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)

To determine the effect of carbonation of lidocaine, a comparison of 1.0% lidocaine hydrochloride (HCl) and 1.1% lidocaine hydrocarbonate (CO2), both with 1:200,000 epinephrine, was made in this study of 50 patients receiving interscalene brachial plexus blocks. Sensory block was determined by the response to pinprick in the C2-T2 dermatomes, while motor block was assessed by the development of paresis and paralysis at the shoulder and hand. The percentage of patients developing analgesia (decreased sensation to pinprick) and anesthesia (total absence of sensation to pinprick) at each dermatome level as well as the percentage of patients developing motor block was not significantly different between the two forms of lidocaine. The initial onset of analgesia [lidocaine HCl, 4.0 +/- 2.4 (SD) minutes; lidocaine CO2, 4.3 +/- 3.8 (SD) minutes] and anesthesia [lidocaine HCl, 10.1 +/- 5.7 (SD) minutes; lidocaine CO2, 7.8 +/- 4.4 (SD) minutes] did not differ significantly between the two groups. At the individual dermatomes, there was no difference in the onset of analgesia except at one dermatome level, C7, which was near the level of local anesthetic injection. Anesthesia onset in each dermatome as well as the onset of motor block did not differ between the two groups. It is concluded that lidocaine CO2 does not offer any significant clinical advantage over lidocaine HCl in interscalene brachial plexus block.
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PMID:Lidocaine hydrocarbonate is not superior to lidocaine hydrochloride in interscalene brachial plexus block. 207 84

In the period from April 1987 to April 1990, 230 patients with pathological changes of the vulva, vagina and cervix uteri were treated with the CO2-laser. The diagnosis and pretreatment stages of the diseases were confirmed by the cytodiagnostic, colposcopic and histopathological results of the biophysics. In most cases, DNA-hybridization of human papilloma viruses confirmed their virus etiology. Twenty patients had peak condyloma of the vulva and vagina, 34 had benign cervical diseases, 65 were at the premalignant and 111 in the first stages of malignant cervical disease. Vaporizations, conical or cylindrical excisions were performed depending on the nature of disease and its localisation. The average age of operated patients was 30.6 years and the average parity 0.69. Operations were performed using analgesia and in rare cases total anesthesia. After the excision treatment, the tissue was checked histo-pathologically according to the principle of series. The complications were very rare. After operation, postoperative control was performed after 3.9 and 15 months, and later once a year. The results have shown that one treatment was sufficient in 80% of patients for curing vulvar and vaginal disease and 20% patients needed repeat because of the condyloma that relapsed. After the first treatment, benign and premalignant cervical diseases were cured in 100% of cases. In 95.4% operated patients at the first stages of cervical malignant diseases, the excisional treatment was final and in 4.6% needed an additional radical therapy because of a higher stage of lesion found by the conular histo-pathological analysis. There were no relapses relating to the cervix.
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PMID:[Use of the CO2 laser in the treatment of pathologic changes in the vulva, vagina and uterine cervix]. 209 98

The influence of two different doses of oral naltrexone on the adverse effects and the analgesia of epidural morphine were compared in a double-blind, placebo-controlled study. Forty-five patients undergoing cesarean section were provided postoperative analgesia with 4 mg epidural morphine. Five minutes later they received 6 mg naltrexone, 9 mg naltrexone, or placebo as an oral solution. Pain relief was assessed by the Visual Analog Scale (VAS) and by direct questioning of the patients. Requirement for additional analgesics and side effects were noted. Respiratory effects of epidural morphine and naltrexone were assessed using the ventilatory responses to CO2 and by monitoring O2 saturation (Spo2) using pulse oximetry. All patients in the placebo group had adequate analgesia. One of the 15 patients who received naltrexone 6 mg had inadequate analgesia versus five of the 15 patients who received naltrexone 9 mg (P less than 0.05), 9 mg versus placebo. Ten patients (67%) in the placebo group had pruritus while no patient in the 6 mg naltrexone group and one patient in the 9 mg group experienced mild pruritus (P less than 0.05), placebo versus other two groups. The CO2 response slopes were depressed compared to control values from 6-16 h in the placebo group, from 6-12 h in the 6 mg naltrexone group. No significant depression was noted in the 9 mg naltrexone group. The authors conclude that oral naltrexone 6 mg significantly reduces the incidence of pruritus associated with epidural morphine without affecting analgesia and that 9 mg naltrexone is associated with shorter duration of analgesia than 6 mg naltrexone.
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PMID:Prophylactic oral naltrexone with epidural morphine: effect on adverse reactions and ventilatory responses to carbon dioxide. 210 73

