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)

Blood cell catecholamine levels were measured in the patients over the course of the postoperative period administered various types of analgesia, the standard mode with narcotic analgetics and the method suggested by the authors, consisting in blocking of the afferent nervous painful pulsation via the anterior abdominal wall. The blocking is carried out with a micro-irrigator placed in the muscular layer of the anterior abdominal wall during surgery. Procaine solution was employed for anesthesia. Postoperative analgesia efficacy was assessed from blood catecholamine levels. Analysis has shown the efficacy of the suggested analgesia mode.
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PMID:[Blood cell catecholamines during different methods of postoperative analgesia]. 172 26

The effects of procaine, mepivacaine and phenylbutazone on pain perception in the equine were studied using two behavioral assays of nociception; the thermal evoked hoof withdrawal reflex and skin twitch reflex. Pain perception threshold was measured as the latency from onset of thermal stimuli to reflex withdrawal of the forelimb or contraction of the cutaneous musculature. Procaine 2% and mepivacaine 2% prolonged the hoof withdrawal reflex latency when administered locally by producing a block of the palmar and metacarpal nerves. Significant analgesia lasted 90 min and 210 min for procaine and mepivacaine, respectively. Phenylbutazone (7.3 mg/kg) failed to alter pain thresholds measured over a 36 h post-treatment period. However, pain thresholds rose over time with successive trials. These data suggest that in the equine (1) phenylbutazone does not alter normal cutaneous pain perception, and (2) successive presentation of painful stimuli increases nociceptive thresholds.
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PMID:Differential effects of phenylbutazone and local anesthetics on nociception in the equine. 652 70

The calcium entry blocker, verapamil, enhanced morphine analgesia, but neither methadone nor propoxyphene analgesia was affected by verapamil in the mouse hot-plate test. To explain this, it was hypothesized that methadione and propoxyphene differ from morphine because they, like verapamil, block calcium channels and subsequent studies were done to confirm this. Verapamil, methadone and propoxyphene all depressed barium-induced bovine adrenal catecholamine release and KCl-induced contractions of guinea pig ileum, which are known to be calcium-dependent events. Calcium reversed opioid-induced inhibition in both tissues. Morphine did not affect either catecholamine release or ileal contractions. Procaine also did not influence catecholamine release or ileal contraction. Therefore, local anesthesia was eliminated as a mechanism for the inhibitory action of methadone and propoxyphene in these tissues. Opioids which block calcium channels should, like verapamil, produce bradycardia and hypotension. In the spinal vagotomized rat, methadone, propoxyphene, and verapamil produced bradycardia and hypotension, whereas, morphine produced tachycardia and (at low doses) hypertension. The results of this work suggest that methadone and propoxyphene, in contrast to morphine, block calcium channels in a manner similar to verapamil, and that some pharmacological and especially toxicological differences between these drugs are due to different degrees of verapamil-like calcium channel blockade.
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PMID:Calcium channel blockade by certain opioids. 666 95

The effects of several anesthetic or analgesic agents (halothane, Na thiopental, ketamine, nitrous oxide, xylazine, and procaine) administered in vivo, on swine adipose tissue metabolism were measured. Adipose tissue samples were collected from the subcutaneous depot before and after administration of the anesthetic or analgesic agent. The rate of oxidation of glucose to CO2 and the lipogenic rate, or the basal and stimulated lipolytic rates, were measured on tissue slices incubated in vitro. There were no effects on the oxidation of glucose to CO2 or the incorporation into lipids except by procaine. Procaine depressed (P less than or equal to 0.05) the lipogenic rate (12%) and tended (P less than or equal to 0.1) to depress the oxidative rate (9%). The only observable effect on the lipolytic rates was a tendency (P less than or equal to 0.1) for ketamine to increase the stimulated lipolytic rate. The minimal effects on adipose tissue metabolism reported herein were obtained with short times of compound administration. Several agents (nitrous oxide, procaine, and xylazine) are not recommended because of poor analgesia.
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PMID:Effect of anesthetic or analgesic drugs on lipogenic and lipolytic adipose tissue activities. 684 43

The analgesic effectiveness of various local anaesthetic solutions was measured in the distribution of the infraorbital nerve of the rat. Using Sprague-Dawley rats sedated with phenobarbitone 25 mg/kg intraperitoneally and a simple stereotactic technique, 0.2 ml of solution was deposited at the infraorbital notch. The onset and duration of analgesia were ascertained by timing the unilateral absence of aversive response to pinching the upper lip, tested at intervals of five minutes. The experiments were performed with coded solutions, the entire code being preserved intact until completion of the study. Solutions were tested on sets of eight animals weighing 500--600 g. The average duration (minutes +/- S.D.) of analgesia produced by the respective injectates was as follows: Lidocaine 0.5% -42+/-12 Lidocaine 1.0% -47+/-10 Mepivacaine 0.5% -58+/-13 Mepivacaine 1.0% -78+/-23 Procaine 0.5% -0+/-0 Procaine 1.0% -34+/-10 Procaine 1.5% -46+/-13 2-Chloroprocaine 1.5% -38+/-9 Bupivacaine 0.5% -100+/-40 Etidocaine 1.0% -59+/-25 Tetracaine 0.2% -0+/-0 Tetracaine 0.3% -0+/-0 Comparison with other animal models used to evaluate conduction block indicates that this technique affords an improved, standardized and reliable experimental guide to the clinical analgesic properties of local anaesthetic agents.
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PMID:Experimental evaluation of local anaesthetic solutions using rat infraorbital nerve block. 698 89

