LOPRESSOR metoprolol tartrate injection solution

Država: Združene države Amerike

Jezik: angleščina

Source: NLM (National Library of Medicine)

Aktivna sestavina:

METOPROLOL TARTRATE (UNII: W5S57Y3A5L) (METOPROLOL - UNII:GEB06NHM23)

Dostopno od:

Novartis Pharmaceuticals Corporation

INN (mednarodno ime):

METOPROLOL TARTRATE

Sestava:

METOPROLOL TARTRATE 5 mg in 5 mL

Tip zastaranja:

PRESCRIPTION DRUG

Status dovoljenje:

New Drug Application

Lastnosti izdelka

LOPRESSOR- METOPROLOL TARTRATE INJECTION, SOLUTION
NOVARTIS PHARMACEUTICALS CORPORATION
----------
LOPRES S OR
METOPROLOL TARTRATE INJECTION, USP
RX ONLY
PRESCRIBING INFORMATION
DESCRIPTION
Lopressor, metoprolol tartrate USP, is a selective beta
-adrenoreceptor blocking agent, available in 5-
mL ampuls for intravenous administration. Each ampul contains a
sterile solution of metoprolol tartrate
USP, 5 mg, and sodium chloride USP, 45 mg, and water for injection
USP. Metoprolol tartrate USP is
(±)-1-(Isopropylamino)-3-[_p_-(2-methoxyethyl)phenoxy]-2-propanol
L-(+)-tartrate (2:1) salt, and its
structural formula is:
Metoprolol tartrate USP is a white, practically odorless, crystalline
powder with a molecular weight of
684.82. It is very soluble in water; freely soluble in methylene
chloride, in chloroform, and in alcohol;
slightly soluble in acetone; and insoluble in ether.
CLINICAL PHARMACOLOGY
MECHANISM OF ACTION
Lopressor is a beta -selective (cardioselective) adrenergic receptor
blocker. This preferential effect
is not absolute, however, and at higher plasma concentrations,
Lopressor also inhibits beta -
adrenoreceptors, chiefly located in the bronchial and vascular
musculature.
Clinical pharmacology studies have demonstrated the beta-blocking
activity of metoprolol, as shown by
(1) reduction in heart rate and cardiac output at rest and upon
exercise, (2) reduction of systolic blood
pressure upon exercise, (3) inhibition of isoproterenol-induced
tachycardia, and (4) reduction of reflex
orthostatic tachycardia.
_Hypertension_
The mechanism of the antihypertensive effects of beta-blocking agents
has not been fully elucidated.
However, several possible mechanisms have been proposed: (1)
competitive antagonism of
catecholamines at peripheral (especially cardiac) adrenergic neuron
sites, leading to decreased cardiac
output; (2) a central effect leading to reduced sympathetic outflow to
the periphery; and (3) suppression
of renin activity.
_Angina Pectoris_
By blocking catecholamine-induced increases in heart rate, i