In a double-blind study the relative postoperative respiratory and analgesic effects of perioperatively administered nalbuphine and fentanyl were compared in 60 females undergoing gynecological surgery under i.v. anesthesia. One milliliter (10 mg) nalbuphine was considered equipotent to 1 ml (100 micrograms) fentanyl. In the recovery period pain was assessed by visual analog score (VAS) and recovery by Pegboard scoring. Respiratory function was evaluated by continuous monitoring of respiratory frequency and end-tidal CO2 (ETCO2) and by frequent arterial blood gas analyses. The total volume of analgesic required for surgical analgesia was similar in the two groups. Patients in the nalbuphine group showed mild to moderate increases in pulse rate during the intubation phase and in blood pressure during surgery. Fentanyl was more effective in suppressing these cardiovascular responses. Within the first 15 min following recovery, increasing PaCO2 and ETCO2 as well as respiratory rates below 10/min were noted in 8 patients, who all belonged to the fentanyl group; in 4 of these patients i.v. naloxone had to be administered to reverse respiratory depression. Prolonged sedation was a common feature in patients receiving nalbuphine. It was concluded that fentanyl was superior to nalbuphine in attenuating the pressor responses to intubation and surgery. However, fentanyl was associated with respiratory depression in a considerable number of patients. The quality and duration of postoperative analgesia were similar in the two groups.
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PMID:Influence of perioperative nalbuphine and fentanyl on postoperative respiration and analgesia. 211 27

The magnitude and duration of analgesia and respiratory depression induced by fentanyl (1.0, 2.0, and 4.0 micrograms/kg) and sufentanil (0.1, 0.2, and 0.4 microgram/kg) after intravenous administration over 30 s were measured in 30 healthy young adult male volunteers divided into three groups and studied in a double-blind, randomized fashion. Each volunteer received one dose of fentanyl or sufentanil and no sooner than 48 h later, the corresponding equipotent dose of the other opioid. End-tidal CO2 and ventilatory and occlusion pressure responses to CO2 rebreathing were used to measure drug-induced respiratory effects. Analgesic effects were assessed by changes in the pain threshold to electric shock applied to the forearm. Plasma levels of fentanyl and sufentanil were measured by radioimmunoassay. Testing and sampling intervals were 5, 30, 60, 90, 120, 240, 300, and 360 min after drug administration. The magnitude and duration of depression of the ventilatory and occlusion pressure response were significantly less with sufentanil compared with fentanyl, irrespective of dose. Ventilatory and occlusion pressure responses returned to control values by 30 and 30 min, respectively, after sufentanil and by 240 and 120 min, respectively, after fentanyl. Statistically significant elevations of the pain threshold were, however, greater and longer lasting after sufentanil compared with fentanyl. Pain threshold returned to control values 180 min after sufentanil but only 90 min after fentanyl. These results suggest that sufentanil may provide better patient comfort with less respiratory depression than does fentanyl.
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PMID:Differences in magnitude and duration of opioid-induced respiratory depression and analgesia with fentanyl and sufentanil. 197 32

This study evaluates the respiratory effects of laparoscopy under epidural anesthesia in seven female patients (ASA physical status I) scheduled for a gamete intrafallopian transfer procedure. Epidural anesthesia was performed with 15-18 mL of 1.5% plain lidocaine using a catheter inserted at the L3-4 level. The upper level of analgesia to pinprick was measured 20 min after lidocaine injection. Ventilatory measurements and arterial blood gas analyses were performed (a) preoperatively, in the horizontal supine position with a T7-9 level of analgesia; (b) in the 20 degrees Trendelenburg position with a T2-5 level of analgesia; (c) during intraabdominal insufflation of CO2 through the laparoscope; and (d) after CO2 exsufflation by manual compression of the abdomen before removal of the laparoscope while in the horizontal position. On-line measurements of VO2, VCO2, VE, VT, F, and PETCO2 were made using a Beckman metabolic cart, while the patients breathed room air through an anesthetic face mask. No significant changes in the ventilatory variables were observed in the Trendelenburg position. In contrast, CO2 insufflation significantly increased VE (from 9.1 +/- 1.0 L/min to 11.8 +/- 2.6 L/min, mean +/- SD), and F (from 16.9 +/- 1.9 breaths/min to 23.1 +/- 3.3 breaths/min, mean +/- SD), whereas VCO2 remained unchanged. PaCO2 remained constant throughout the study. These results suggest that epidural anesthesia may be a safe alternative to general anesthesia for outpatient laparoscopy, as it is not associated with ventilatory depression.
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PMID:Ventilatory effects of laparoscopy under epidural anesthesia. 213 37

A significant association exists between the use of epidural morphine (EM), reactivation of herpes labialis (HL) commonly known as coldsores, and pruritus in the obstetric population. A randomized prospective study was designed to eliminate previously identified confounding variables. Immediately following delivery, parturients having undergone cesarean section with epidural anesthesia with carbonated lidocaine (Xylocaine CO2, Astra, Mississauga, Ontario, Canada) with 1:200,000 epinephrine were sequentially randomized to receive either EM or im opioids for postoperative analgesia. One blood sample was collected for viral serology and two mouthwashes (day 0 and 2) were collected to determine oral viral shedding. The patients were observed daily for 5 days. Coldsores were cultured for herpes simplex virus (HSV). Of 187 patients, 96 received EM and 91 im opioids; herpes labialis occurred in 14 of 96 (14.6%) of the former but in 0 of 91 of the latter (P = 0.0004). All 14 experienced facial pruritus. The two groups were at equal risk for reactivation (seropositivity 64.6% and 62.6%, respectively). Analysis of data for those with positive HSV serology reveals 14 of 62 (22.5%) had EM and herpes labialis compared with 0 of 57 in the im group (P less than 0.0001). The incidence of oral viral shedding was low. Surgical stress, the local anesthetic solution, and epinephrine addition to the local anesthetic were eliminated as confounders. Stepwise logistic regression analysis revealed that EM and a history of herpes labialis in these patients were predictive for reactivating oral HSV.
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PMID:Herpes labialis in parturients receiving epidural morphine following cesarean section. 184 64

