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)

The effects of high dose alfentanil on the cerebral vascular responses to alterations in mean arterial pressure (MAP), arterial oxygen tension (PaO2) and arterial carbon dioxide tension (PaCO2) were studied in 17 dogs, using the cerebral venous outflow technique. In six animals anaesthetized with sodium pentobarbitone 30 mg kg-1 i.v., bolus injection of alfentanil 0.32 mg kg-1 i.v. decreased MAP without a change in cerebral blood flow (CBF). In another group of animals(n = 5) anaesthetized with pentobarbitone 30 mg kg-1 i.v. the CBF responses to changes in MAP, PaO2, and PaCO2 were studied. In a third group of animals (n = 6) anaesthetized with alfentanil 0.32 mg kg-1 i.v. plus pentobarbitone 1-2 mg kg-1 i.v. and an infusion of alfentanil 0.32 mg kg-1 h-1, the CBF response to alterations in MAP, PaO2, and PaCO2 were studied and compared with the barbiturate-anaesthetized animals. The CBF responses to hypercapnia and hypoxia in the alfentanil-anaesthetized animals were not different from those observed in animals anaesthetized with barbiturate only. The lower and upper limits of cerebral autoregulation in alfentanil-anaesthetized animals were not different from those observed in animals anaesthetized with barbiturate only. The data suggest that alfentanil, in doses sufficient to cause profound analgesia and anaesthesia, does not alter cerebral reactivity to changes in PaO2, PaCO2 and MAP.
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PMID:Effects of alfentanil on cerebral vascular reactivity in dogs. 393 29

A therapeutic regimen is described for sedative, analgesic, and anti-emetic effect in patients receiving intra-arterial carmustine (BCNU) for malignant gliomas. This regimen consists of nalbuphine, 30 mg, i.v., and droperidol, 2.5 mg, i.v., given immediately prior to intra-carotid BCNU infusion. Droperidol, 2.5 mg, i.v., is then administered on four hour intervals for sixteen hours post-procedure. This combination provided excellent effect in nine patients treated for twelve intra-carotid infusions. None of the nine patients experienced vomiting, one experienced mild nausea several hours post-infusion, and non complained of severe pain or discomfort. Thirteen additional patients received diazepam, 10 mg, P.O., prior to the intra-carotid BCNU infusion, with fentanyl, 100 mcg, i.v., and prochlorperazine, 10 mg, i.m. at the onset of infusion. All thirteen patients suffered from severe nausea, vomiting, and orbital pain. The nalbuphine/droperidol combination is thought to provide a superior alternative to the traditional narcotic/pheonothiazine/benzodiazepine combination for carotid BCNU infusion. This combination has theoretical advantages for the patient with intracranial mass lesions by providing analgesia and sedation with minimal potential for respiratory depression and carbon dioxide retention.
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PMID:Nalbuphine and droperidol in combination for sedation and prevention of nausea and vomiting during intra-carotid BCNU infusion. 395 77

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

Two groups of 100 children each who underwent adenoidectomy and/or tonsillectomy were anaesthetised by halothane 1% or by a neuroleptic technique (NLA) using fentanyl 0.0025 mg/kg and droperidol 0.125 mg/kg as a fixed combination (Thalamonal). Both techniques were supplemented with nitrous oxide/oxygen 4/2 l. All children were premedicated with atropine 0.015 mg/kg, fentanyl 0.0025 mg/kg and droperidol 0.125 mg/kg i.m. Quality of premedication and postoperative behaviour and analgesia were assessed by standardised criteria. 93% of the patients arrived at the theatre sleeping or detached, 75% showed almost no reactions to venipuncture. Heart rate during surgery in both groups increased by 13%, mean arterial blood pressure in the NLA group increased by 9% and in the halothane group dropped by 5%. Postoperatively blood pressure in NLA patients returned to normal, while in the halothane group there was a transient rise by 10%. Protective reflexes and consciousness were restored in the NLA group earlier. After halothane, stridor occurred in eight cases upon extubation. Postoperative analgesia scores in NLA patients were double those in the halothane group. Moderate metabolic acidosis and slight hypercapnia were postoperatively present in both groups twice. Modified neuroleptanaesthesia proved equal to halothane anaesthesia for ENT surgery. No respiratory depression was seen. Advantages like uncomplicated quick recovery and protracted postoperative analgesia are opposed by disadvantages like inferior vegetative blockade and inferior pharmacokinetics. Close postoperative supervision in a recovery room is a prerequisite to using this NLA technique.
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PMID:[The use of neuroleptanesthesia in adenotonsillectomy in children]. 643 37

