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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Anasthetic and class Ib antiarrhythmic agent.?Blocks voltage-gated sodium channels in the inactivated state.
Cell lines
Fresh bovine articular chondrocytes, sarcoplasmic reticulum
Preparation method
The solubility of this compound in DMSO is >11.7 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.
Reacting condition
1% or 2% lidocaine, 30 minutes
Applications
Lidocaine (1%, 15-minute) decreased chondrocyte viability. Longer exposures to 1% and 2% lidocaine further reduced chondrocyte viability. Lidocaine (40 μM) showed reverse frequency-dependent depression of myocardial contractility. Lidocaine(40 μM, 100 μM) caused a marked depression of the late-peaking contractile responses, attributed to Ca2+ release from the sarcoplasmic reticulum.
Animal models
Dogs with 2-hour-old myocardial infarctions
Dosage form
Intravenous bolus injection, 2-8 μg/ml
Application
Lidocaine prolonged the Q-EG intervals in the infarcted zones of the heart 17-26% at peak effect, but it had no effect on the Q-EG intervals in the normal zone except for a slight (1.5%) prolongation shortly after the initial intravenous bolus injection. Lidocaine prolonged the effective refractory period of the infarcted zone 23% at peak effect but had no effect on the effective refractory period of the normal zone.
Other notes
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
References:
[1]. Karpie J C, Chu C R. Lidocaine exhibits dose-and time-dependent cytotoxic effects on bovine articular chondrocytes in vitro[J]. The American journal of sports medicine, 2007, 35(10): 1622-1627.
[2]. Lynch III C. Depression of myocardial contractility in vitro by bupivacaine, etidocaine, and lidocaine[J]. Anesthesia & Analgesia, 1986, 65(6): 551-559.
[3]. Kupersmith J, Antman E M, Hoffman B F. In vivo electrophysiological effects of lidocaine in canine acute myocardial infarction[J]. Circulation research, 1975, 36(1): 84-91.