The concentration of procaine in the CSF of 10 adult nonpregnant cows was determined after epidural injection of 5% procaine hydrochloride solution. Samples of CSF were removed through a catheter introduced into the subarachnoid space at the lumbosacral intervertebral space and advanced craniad to the same level as the epidural injection site. The position and the location of the catheter and spinal needle were confirmed radiographically. Segmental analgesia was achieved 8 to 20 minutes after completing the procaine hydrochloride injection and extended between spinal cord segments T12 and L3 on one or both sides of the animal. The average duration of analgesia, as determined by response to superficial and deep muscular pinpricks at the L1 dermatome, was 81.3 +/- 22.8 minutes (min-max, 45-127 minutes). The average subarachnoid concentration of procaine 10 minutes after epidural injection was 120.4 +/- 42.9 microgram/ml. The highest average procaine concentration recorded was 160.7 +/- 63.7 microgram/ml at 25.0 +/- 6.7 minutes after injection. Average procaine concentration was 47.8 +/- 13.5 microgram/ml at cessation of analgesia. A similar concentration of procaine was recovered from the subarachnoid space during either unilateral or bilateral analgesia. Procaine was not found in arterial plasma after the epidural administration of procaine hydrochloride. Subarachnoid threshold concentrations of local anesthetic necessary to produce spinal analgesia were reached after repeated epidural injections, but not after a single administration. It is concluded that segmental epidural analgesia is principally due to anesthesia of dura-covered nerve roots within and outside the epidural space and is minimally, if at all, dependent on the production of analgesia of nerves within the subarachnoid space.
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PMID:Appearance of procaine in spinal fluid during segmental epidural analgesia in cows. 733 26

The recognition and alleviation of animal pain is a growing veterinary and public concern. Pain can be of an acute or chronic nature with different behavioral manifestations. Physiologically, pain is a dynamic and complex phenomenon that produces changes in the central and autonomic nervous systems as well as in the endocrine system. Horses and other animals appear to possess an endogenous pain-suppressing system involving the brainstem and spinal cord. This system can modulate pain perception and the responses to it. The recently discovered endogenous opioid peptides (endorphins and enkephalins) appear to play a role in this system, which is activated by stress. Opioids (narcotic analgesics) act to selectively depress pain-sensitive cells. Opioid analgesics may act via multiple opioid receptors. Each subclass of opioid receptor has a different pharmacologic profile. Classical opioids that act at mu (morphine) receptors typically produce analgesia, increased locomotor activity, cardiorespiratory stimulation, and a decrease in intestinal peristalsis in the horse. Opioids that act at kappa receptors produce analgesia, sedation, ataxia, and minimal autonomic effects in the horse. Owing to their lack of excitatory actions, the kappa opioids represent a potentially useful class of analgesics for use in equine species. Local anesthetics depress all excitable cells and can diminish sensory, motor, and muscular function. They do not act selectively on pain fibers, although pain is among the first sensations lost following a nerve block. Local anesthetic activity is enhanced by increased extraneuronal pH, nerve cooling, increased nervous activity, coadministration of a vasoconstrictor or hyaluronidase, delayed systemic absorption, prolonged drug metabolism, and by using agents with high lipid solubility. Procaine, lidocaine, and mepivacaine are among the most widely used and studied agents in horses. These agents and/or their metabolites can be readily detected in urine; in some cases, for prolonged periods.
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PMID:Narcotics and local anesthetics. 829 18

Local anaesthetics potentiate epidural or intrathecal opioid analgesia via a poorly defined mechanism. In this study, we have examined the interaction of local anaesthetics (lidocaine, bupivacaine and its optical isomers, tetracaine, procaine and prilocaine) with recombinant mu-, kappa-, and delta-opioid receptors expressed in Chinese hamster ovary cells (CHO-mu, kappa, and delta, respectively). Lidocaine produced a concentration-dependent displacement of radiolabelled opioid antagonist [3H]diprenorphine ([3H]DPN) binding with the following rank order of inhibitor constant (Ki): kappa (210 microM) > mu (552 microM) > delta (1810 microM). Procaine, prilocaine, tetracaine and bupivacaine also displaced [3H]DPN binding in CHO-mu with Ki values of 244, 204, 43 and 161 microM respectively. Lidocaine produced a concentration-dependent and naloxone-insensitive inhibition of cAMP formation in all cell lines including untransfected cells. Concentration producing 50% inhibition of maximum was mu, 1.32 mM; kappa, 2.41 mM; delta, 1.27 mM; untransfected, 2.78 mM. When lidocaine (300 microM) was co-incubated with spiradoline (kappa-selective) and [D-Ala2, MePhe4, Gly(ol)5] enkephalin (DAMGO mu-selective) in CHO-kappa and mu cells we did not observe an additive interaction for cAMP formation. In contrast, there was an apparent inhibitory action of the combination at the kappa receptor. This study suggests that clinical concentrations of local anaesthetics interact with mu and kappa but not delta opioid receptors. As there was no synergism between local anaesthetics and opioids we suggest that the interaction of these agents in the clinical setting does not occur at the cellular level.
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PMID:Interaction of local anaesthetics with recombinant mu, kappa, and delta-opioid receptors expressed in Chinese hamster ovary cells. 1109 91