The ventilatory effects of tramadol (T) and nefopam (N) are evaluated in anesthetized patients with enflurane in a closed circuit breathing system and compared with the effects of pentazocine (P). The following parameters tidal volume (VT), minute ventilation (V), CO2 (capnometry) occlusion pressure (OP), ventilatory response to hypercarbia are recorded after 30 minutes of anaesthesia, before and after repeated injections of the analgesics, P: 15 mg, N: 40 mg, T: 100 mg are injected I.V., and analgesics administration is repeated at 30 minutes interval, so that the patients receive a total P dose of 30 mg, a total N dose of 60 mg and a total T dose of 200 mg. The administration of 15 mg of P induces a change in VT (-24%), ventilatory frequency (-40%), OP (-18) OP only returns to basal values after a second dose. The ventilatory response to hypercarbie is indeed satisfying (increase of 61% in V). After N and T, ventilatory frequency is not disturbed. V increases of 16% and 11% respectively after the first injection, and of 31% and 2% after the second injection. OP increases by 39% and 56% respectively after the first injection and gets better over time with nefopam (+ 58%), 30 mg of P. 20 mg of N and 100 mg of T are equivalent for analgesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Choice of a central analgesic for anesthesia with spontaneous respiration]. 652 78

The influence of anaesthesia and surgery on the pharmacokinetics of morphine was studied in 10 patients. Plasma concentrations of morphine were assayed by gas chromatography with electron capture detection. All patients were studied on the day of surgery and again 3 to 7 days later. Mean +/- SD for peroperative Vd(area) was 6.3 +/- 3.6 L/kg and for the terminal half-life was 3.8 +/- 2.3 h. In the postoperative period, Vd(area) decreased to 3.7 +/- 1.4L/kg and the terminal half-life to 2.2 +/- 1.1 h. Plasma clearance (Clp) remained constant, peroperative Clp being 20 +/- 7.0 ml/min/kg and postoperative Clp 21 +/- 6.0 ml/min/kg. Postoperative pain was relieved by patient-controlled administration of intravenous doses of morphine by means of a programmable drug injector. The mean morphine consumption was 2.6 +/- 1.2 mg/h, which produced a mean plasma concentration of 21 +/- 12 ng/ml with a calculated mean minimum effective concentration (MEC) of 16 +/- 9 ng/ml. In 1 patient, temporary hypercapnia was seen during a period of hypovolaemia. Analgesia was considered satisfactory by all patients.
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PMID:Patient-controlled analgesic therapy, Part IV: pharmacokinetics and analgesic plasma concentrations of morphine. 709 1

A few effects of carbon dioxide on pain threshold and acid-base balance are known. The purpose of this study was to investigate specifically the variations of analgesia in relation to hypercapnia during general anaesthesia and the respective roles played by carbon dioxide and [H+]. The nociceptive jaw opening reflex was studied on five beagle dogs anaesthetized with alfathesin administered at constant rate under acute hypercapnic conditions and acute metabolic acidosis. Acute hypercapnia did not decrease the jaw opening reflex significantly until a level was reached where PaCO2 values modified blood [H+] (pH) significantly (10 +/- 1.04 kPa corresponding to [H+] 91.5 +/- 13.24 nmol/l (pH 7.04 +/- 0.06) p less than 0.05)). At [H+] 176.2 +/- 42.77 nmol/l (pH 6.7 +/- 0.13) (p less than 0.01) the reflex was only 9.3 +/- 3.9 per cent (p less than 0.001) of its initial value. The infusion of decinormal solution of HCl during constant capnia caused an abrupt drop of the reflex. There was a correlation between reflex and metabolic acidosis (p less than 0.05). The authors conclude that modification of the jaw opening reflex occurs with extreme values of arterial [H+] incompatible with safe anaesthesia and they discuss the mechanisms involved.
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PMID:[Comparison of the effects of acute respiratory acidosis and acute metabolic acidosis on the jaw-opening reflex in the anesthetized dog]. 723 18

