Disease relevance of Xylocitin

• Intramuscular lidocaine for prevention of lethal arrhythmias in the prehospitalization phase of acute myocardial infarction [1].
• CNS toxicity after ingestion of topical lidocaine [2].
• Lidocaine to prevent ventricular fibrillation: easy does it [3].
• Ventricular tachycardia terminated a mean of 10 minutes after injection in six of nine lidocaine-treated patients with acute myocardial infarction but in none of five control patients with infarction (P less than 0.02) [1].
• Effect of hypotension on liver blood flow and lidocaine disposition [4].

Psychiatry related information on Xylocitin

• Afferent responses were unrelated to intestinal motor activity, and the response to luminal antigen was attenuated by luminal anesthetic (1% lidocaine) [5].
• Electroconvulsive shock and lidocaine reveal rapid consolidation of spatial working memory in the water maze [6].
• Of 15 patients with psychiatric reactions to lidocaine, 12 (80%) had mood changes, 11 (73%) had "doom anxiety," eight (53%) had overt confusional states, and six (40%) had hallucinations and delusions [7].
• We also suggest that the concept of a single value for the upper limit of the therapeutic level of lidocaine in serum is an oversimplification because it does not take into account individual differences in drug-protein binding or accumulation of active metabolites [8].
• Cutaneous application of naphthalene provoked a decrease in the RIII,Cu threshold and relative pain threshold, whereas lignocaine increased them [9].

High impact information on Xylocitin

• CONCLUSIONS: Tumescent liposuction can be fatal, perhaps in part because of lidocaine toxicity or lidocaine-related drug interactions [10].
• Although the recommended doses of lidocaine are as high as 55 mg per kilogram of body weight, few safety data are available [10].
• Lidocaine for severe hiccups [11].
• Lidocaine kinetics predicted by indocyanine green clearance [12].
• To evaluate the importance of hepatic blood flow in lidocaine kinetics, we compared indocyanine green clearance, an estimate of hepatic plasma flow, to lidocaine clearance in 26 patients, half with and half without congestive heart failure, who received a lidocaine infusion for 24 hours as clinically indicated [12].

Chemical compound and disease context of Xylocitin

• The normal elimination of morphine in cirrhosis is in contrast to the decreased elimination of high clearance drugs metabolized by oxidation, such as lidocaine and meperidine [13].
• The relative safety and efficacy of intravenous administration of adenosine, lignocaine, disopyramide, flecainide, and sotalol for termination of stable, induced ventricular tachycardia was assessed in serial trials [14].
• Tachycardia ceased in 7 (50%) patients who crossed over to sotalol, and in 1 patient who crossed over to lignocaine [15].
• RESULTS: After intracolonic injection of glycerol, a strong abdominal colic occurred and was associated with an increase in long spike burst activity (+280%), which was eliminated by previous administration of lidocaine and was not observed after paraffin oil [16].
• Propranolol (tested in three patients) and lidocaine (tested in two patients) effectively prevented exercise provocation of tachycardia [17].

Biological context of Xylocitin

• Prolonged suppression of cough after inhalation of lidocaine in a patient with sarcoid [18].
• After lidocaine, blood pressure and sympathetic nerve discharge were unchanged [19].
• Lidocaine accelerated the decay of whole-cell FQ currents in Xenopus oocytes, reestablishing the wild-type phenotype; peak inward current at -20 mV was blocked with an IC50 of 513 microM, while plateau current was blocked with an IC50 of only 74 microM (P < 0.005 vs. peak) [20].
• 0. Local irrigation of HP by 2% xylocaine and intravenous infusion of atropine (100 mug per kg per hr) or metiamide (2.9 mg per kg per hr) reduced but did not abolish HP response to chemical stimulation and the pH dependency of this response [21].
• The concentration of lidocaine required to block cell fusion was dependent on the concentration of calcium or magnesium in the medium [22].

