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)

On the basis of two case histories, the most recent literature concerning hydrofluoric acid injuries is reviewed with particular attention to the pathogenesis and the therapeutic possibilities. It is concluded that washing with water is the primary and most important treatment. Depending upon the extent of the injury, surface treatment with 2.5% calcium gluconate solution or gel may then be employed and/or infiltration treatment with a 5-10% calcium solution. Possibly combined with local analgesia and hyaluronic acid. Intravenous or intra-arterial infusion of calcium compounds and surgical excision may be considered as specialist treatment.
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PMID:[Hydrofluoric acid injuries: pathogenesis and treatment]. 236 Feb 78

Determinations were made of the effects of the calcium channel blockers, nifedipine and verapamil, on the antagonistic effects of FMRFamide (Phe-Met-Arg-Phe-NH2) and naloxone on morphine- and immobilization-induced opioid analgesia in mice. Intraperitoneal (i.p.) administrations of the calcium channel antagonists significantly reduced the inhibitory effects of intracerebroventricular (i.c.v.) FMRFamide, but had no effects on i.p. or i.c.v. naloxone-mediated inhibition of either morphine- or immobilization-induced analgesia. These results suggest that the antagonistic effects of FMRFamide, (or other endogenous FMRFamide-like peptides) on both opiate- and opioid-mediated analgesia in mice may involve alterations in the functioning of calcium channels.
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PMID:Calcium channel blockers inhibit the antagonistic effects of Phe-Met-Arg-Phe-amide (FMRFamide) on morphine- and stress-induced analgesia in mice. 244 May 27

An exposure for 60 min to a weak 0.5 Hz rotating magnetic field significantly reduced the day-time analgesic effects of morphine in male mice. The dihydropyridine (DHP) calcium channel antagonists diltiazem and nifedipine and the non-DHP antagonist verapamil, as well as the inorganic calcium channel blockers, La3+ and Co2+, differentially reduced, while the DHP calcium channel agonist, BAY K 8644, enhanced the inhibitory effects of the magnetic stimuli. In a similar manner, though to a lesser degree, the calcium channel antagonists and agonist, increased and decreased, respectively, the inhibitory effects of intracerebroventricular administrations of Ca2+ on morphine-induced analgesia. The calcium channel antagonists and agonists had no significant effects on naloxone-mediated reductions of morphine-induced analgesia. These results suggest that exposure to magnetic stimuli affects the functioning of calcium channels and the distribution of calcium ions, thereby, altering the effects of opiates.
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PMID:Calcium channel involvement in magnetic field inhibition of morphine-induced analgesia. 244 52

The study included 48 cases of pulpitis grade II of one-root teeth in 42 patients of either sex aged 21-35 years treated by pulp extirpation under analgesia with immediate filling of canals. In 28 teeth Biopulp was used as an intercalated substance between the periapical tissues and the material filling the canal. The control group comprised 20 teeth filled only with Endomethasone paste. The observations made immediately after filling and clinical-radiological control examination after from 6 months to 3 years showed a high usefulness of calcium hydroxide. Good results were achieved in 100% of cases while in the control group in 70% of cases.
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PMID:[Use of calcium hydroxide in the treatment of pulpitis by extirpation under analgesia]. 248 38

Lappaconitine (LA), isolated from Aconitum sinomontanum Nakai, was characterized as analgesic principle by our laboratory. The analgesic effect of ip LA 6 mg/kg as measured in the rat tail-flick test was reduced by icv CaCl2 or MgCl2 0.1 or 1 mumol/rat. BaCl2 was inactive. The analgesic action induced by LA was potentiated by ethylene glycol tetraacetic acid (EGTA, 0.2 mumol/rat icv) but not by ethylenediamine tetraacetic acid (EDTA, 0.2 or 0.4 mumol/rat icv). The calcium antagonists nifedipine (5 mg/kg ip) and verapamil (1 mumol/rat icv) partially reversed the Ca2+ antagonistic effect on LA analgesia, although nifedipine did not enhance LA analgesic action and only at 15 min after medication did verapamil exhibit enhancement of LA analgesia. The analgesic activity of LA was reduced and augmented by microinjection of CaCl2 0.5 mumol and EGTA 50 nmol to periaqueductal gray (PAG) area, respectively. These results suggest that LA can produce analgesia, possibly through a decrease in cellular calcium availability and PAG may be involved in the Ca2+ antagonistic effect on LA analgesia.
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PMID:[Effects of central Ca2+ on analgesic action of lappaconitine]. 251 40

