we investigated whether pre-incisional injection of bupivacaine during general anaesthesia reduces the pain experienced after tonsillectomy. The patients were randomized into three treatment groups: 43 patients were injected with 5 ml of bupivacaine (2.5 mg/ml)+ epinephrine (5 microg/ml) solution in both tonsillar fossa, 41 had epinephrine (5 microg/ml) + saline (9 mg/ml) and 42 patients received saline (9 mg/ml) only. Self-assessment of pain during the first postoperative week (repeated measures) was recorded. Use of analgetics, experience of the surgeons, peroperative bleeding and several other clinical parameters were assessed. Analyses of covariance with repeated measures was carried out for each pain score. In general there was no statistical significant difference in pain scores, represented by a visual analogue scale (VAS) between the three treatment groups. However, injection of bupivacaine into the tonsillar fossa seemed to reduce pain shortly after the operation in the age group 19-24 years. Further, females and older patients reported more pain and used more analgetics than males and younger patients. Increasing experience of the surgeon was related to a lower score for baseline pain shortly after the operation. Epinephrine in bupivacaine or saline reduced peroperative bleeding. We conclude that bupivacaine does not provide significant postoperative analgesia after tonsillectomy in an unselected group of patients.
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PMID:Effect of bupivacaine on pain after tonsillectomy: a randomized clinical trial. 1038 Jul 45

The mixture of 1% lidocaine and 0.2% tetracaine with 1:200,000 epinephrine, so-called "supercaine," has been used extensively for axillary brachial plexus blockade for several decades. Since the advent of bupivacaine, the supercaine mixture has fallen into relative disuse despite its record of effectiveness and safety. No studies have been done recently to evaluate quality of anesthesia, duration of postoperative analgesia, and degree of patient satisfaction with this mixture when used for axillary brachial plexus blockade. The assumptions were as follows: surgical anesthesia will be adequate, length of postoperative analgesia will be approximately 4 to 9 hours, and patients will be highly satisfied. The specific aim of the present study was to describe the anesthetic characteristics of supercaine. Patients between 18 and 65 years of age received a standard mixture of supercaine, totaling 450-500 mg of lidocaine and 90 to 100 mg of tetracaine. Epinephrine in a solution of 1:200,000 and an 8.4% solution of sodium bicarbonate were added, and the transarterial technique was used. Patients were contacted on postoperative day 1 to determine the duration of sensory and motor block; overall satisfaction with the block was rated. Data were analyzed with the Statistical Program for the Social Sciences (SPSS, Chicago, Ill) and Stata (Stata Corp., College Station, Tex) computer programs. The mean +/- SD findings were as follows: duration of sensory block, 465 +/- 204 minutes; duration of motor block, 473 +/- 214 minutes; patient satisfaction score, 9 +/- 1 on a 1 to 10 scale. Data are reported within a 95% confidence interval. Variables examined and compared were not statistically significant. We concluded that the duration of block supports findings reported in the literature, patients equate duration of sensory block with duration of motor block, differences in duration were probably due to levels of provider experience, and patients were extremely satisfied with the anesthetic.
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PMID:Evaluation of lidocaine and tetracaine mixture in axillary brachial plexus block. 1049 55

A 71-year-old woman on chronic therapy with mianserine and amantadine was scheduled to undergo abdominal hysterectomy under spinal anesthesia. Following spinal anesthesia she developed hypotension refractory to continuous intravenous fluid infusion as well as multiple boluses of ephedrine. Because the maximum level of analgesia was T 8, general anesthesia was added using laryngeal mask airway. Immediately after anesthetic induction, a marked hypotension occurred. Blood pressure again did not respond to ephedrine but went up excessively to a small dose of epinephrine without any changes in heart rate. Epinephrine infusion at a low dose rate was needed to sustain the blood pressure during surgery. Both depletion of presynaptic norepinephrine store and down-regulation of postsynaptic beta-receptor may have led to abnormal response to catecholamines in this case.
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PMID:[Severe hypotension during anesthesia in a patient on long-term antidepressant therapy]. 1270 73

