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)

In 91 patients who had undergone surgery under C.E.C. the influence of the analgesia on adrenal cortex system was studied. With the exception of the analgesic used, the anaesthesia was performed following the same guidelines in all of the operations. Concentrations of cortisol in plasma were maximum with Pentazocina, the weakest analgesic used by us, and minimum with Fentanest. In view of these results, we can affirm that, in the absence of alterations haemodynamic, metabolic and neurological, concentrations of cortisol in plasma are a true reflexion of the amount of analgesic protection that different drugs offer against noxins stimuli triggered by the surgical act. These findings guarantee the intimate relationship that exists between the nervous system and the endocrine system and they are further confirmed by results obtained with a recently acquired analgesic Fentathienil, which is more potent than Fentanyl.
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PMID:[Analgesics and neuroendocrinic response in cardiac surgery. I. Adrenal cortex response]. 447 Oct 78

Many critically ill patients suffer pain which can produce by itself undesirable effects. Consequently, pain must be carefully prevented, or at least, treated early and effectively. Basal analgesia can be provided by repeated intramuscular administration of narcotics, or rather by continuous intravenous infusion of morphine or meperidine or by a regional anesthetic procedure such as an epidural block. Computer-assisted intravenous "on demand" analgesia with Fentanyl can also be used. When pain coverage is required during transient events such as active physiotherapy or dressing changes, additional intravenous of a narcotic (1-2 mg morphine e.g.) or inhalation of nitrous oxide with oxygen are usually effective.
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PMID:Relief of pain in intensive care patients. 614 50

The effects of several anaesthetics on spinal cord nociceptive neural mechanisms and their interactions with the opiate antagonist, naloxone, were studied in acute, spinal cord transected cats. Intra-arterial injection of bradykinin was used as the noxious test stimulus. Spontaneous activity and the neural response induced by bradykinin were recorded by the multi-unit activity technique in the lateral funiculus of the spinal cord. Naloxone, 0.1 or 2.0 mg/kg i.v. had little effect on the bradykinin-induced response, but enhanced the spontaneous firing of the lateral funiculus significantly. Fentanyl, 30 micrograms/kg i.v., depressed both the bradykinin-induced response and spontaneous firing. These effects of fentanyl were antagonized completely by naloxone, 0.1 mg/kg i.v. Nitrous oxide, thiamylal, halothane and ether depressed the bradykinin-induced response considerably, but it was not antagonized by naloxone, 0.1-2.0 mg/kg i.v. Enflurane had little effect on the bradykinin-induced response. The effects of these anesthetics on spontaneous firing were divergent: nitrous oxide enhanced it while other drugs depressed it, to various degrees. All these data suggest that the neural and/or neurochemical mechanisms of anesthetic-induced analgesia differ from mechanisms related to opioids.
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PMID:Naloxone does not antagonize the anesthetic-induced depression of nociceptor-driven spinal cord response in spinal cats. 628 89

Fentanyl (FEN) and diprenorphine's (DIPR) potentials for analgesia and reinforcement were assayed using rats. Analgesia was measured by the classic tail-flick test. The test germane to opioid reinforcement involved measuring pressing rates for direct electrical stimulation of the lateral hypothalamus and ventral tegmental area. FEN, as does morphine and heroin, produced strong analgesia and enhanced pressing rates for brain stimulation. DIPR produced no analgesia and antagonized FEN's analgesia. DIPR, at doses antagonizing FEN's analgesia, enhanced pressing for brain stimulation. DIPR's enhancement of pressing was antagonized by naloxone (100 micrograms/kg). When FEN and DIPR were given concurrently, pressing for brain stimulation was not reduced and was greater than after FEN alone was given. These data support a conclusion that different types of receptors are associated with opioid analgesia and reinforcement.
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PMID:Opioid antinociception and positive reinforcement are mediated by different types of opioid receptors. 631 75

This prospective study was designed to evaluate the benefit of a bupivacaine-fentanyl mixture vs bupivacaine alone in epidural anaesthesia for caesarean section. In 10 women, 0.5% bupivacaine (1.18 ml per metamer) was injected in the epidural space. In 20 women, 0.5% bupivacaine (1.06 ml per metamer) was injected by the same route together with fentanyl (1.70 +/- 0.09 micrograms X kg-1). The bupivacaine-fentanyl group showed a significantly shortened onset of analgesia (p less than 0.001), as well as a significant reinforcement of this analgesia graduated from 0 to 4 (p less than 0.01 at 25 min, p less than 0.001 at 75 min and at the maximum of pain, for the two sets of scores). All the Apgar scores were maximal at 5 min. No clinical respiratory depression was observed in either the mothers or the neonates. Fetal and maternal blood concentrations were in favour of respiratory innocuousness of the method (peak fentanyl concentrations: in mothers 1.5 ng X ml-1, in neonates 0.8 ng X ml-1). Fentanyl never induced any significant haemodynamic variations. Pruritus and nausea respectively occurred in six and two patients respectively in the bupivacaine-fentanyl group. In conclusion, in caesarean section, the adjunction of fentanyl to bupivacaine significantly improved analgesia without any clinical respiratory depression both in the mother and the neonate.
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PMID:[Epidural anesthesia using the bupivacaine-fentanyl combination for cesarean section]. 635 72