Multiple modulatory effects of opioids on the duration of the calcium component of the action potential (APD) of dorsal-root ganglion (DRG) neurons of mouse spinal cord-ganglion explants were studied. The APD of DRG neuron perikarya has been previously shown to be shortened by exposure to high concentrations of opioids (ca. 0.1-1 microM) in about 1/2 of the cells tested. The present study demonstrates that in addition to these inhibitory modulatory effects of opioids, lower concentrations (1-10 nM) of present study demonstrates that in addition to these inhibitory modulatory effects of opioids, lower concentration (1-10 nM) of delta- mu, and kappa-opioid agonists elicit excitatory modulatory effects, i.e. prolongation of the APD, in about 2/3 of the sensory neurons tested. APD prolongation as well as shortening elicited by delta, mu, and kappa agonists were prevented by coperfusion with the opioid antagonists, naloxone or diprenorphine (10 nM). APD prolongation induced by the delta-agonist [D-Ala2-D-Leu5]enkephalin (DADLE) was prevented in the presence of multiple K+ channel blockers, whereas excitatory modulation by the specific kappa-agonist, U-50,488H was not attenuated under these conditions. After treatment of DRG neurons with pertussis toxin (1 micrograms/ml for several days) or forskolin (50 muM for less than 15 min), a much smaller fraction of cells showed opioid-induced APD shortening; moreover, a much larger fraction of cells showed opioid-induced APD prolongation, even when tested with high concentrations of DADLE (1-10 muM). These data indicate that opioid-induced APD prolongation is not mediated by pertussis toxin-sensitive G proteins (which have been shown to regulate opioid inhibitory effects) and suggest that elevation of cyclic AMP levels may enhance opioid excitatory responsiveness. Furthermore, our analyses indicate that mu-, delta- and kappa-subtypes of excitatory as well as inhibitory opioid receptors may be expressed on the same DRG neuron perikaryon under in vitro conditions. If dual opioid modulation of the APD of DRG perikarya also occurs in central DRG terminals this may play a significant role both in nociceptive signal transmission as well as tolerance to opioid analgesia.
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PMID:Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture. 254 63

It is widely accepted that the nociceptive state and opiate-induced nociception are regulated at least in part by calcium ions. Animal experiments suggest that systemically or intracerebroventricularly applied calcium antagonizes analgesic effects, whereas calcium chelating agents or calcium channel blockers enhance them. Recently, von Bormann et al. [3] reported a fentanyl-saving effect in cardiovascular patients who had received an intraoperative infusion of nimodipine; this finding was discussed as a possible synergistic analgesic interaction. Since doubts remained as to whether this interpretation was justified, the present study aimed to verify, in awake postoperative patients, whether nimodipine increased the analgesic efficacy of fentanyl. Forty ASA I-II patients (mean age 43-44 years) undergoing elective hysterectomy under standardized balanced anesthesia were investigated. In the recovery room, they were allowed to self-administer fentanyl by means of the On-Demand Analgesia Computer (ODAC). Demand dose was 34.5 micrograms, infusion rate 4 micrograms/h, lockout time 1 min, hourly maximum dose 250 micrograms. The patients were randomly and double-blindly assigned to have an additional infusion of either placebo (P) or nimodipine (N: 15 micrograms/kg/h during the first 2 h, 30 micrograms/kg/h from the 3rd to the 12th h). Fentanyl consumption, pain scores (actual and retrospective), blood pressure, heart rate, respiratory rate, and side-effects were monitored. The mean duration of patient-controlled analgesia was 16 (P) to 19 (N) h, during which time 0.64 +/- 0.46 (N) to 0.79 +/- 0.43 (P) micrograms fentanyl/kg/h was demanded. Pain relief was very satisfactory in 92.5% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The clinical significance of drug interactions between opiates and calcium antagonists. A randomized double-blind study using fentanyl and nimodipine within the framework of postoperative intravenous on-demand analgesia]. 256 86

