Sell Milrinone (CAS:78415-72-2)

Price:

NEGOTIABLE

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Origin:

China

Payment Method:

Telegraphic Transfer (T/T)

Pack. & Delivery:

100/500G TIN

Other name: two-pyridone; Fenpropathrin pyrazole ketone; cyanide double pyrazole ketone; Milrinone
chemical name: 2 - methyl -6 - oxygen -1,6 - dihydro - [3,4 'dual-pyridyl] -5 A nitrile
Molecular formula: C10H9N3O
MW: 211.22
Characters:
This product is a colorless liquid clarity.
Pharmacological effects
This product is a phosphodiesterase inhibitor, for amrinone similar drugs, the role of mechanism and the same amrinone. Oral and intravenous administration were effective, the role of both positive inotropic and vasodilator effect. However, its role amrinone than strong 10 ~ 30 times. Better tolerability. This product is positive inotropic effect mainly by inhibiting phosphodiesterase so that cAMP inner myocardial cells (CAMP) concentration increased intracellular calcium increase in myocardial contractility strengthened to increase cardiac output. With the B1-adrenergic receptor or cardiac myocyte Na +, K +-ATP enzyme has nothing to do. The role of its vasodilator effect may be direct or due to the small arteries, which can reduce the heart before and after the load, reducing left ventricular filling pressure and improve left ventricular function, increase cardiac index, but mean arterial pressure and heart rate had no significant effect. Milrinone cardiovascular effect and dose-related, low-dose mainly manifested as positive inotropic effect, when the dose increased gradually to reach the maximum steady-state positive inotropic effect, its role in the expansion of blood vessels can also be with the dose of increase gradually strengthen. This product is on the block with the safety of patients. This product, when adverse reactions oral heavier, not long-term application.
Pharmacokinetics :
Intravenous administration of 5 ~ 15 minutes to take effect, clear the half-life of 2 ~ 3 hours. Protein binding rate of 70%.
Indications:
Milrinone PDE inhibitors as representatives of drugs, degradation of cAMP can selectively inhibit the PDE, so that degradation of cAMP to 5'-AMP blocked the process, an increase of myocardial and vascular smooth muscle content of cAMP.
Apply to digitalis, diuretics, vasodilator therapy is invalid or ineffective for a variety of reasons caused by acute and chronic refractory congestive heart failure.

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