In summary, these findings indicate the importance of designing future experiments that delineate between opioid and nonopioid forms of respiratory disease and dysfunction, and the need to identify means of diagnosing them in order to achieve successful recovery. Apparently there is great diversity between animal species in terms of contributions of endogenous opioids to tonic control of ventilation, and future work should strive to identify which species is most appropriate as a model of human ventilatory control and disease. Certain opioid receptor types appear to be linked to independent respiratory functions. For instance, mu receptors in the brain stem produce strong inhibitory actions on respiratory parameters, including RR, VT, VE, and CO2 sensitivity. These effects have been observed in vivo and by electrophysiologic recordings in vitro. Delta receptors may also exert some inhibitory effect on respiration, especially in the NTS. In the CNS, the ventral surfaces of the medulla and pons, especially the NTS and NA, seem to be important sites for opioid-induced inhibition of respiration, whereas the spinal cord probably is not involved in opioid-mediated ventilatory depression. Kappa receptors appear to be devoid of respiratory depressant activity, whereas sigma receptors may stimulate some ventilatory parameters. Morphine and similar pure mu agonists, such as fentanyl and oxymorphine, probably produce their analgesic and respiratory depressant effects through stimulation of mu receptors. Mixed agonists/antagonists that have mu antagonist (or partial agonist) activity plus kappa agonist and/or sigma agonist activity show a ceiling effect for respiratory depression. Future tests need to determine which opioid receptor may be responsible for the ceiling effect. In addition, the effects of mu, delta, kappa, and sigma selective agonists on hypoxic drive should also be determined, as a drug that stimulates hypoxic sensitivity in the face of hypercapnic depression may produce less overall respiratory depression due to counteractive effects. In the future, clinically optimal opiates should have more specificity of action than those available now. This may be achieved by creating drugs selective for single receptors or by creating drugs with desirable combinations of receptor selectivities. The combinations of mixed agonists/antagonists with pure mu agonists currently in use today are promising, as they provide analgesia with reduced respiratory depression. In the early days of opiate research and development, combination drug regimens were thoroughly tested to determine the "ideal ratios" that would retain analgesic properties but not the other undesirable effects such as respiratory depression (196).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differential roles of opioid receptors in respiration, respiratory disease, and opiate-induced respiratory depression. 217 88

Nalbuphine hydrochloride, an agonist-antagonist opioid, is reported to reverse the respiratory depression of moderate doses of fentanyl (20 micrograms.kg-1) and still provide good analgesia. We report four patients having abdominal aortic aneurysm repair in which we attempted to reverse the respiratory depression of large doses of fentanyl (50-75 micrograms.kg-1) with nalbuphine (0.3 mg.kg-1, 0.1 mg.kg-1 or 0.05 mg.kg-1). Nalbuphine reversed respiratory depression in all four patients and the respiratory rate increased from 10 to 23 breaths per minute, end-tidal CO2 decreased from 7.0 +/- 0.3 per cent to 5.6 +/- 0.7 per cent, and peak inspiratory pressure after 0.1 seconds increased from 4 +/- 1.4 to 13 +/- 2.6 mmHg. However, hypertension, increased heart rate, and significant increase in analogue pain scores accompanied reversal of respiratory depression. Agitation, nausea, vomiting, and cardiac dysrhythmias also were observed frequently. We do not recommend the use of nalbuphine to facilitate early extubation of the trachea after large doses of fentanyl for abdominal aortic surgery.
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PMID:Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases. 165

Hypoventilation produces hypercapnia which can elevate pain thresholds. Hypercapnia is a potent stressor which releases catecholamines and activates the sympathetic nervous system. Some stressors produce analgesia by releasing endogenous opioids. To determine the roles of endogenous opioids and catecholamines in hypercapnic analgesia, we administered CO2 in the inspired gas mixture to conscious rats. CO2 in the range 5-10% elevated tail flick and leg flexion latencies 2- to 3-fold in both intact and spinalised animals. The effects on reflex latencies but not on paCO2 or pHa were blocked by naloxone (2 mg/kg), and were not present in morphine-tolerant animals. The effects were reduced by dexamethasone but were not changed either by adrenalectomy or by systemic guanethidine, propanolol or phentolamine. Hypercapnia delayed the onset of the late phase of behavioural responses to formalin injected into the plantar surface of the hindpaw. We conclude that moderate hypercapnia powerfully depresses flexor withdrawal responses to noxious stimuli, by a mechanism involving release of endogenous opioids but not systemic catecholamines. This effect may account in part for the elevation in pain threshold during hypoventilation.
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PMID:Hypercapnia depresses nociception: endogenous opioids implicated. 235 37


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