Many drugs potentiate the action of non depolarizing relaxants. These interactions are of clinical importance if such drugs are administered during the perioperative period. H2 Antagonists are increasingly often used for premedication. Cimetidine inhibits the elimination of a number of drugs used in the perioperative period. We therefore investigated whether H2 antagonists enhanced neuromuscular blockade by vecuronium, a medium short acting non depolarizing muscle relaxant. METHODS. The study was carried out in 24 female patients (ASA class I or II) scheduled for microsurgical procedures. Neuromuscular transmission was recorded electromyographically using four stimulations every 20 s to the ulnar nerve. After induction with thiopentone, anesthesia was maintained with fixed concentrations of volatile anesthetics. Fentanyl was administered for additional analgesia. Vecuronium was used as the sole muscle relaxant. Fixed repetitive doses of vecuronium (0.8-1.2 mg) were injected whenever the T1 returned to 25%. This time interval was defined as the T1-25 period. The study proper started when the T1-25 period had stabilized. After two control periods, six patients in each group received either 200 or 400 mg cimetidine or 100 mg ranitidine. The fourth group was the control group. The T1-25 periods and the maximal EMG depression were recorded automatically for at least two further periods. The first measured period was recorded as 100% and the length of each other periods was calculated as a percentage of the control period. This method enables an intraindividual comparison of the length of the T1-25 period and the maximal EMG depression before and after administration of the H2 antagonists. A two-tailed Student's t-test was used to test statistical significance, P less than 0.05 being accepted as significant. RESULTS. In the control group and in the group with 200 mg cimetidine or 100 mg ranitidine no statistical significant prolongation of the T1-25 period or of the maximal EMG depression could be observed, while after 400 mg cimetidine there was significant prolongation (mean 161 +/- 14.8%) of the T1-25 period and significantly greater EMG depression compared with the pre-cimetidine values. In the groups with 200 mg cimetidine or 100 mg ranitidine few patients showed prolongation of the T1-25 period up to 130%. DISCUSSION. Our results confirm experimental studies that have shown cimetidine to enhance aminoglycoside--relaxant interactions. Because we found an immediate response to the administration of the H2 antagonists, the interaction cannot be on the elimination side; it must be at the neuromuscular junction. Experimental investigation has shown that calcium reverses the cimetidine effects. It is therefore probable that the cimetidine--relaxant interaction occurs at the presynaptic level. Careful observation seems to be necessary if H2 antagonists, especially cimetidine, are administered intraoperatively at the same time as drugs that also enhance
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PMID:[Interactions of H2 antagonists and non-depolarizing muscle relaxants]. 256 80

Research conducted at the University of Dayton has shown that alumino-calcium-phosphorous (ALCAP) ceramics impregnated with polylactic acid (PLA) are capable of sustained delivery of polypeptides and steroids. Recent experiments conducted at the university have shown that ALCAP ceramics are capable of delivering aspirin in vitro. Based on this work, ALCAP ceramics containing 25 mg, 50 mg, or 75, mg aspirin were implanted subcutaneously in random bred albino male rats. There were eight rats in each dosage group. Six rats were implanted with empty ceramics (sham-operated). Eight nonimplanted rats served as controls. Levels of analgesia among the groups were determined using a pressure analgesia meter. The data collected showed that aspirin delivered by ALCAP was capable of producing analgesia in rats as early as 24 hours after surgery. The level of analgesia increased over the first seven days before declining gradually over a period of one month. Levels of analgesia were directly related to the amount of aspirin stored initially within the ceramic.
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PMID:Sustained delivery of aspirin by means of ALCAP ceramics. 274 67

Behavioral observations have repeatedly shown that the analgesic effect of morphine can be antagonized by intracerebroventricular injection of angiotensin I (A I), although mechanisms underlying the action were obscure. Since a prevention of Ca2+ uptake into the nerve terminals was considered as one of the mechanisms for morphine analgesia, we examined the effect of A I and morphine on the 45Ca uptake by rat brain synaptosomal preparations. Morphine of 10(-8)-10(-6) mol/L produced a dose-related suppression on synaptosomal 45Ca uptake, which was completely reversed by the opioid antagonist naloxone of 10(-6) mol/L. A I of 10(-8)-10(-6) mol/L, on the contrary, enhanced 45Ca uptake. This effect was totally abolished by saralasin, a A I antagonist, at 10(-6) mol/L. When synaptosomal preparations were incubated in a mixture of morphine (10(-6) mol/L) and A I (10(-8)-10(-6) mol/L), the effect of morphine was almost completely reversed. The results suggest that the distinct effect of A I may account for, at least in part, the antagonistic effect of A I on morphine analgesia.
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PMID:[Antagonistic effects of angiotensin II and morphine on synaptosomal calcium uptake]. 276 44


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