Estimation of the quality of the epidural anaesthesia of the patients sedated with Alprazolam and Midazolam in premedication before arthroscopy or arthrotomy of the knee was the goal of our study. Forty six (34 men and 12 women) ASA physical status 1-2 patients were divided into groups depending on the drugs orally applied in premedication (Alprazolam 0.5 mg, n = 29 or Midazolam 15 mg, n = 17) and of the kind of analgesia. The patients subjected to arthroscopy were treated with a single-shot epidural analgesia (n = 38), while those subjected to arthrotomy--with a continuous epidural analgesia (n = 8). 2% Lignocain with addition of Epinephrine and Fentanyl was used in the perioperative analgesia, while 0.25% Bupivacain with addition of Morphine was used in the postoperative period when continuous epidural analgesia was applied. The ISAS, VAS and Ramsey scales were used and the data were analysed with the Kormogolov test. The perioperative sedation in arthroscopy and arthrotomy of the knee is good without any significant differences associated with a kind of the drugs applied. The single-shot epidural anaesthesia is inadequate only during a prolonged arthroscopy of the knee. The postoperative continuous epidural analgesia, expressed in the VAS scale, was inadequate. A level of general satisfaction of the patients of the sedation and analgesia, expressed in the points of the ISAS scale, was satisfactorily good.
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PMID:[Perioperative sedation and analgesia for complications from arthroscopy and arthrotomy of the knee joint]. 1281 76

While it is well established that acute stress can produce antinociception, a phenomenon referred to as stress-induced analgesia, repeated exposure to stress can have the opposite effect. Since, chronic pain syndromes, such as fibromyalgia and rheumatoid arthritis, may be triggered and/or exacerbated by chronic stress, we have evaluated the effect of repeated stress on mechanical nociceptive threshold and inflammatory hyperalgesia. Using the Randall-Selitto paw pressure test to quantify nociceptive threshold in the rat, we found that repeated non-habituating sound stress enhanced the mechanical hyperalgesia induced by the potent inflammatory mediator, bradykinin, which, in normal rats, produces hyperalgesia indirectly by stimulating the release of prostaglandin E2 from sympathetic nerve terminals. Hyperalgesia induced by the direct-acting inflammatory mediator, prostaglandin E2 as well as the baseline nociceptive threshold, were not affected. Adrenal medullectomy or denervation, reversed the effect of sound stress. In sound stressed animals, bradykinin-hyperalgesia had a more rapid latency to onset and was no longer inhibited by sympathectomy, compatible with a direct effect of bradykinin on primary afferent nociceptors. In addition, implants of epinephrine restored bradykinin-hyperalgesia in sympathectomized non-stressed rats, lending further support to the suggestion that increased plasma levels of epinephrine can sensitize primary afferents to bradykinin. These results suggest that stress-induced enhancement of inflammatory hyperalgesia is associated with a change in mechanism by which bradykinin induces hyperalgesia, from being sympathetically mediated to being sympathetically independent. This sympathetic-independent enhancement of mechanical hyperalgesia is mediated by the stress-induced release of epinephrine from the adrenal medulla.
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PMID:Repeated sound stress enhances inflammatory pain in the rat. 1593 44

Adrenaline has been added to local anaesthetic solutions for more than a century. The aim has been to delay the absorption of the local anaesthetic drug and to prolong and enhance its anaesthetic effect, both in peripheral and central neuraxial blockades. The intention in this chapter has been to give up-to-date knowledge about adrenaline as an adjuvant to local anaesthetics and/or opioids in clinical peripheral and central blockades. My own research has focused on optimizing postoperative epidural analgesia by adding adrenaline and/or fentanyl to an epidural mixture with dilute bupivacaine or ropivacaine. The main part of this chapter will therefore focus on the advantages and disadvantages of adrenaline in epidural analgesia. However, recent knowledge about adrenaline in peripheral blockade will also be covered, together with some pharmaceutical comments on the shelf-life of local anaesthetic mixtures containing adrenaline.
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PMID:Advantages and disadvantages of adrenaline in regional anaesthesia. 1596 95


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