Anatomical context of Xylocitin

• It is now thought that amine local anaesthetic compounds (procaine, lignocaine and related molecules) depress electrical activity in nerve and muscle cells by binding to sites within ion channels and blocking current flow [23].
• Lidocaine applied topically to the left ventricle completely prevented these alterations [24].
• Thioglycolate-stimulated mouse peritoneal macrophages cultured in the presence of macrophage growth factor (MGF) will continue to proliferate when they are removed from culture dishes with the local anesthetic lidocaine and subcultured [25].
• However, an early lidocaine outflow peak related in time to the peak erythrocyte curve was observed in cirrhotic, but not in noncirrhotic, rats [26].
• We speculate that this effect is due to central nervous system effects of the drug and that this effect may contribute to the antiarrhythmic actions of lidocaine [27].

Associations of Xylocitin with other chemical compounds

• The blocking action of lidocaine and disopyramide were studied over a range of [Na]o. Both whole-cell voltage clamp and single-channel recordings were performed on isolated rabbit myocytes at 17 and 22 degrees C, respectively [28].
• We examined possible mechanisms of the reversal by measuring INa in rabbit atrial myocytes during exposure to propoxyphene and the combination of propoxyphene and lidocaine (60 and 80 microM, respectively) [29].
• A method for rapid assessment of hepatic function in liver donors based on the formation of the lignocaine metabolite monoethylglycinexylidide (MEGX), was used in a prospective study of 69 donor-recipient pairs [30].
• The response to capsaicin was completely abolished by a previous intraluminal application of the local anesthetic lidocaine, and was inhibited by an intraarterial injection of somatostatin [31].
• Sotalol was significantly more effective than lignocaine whether analysed on an intention-to-treat basis (69% vs 18%; 95% confidence interval for absolute difference of 51% 22-80%, p = 0.003) or by analysis limited to the 31 patients with subsequent electrophysiologically proven VT (69% vs 20%) [15].

Gene context of Xylocitin

• Negligible metabolism of tolbutamide and S-mephenytoin, substrates of the 2C sub-family, and of p-nitrophenol, a substrate of CYP2E1, was detected, although a trace of the N-deethylated metabolite of lignocaine, thought to be metabolised by CYP3A4, was detected with microsomes from CYP2D6-expressing yeast cells [32].
• The in vitro inhibitory potencies in human liver microsomes (mexiletine > lidocaine > tocainide) are consistent with the structural interactions found in a molecular model of the active site of CYP1A2 [33].
• METHODS: To investigate the effect of lidocaine (4 microM-40 mM) on epidermal growth factor (EGF)-stimulated autophosphorylation of EGFR, the authors studied purified EGFR in microtubes [34].
• Human CYP2B6 and rat CYP2B1 had high lidocaine N-deethylation activity [35].
• Neuropeptide depletion of sensory neurons, treatment with the ganglionic blocker hexamethonium, or in situ skin infiltration with the local anesthetic lidocaine did not affect Ucn-induced vascular permeability, indicating that its in situ effect was not mediated through the peripheral nervous system [36].

Analytical, diagnostic and therapeutic context of Xylocitin

• RESULTS: There was minimal change in the degree of pain in the lidocaine-only and control groups during and after the treatment period [37].
• Therapeutic blood lidocaine concentrations after local anesthesia for cardiac electrophysiologic studies [38].
• BACKGROUND: The technique of tumescent liposuction involves the subcutaneous infusion of a solution containing lidocaine, followed by the aspiration of fat through microcannulas [10].
• In a randomized controlled study examining the value of an intramuscular injection of lidocaine in the prehospitalization phase of suspected acute myocardial infarction, paramedics used an automatic injector to administer 400 mg of the drug into the patient's deltoid muscle before transport to the hospital [1].
• Among those with initial relief of headache, relapse of headache occurred in 10 (42 percent) of 24 in the lidocaine group vs 5 (83 percent) of 6 in the control group (P=.17), usually within the first hour after treatment [39].

References