Although results obtained in baboons and rats have demonstrated that the fatty acid cyclo-oxygenase inhibitor indomethacin reduces cerebral blood flow (CBF) under control conditions and markedly attenuates the CBF response to hypercapnia, nonconfirmatory results have been obtained in rabbits and cats. Since these latter studies were carried out under barbiturate anesthesia, we tested the effect of indomethacin (10 mg kg-1) on CBF and cerebral oxygen consumption in rats anesthetized with 150 mg kg-1 of phenobarbital. At normocapnia the barbiturate reduced CBF, measured with a 133Xe modification of the Kety-Schmidt technique, to about 50% of nitrous oxide control values as previously determined with a similar technique. At this CBF level, indomethacin induced a small, albeit highly significant decrease in CBF. We suggest that a reduction of this magnitude will escape detection with some CBF techniques in current use. Indomethacin induced a highly significant decrease in CBF during hypercapnia, demonstrating that the barbiturate does not eliminate the effect of indomethacin on CO2 responsiveness. The magnitude of the reduction in CO2 response was so large that is should be detected with most methods for measuring CBF. A comparison with previous data on animals under 70% N2O demonstrated that phenobarbital reduced the CO2 responsiveness. defined as the ratio deltaCBF/deltaPCO2, to 39% of that observed under nitrous oxide analgesia. With both types of anesthesia, indomethacin curtailed the CO2 responsiveness 4- to 5-fold.
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PMID:Effects of indomethacin on cerebral blood flow and oxygen consumption in barbiturate-anesthetized Normocapnic and hypercapnic rats. 732 33

Patients in the ICU who require intubation and mechanical ventilation benefit from adequate sedation and analgesia. Traditionally, this has been achieved using benzodiazepines and opioids. Alternatively, propofol is being administered for sedation of patients in the ICU with increasing frequency. Propofol has a number of properties that make it a potentially superior choice for sedation of intubated ICU patients. The rapid onset and offset of sedation with propofol, even after prolonged administration, allow for greater control over the level of sedation and more rapid weaning from mechanical ventilation. In addition, long-term administration of propofol does not appear to be associated with the development of tolerance, addiction, or withdrawal following discontinuation. Propofol suppresses cellular oxygen consumption and carbon dioxide production without increasing anaerobic metabolism. This may be beneficial in patients with severe hypoxemia, hypercarbia, or myocardial ischemia. Finally, the use of propofol may reduce or eliminate the need for other medications in these patients such as muscle relaxants, antihypertensives, lipid nutritional supplements, and analgesics, thereby simplifying their medication regimens and reducing the overall cost of their care while in the ICU. Propofol can be administered to critically ill patients for sedation with a high degree of safety and efficacy. Propofol causes systemic vasodilatation which may result in unwanted hypotension, especially in patients who are already hemodynamically compromised. Propofol also causes ventilatory depression, so its use should be restricted in the ICU to patients whose airway is protected by an endotracheal tube and whose ventilation is closely monitored. Finally, continuous administration of propofol may cause clinically significant hypertriglyceridemia in patients with disordered triglyceride metabolism, or in patients receiving excessive doses of propofol or parenteral lipid supplements. Although propofol is more expensive than equipotent doses of other sedative agents, the additional cost of using propofol for sedation of critically ill patients in the ICU may be more than offset by the savings accrued from faster times to extubation, shorter ICU stays, and the use of fewer medications to manage these patients. Further research needs to be done to determine the potential clinical and cost benefits of using propofol for sedation of patients in the ICU.
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PMID:Propofol: a new drug for sedation in the intensive care unit. 763 54

Respiratory depression is a limiting factor in the therapeutic use of opioid analgesics. It has been suggested that respiratory depression is mediated by mu rather than kappa receptors and may involve a decrease in central nervous system sensitivity to hypercapnia. This study investigated opioid receptor mechanisms underlying respiratory depression in unanesthetized rhesus monkeys (n = 3) breathing air or 5% CO2 in air into a pressure displacement head plethysmograph. Apparent pA2 analyses of s.c. quadazocine (a mu-selective antagonist) were carried out on the effects of cumulative doses of s.c. bremazocine, ethylketocyclazocine (EKC) and (+/-)-(1-R/S,5-R/S,2 = R/S)-5,9-dimethyl-2'-hydroxy-2- tetrahydrofurfuryl-6,7-benzomorphan (Mr2033) (compounds with kappa agonist effects in other in vivo assays), alfentanil and etonitazene (compounds with mu agonist effects in other in vivo assays). Alfentanil, bremazocine, EKC and Mr2033 were approximately equipotent in causing dose-dependent depression of respiratory minute volume of CO2-stimulated and air respiration, whereas etonitazene was approximately 10-fold more potent than the above compounds. Dose-effect curves for respiratory frequency, tidal volume and respiratory minute volume for all of the agonists except bremazocine were shifted to the right by increasing quadazocine doses. Together with data previously obtained in drug discrimination and analgesia assays, results of the present study demonstrating homogeneous pA2 values for quadazocine with alfentanil, etonitazene, EKC and Mr2033 strongly suggest that the latter two compounds decrease respiratory function in rhesus monkeys by acting on mu receptors.
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PMID:Apparent pA2 analysis on the respiratory depressant effects of alfentanil, etonitazene, ethylketocyclazocine (EKC) and Mr2033 in rhesus monkeys. 809 21


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