The analgesic effects of the synthetic opiate fentanyl citrate (0.1 mg) on subjective pain reports (SPR) and late-wave event-related potentials (ERP) recorded during painful dental stimulation were examined in human subjects. Such waves have been shown to reflect the contribution of cognitive variables, such as expectancy and belief, to perception. In addition, the study was intended to demonstrate a dose-related narcotic antagonism with injection of naloxone (1.2 or 0.4 mg) or normal saline (double-blind) following IV fentanyl administration. Fentanyl reduced both ERP waveform amplitudes and SPR as have previously studied analgesic agents, such as nitrous oxide, acupuncture, and aspirin. Naloxone injection reversed both ERP and SPR changes, but surprisingly, a reversal of narcotic analgesia equal to that of 0.4 mg naloxone was seen with saline injection. By chance, all subjects were health-science students or professionals who were knowledgeable in opiate pharmacology, and so placebo reversal was hypothesized. Alternatively, it was hypothesized that fentanyl cleared more rapidly than predicted, thus, producing apparent reveal. In a second experiment involving similarly knowledgeable subjects with identical procedures and testing intervals, subjects received 0.1 mg fentanyl, but no reversal injection. The fentanyl effect was constant across this time period. The data, thus, support the hypothesis where the subjects were knowledgeable in opiate pharmacology, was placebo opiate antagonism.
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PMID:Opiate analgesia and its antagonism in dental event-related potentials: evidence for placebo antagonism. 640 47

The effect of high-dose fentanyl on the cerebral vascular response to alterations in mean arterial blood pressure, arterial O2 tension (PaO2), and arterial CO2 tension (PaCO2) was studied in 28 mongrel dogs using the cerebral venous outflow technique. In 13 animals anesthetized with sodium pentobarbital (30 mg/kg, iv), bolus injection of fentanyl (25 micrograms/kg, iv) decreased mean arterial blood pressure (MABP) without a change in cerebral blood flow (CBF). In these animals, the response of the cerebral circulation to changes in PaO2, PaCO2, and MABP was determined before and after fentanyl administration. Fentanyl did not alter the increase in CBF caused by hypoxic hypoxia or hypercapnia. The lower and upper limit of cerebral autoregulation determined by hypovolemic hypotension and norepinephrine infusion, respectively, also were unaltered by fentanyl administration. The CBF response to alterations of MABP, PaO2, and PaCO2 were studied in another group of 15 dogs anesthetized with fentanyl (100 micrograms/kg) plus small doses (3-5 mg/kg) of pentobarbital. The CBF response to PaO2, and PaCO2 in these animals was not different from that observed in animals anesthetized with barbiturates only. The lower and upper limit of cerebral autoregulation also were not different from that observed in animals anesthetized with barbiturates only. These data suggest that fentanyl in doses sufficient to cause profound analgesia and anesthesia did not alter cerebral responsivity to changes in PaO2, and PaCO2, and MABP.
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PMID:Fentanyl and cerebral vascular responsivity in dogs. 642 Nov 99

Fentanyl or alfentanil (at a dose ten times that of fentanyl) was administered to fifty healthy patients undergoing elective surgery. They were given in a double-blind manner for analgesia in a total intravenous anaesthesia technique to see if differences existed in their respiratory depressant, analgesic or sedative effects. They were combined in the same syringe with etomidate and given by intravenous bolus injection followed by a continuous intravenous infusion. Analgesia was generally adequate for the operations in this study. Respiratory depression (respiratory rate less than ten) lasted about ten minutes after drug administration, ceased in all patients. The return of respiratory rate, consciousness, and psychomotor performance to control was similar in the groups receiving fentanyl or alfentanil. This study showed that alfentanil and fentanyl have equivalent potency and duration of action when used in a ten to one ratio. Furthermore, the technique provided good operating conditions but there was a high incidence of postoperative drowsiness, nausea and vomiting.
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PMID:[Double-blind testing of alfentanyl and fentanyl in total intravenous anesthesia]. 642 98

Application of 0.1 mg Fentanyl and 5 mg Droperidol iv. (obstetric neurolept-analgesia) causes an enduring pain relief. Labor is not influenced. The obstetric neuroleptanalgesia appears to accelerate labor indirectly. The condition of the fetus will be not affected by obstetric neuroleptanalgesia. In respect of this obstetric neuroleptanalgesia can be recommended as a method of analgesia during parturition.
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PMID:[Use of small neuroleptanalgesia sub partu]. 648 16

The present study examined the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of decerebrate, spinal cord-transected cats. This work was performed in order to evaluate the dose-response relationship, time course, and naloxone reversibility of fentanyl suppression of neurons that are involved with the transmission of information about pain. Extracellular single neuron recordings were obtained from 18 WDR neurons in the lumbar enlargement. These neurons were activated by a radiant heat stimulus on the footpads of the hindpaw. Fentanyl (10, 15, 25 micrograms in 0.5 ml of physiologic saline) was placed on the spinal cord following control studies of each neuron and the effect was observed. In 12 cats, 31 min after fentanyl administration, naloxone (0.1 mg) was administered intravenously, and its effect on the fentanyl suppression was determined. All three doses of fentanyl suppressed both the spontaneous and evoked activity of all the neurons studied. Thirty minutes after fentanyl the mean evoked activity was reduced to 47, 23, and 11% of control values by 10, 15, and 25 micrograms, respectively. The spontaneous activity was reduced to similar levels. Intravenous naloxone (0.1 mg) caused a significant reversal of the fentanyl suppression. The results of the present study indicate that fentanyl causes a naloxone-reversible, dose-dependent suppression of noxiously evoked WDR neuron activity. Such results support the concept that fentanyl is acting through a specific drug-receptor interaction. The onset of neuronal suppression occurred more rapidly, and the duration of the suppression was longer following fentanyl than that seen following spinal morphine. The onset and duration of this suppression correlates well with human clinical data, providing further evidence that alterations of WDR neuronal activity may be important in the production of spinal opioid analgesia.
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PMID:Dose-response suppression of noxiously evoked activity of WDR neurons by spinally administered fentanyl. 685 81


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