Professional Documents
Culture Documents
Pharmaceutics
MOA Direct agonist, at lower Direct and indirect action,
doses alpha selectivity, at mainly alpha1, some beta
higher doses beta activity Not metabolised by COMT –
Structure Metabolised by COMT – OH no C3 OH group
group on C3 Not metabolised by MAO –
Metabolised by MAO – no alkyl group on alpha C
alkyl group on alpha C Indirect activity – alkyl group
Less beta effect – no group on alpha C
on terminal amine Increased lipid solubility/CNS
effects – no substitutions on
benzene ring
Alkyl substitution on
terminal amine – beta effect
Pharmacokinetics IV only (metabolised in GIT) IV, IM, PO
Poorly lipid soluble, does More lipid soluble, can cross
not cross BBB BBB
Metabolised by COMT and Not metabolised by MAO or
MAO COMT, 35% hepatic
97% excreted renally as metabolism, 65% excreted
VMA, 3% normetanephrine unchanged in urine
T1/2b 2 mins T1/2b 5 hrs
Onset <1 min, duration 5 Onset 1 min, duration 1hr
mins
Pharmacodynamics
CVS Alpha effects low dose – Alpha and beta effects,
vasoconstriction, decrease in increase vasoconstriction,
HR due to BRR, potential inotropy, HR. Indirect action
decrease in CO. Beta effects can cause tachyphylaxis if
at higher dose – increased NAdr stores depleted
inotropy and HR
Respiratory Increased PVR, Similar
bronchodilator, respiratory
stimulant
CNS Decreased CBF from Does cross BBB, thus can get
vasoconstriction. Mydriasis. agitation, confusion,
Does not cross BBB increased MAC requirement
Other Decreases RBF, splanchnic BF Similar
flow, uterine BF. Increases
BGL, FFA, renin release
Side effects Tissue necrosis if Can be given IM and
extravasation (thus use CVC), peripherally, HTN crisis if on
effects prolonged if on MAOi
MAOis, metabolic acidosis,
HTN crisis, tachyarrythmia,
MI
Uses Vasopressor in critically treat hypotension (e.g. with
ill/vasodilatory shock GA or regional),
bronchospasm, nasal
decongestant, narcolepsy