Cevadine

Cevadine
Product Name Cevadine
CAS No.: 62-59-9
Catalog No.: CFN70426
Molecular Formula: C32H49NO9
Molecular Weight: 591.7 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: Potassium Channel
Source: The herbs of Veratrum nigrum L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Cevadine-induced changes of membrane potential and sodium transport of muscle membrane in a chloride-free solution.Membrane potential dependence of potential oscillation induced by cevadine in striated muscle.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Acta physiologica hungarica, 1985, 65(2):199-211.
    Cevadine-induced changes of membrane potential and sodium transport of muscle membrane in a chloride-free solution.[Reference: WebLink]
    Cevadine-induced changes in membrane potential, sodium transport, intracellular Na, K, and water content were investigated in sartorius muscles incubated in chloride-free (glutamate) Ringer.
    METHODS AND RESULTS:
    Cevadine sensitivity of muscles incubated in glutamate Ringer was about five times greater than that of muscles incubated in normal Ringer. Therefore, even 0.005 mmol/l Cevadine could induce depolarization and membrane potential oscillations. The membrane potential oscillations were recorded much longer from muscles incubated in chloride-free Ringer (even in the 15th hour of treatment) than in normal Ringer. Depolarization and membrane potential oscillations reversed more slowly in Cevadine-free glutamate Ringer than in alkaloid-free normal Ringer. The rhythmic activity could be recorded even in the 10th-15th hour of incubation in Cevadine-free glutamate Ringer. Cevadine increased the 24Na uptake of muscles incubated in glutamate Ringer by an average of 230%. In comparison, the Cevadine-induced increase of 24Na uptake of muscles incubated in normal Ringer was approximately 350%. In the presence of Cevadine the 24Na loss of muscles incubated either in glutamate or in normal Ringer increased to the same degree, i.e. three times. The increase of 24Na loss developed faster in glutamate Ringer than in the presence of chloride. The water content of muscles incubated in Cevadine containing, chloride-free (glutamate) Ringer did not increase significantly. Muscles incubated in normal Ringer with Cevadine showed a 42.7% increase of water content in 2 hours. Intracellular Na content and Na concentration increased by about 60% during a 2-hour-treatment with Cevadine in a chloride-free environment. At the same time, Cevadine treatment increased the intracellular Na content and Na concentration of muscles incubated in normal Ringer by about 160% and 80%, respectively. The Cevadine-induced decrease of intracellular K content and concentration of muscles incubated in glutamate Ringer was 5% and 10%, respectively, in 2 hours. On the other hand, the decrease of intracellular K concentration in muscles incubated in Cevadine-containing normal Ringer occasionally reached 30% due to the increase of water content of the muscles.
    CONCLUSIONS:
    The Cevadine-induced increase of the wet weight of muscles incubated in normal Ringer was practically irreversible. It was not possible to eliminate the increase of wet weight even by washout lasting for 10-15 hours.
    Acta physiologica academiae scientiarum hungaricae, 1981, 58(4):275.
    Membrane potential dependence of potential oscillation induced by cevadine in striated muscle.[Reference: WebLink]
    The dependence of the membrane potential oscillation induced by Cevadine on the actual transmembrane potential was studied in the frog sartorius muscle.
    METHODS AND RESULTS:
    1. If the membrane potential oscillation is recorded for hours, its amplitude is seen to decrease slowly and smoothly and the membrane potential measured during the resting period among the waves of oscillation also decreases simultaneously. This means that the depolarization increases. 2. The increase of depolarization results not only in a decrease in the amplitude of the oscillation but the oscillation ceases between -40 and -55 mV as well. 3. The phenomenon reappears if the membrane is partially repolarized on a Cevadine treated muscle fibre on which the membrane potential oscillation has already ceased as a consequence of the relatively marked depolarization. 4. Changing the membrane potential either to a value more positive than -40 mV, or to one more negative than -90 mV the developed oscillation activity may reversibly be suspended.
    CONCLUSIONS:
    5. According to the above results, the amplitude of the membrane potential oscillation depends on the actual membrane potential. If other factors which may influence the oscillation parameters are unchanged, the relationship between the oscillation amplitude and the membrane potential can be characterized by a linear equation. In these cases there is a close correlation between the measured values and the calculated ones.
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