Vasoconstriction sympathomimetics causing

Ephedrine is an alkaloid that is present in various forms of the ephedrine family, and which is still extracted from Ephedra sinica and Ephedra equisetina. Because of the presence of two asymmetric atoms, there are four isomeric forms. Pseudoepinephrine (d-isoephrine) is a stereoisomer with pharmacological action that differs slightly from ephedrine. The pharmacological action of ephedrine is typical of noncatecholamine sympathomimetics of mixed action. It stimulates both a- and 8-adrenoreceptors, and simultaneously causes a release of norepinephrine from synaptic neurons. Its vasoconstrictive ability is approximately 100 times weaker than that of epinephrine however, the duration of action is approximately 10 times longer. It is much less toxic than epinephrine, which allows it to be used widely in medicine. 

Pharmacology Sympathomimetic agents produce -adrenergic stimulation (vasoconstriction), - -adrenergic stimulation (increase myocardial contractility, heart rate, automaticity, and AV conduction), and 2-adrenergic activity (peripheral vasodilation). Dopamine also causes vasodilation of the renal and mesenteric, cerebral, and coronary beds by dopaminergic receptor activation. 

Pharmacology Epinephrine, a direct-acting sympathomimetic agent, acts on and receptors. Topical application, therefore, causes conjunctival decongestion (vasoconstriction), transient mydriasis (pupillary dilation), and reduction in intraocular pressure (lOP). It is believed lOP reduction primarily is caused by reduced aqueous production and increased aqueous outflow. The duration of decrease in lOP is 12 to 24 hours. 

Uses Postpartum bleeding (uterine subinvolution) Action Ergotamine derivative Dose 0.2 mg IM after placental deliv y, may repeat 2-4-h intervals or 0.2-0.4 mg PO q6-12h for 2-7 d Caution [C, ] Contra HTN, PRO Disp Inj, tabs SE HTN, N/V Interactions t Vasoconstriction W/ ergot alkaloids, sympathomimetics, tobacco EMS Tobacco use can t vasoconstriction and lead to a hypertensive crisis OD May cause N/V/D, chest/abd pain, limb numbness, and possibly distal gangrene d/t vasoconstriction activated charcoal may be effective for PO form... 

Pseudoephedrine (Sudafed, Novafed, Afrinol, Others) [OTC] [Decongestant/Sympothomimetic] Uses Deconge tant Action Stimulates a-adren gic rec tors w/ vasoconstriction Dose Adults. 30-60 mg PO q6—8h Peds. 4 mg/kg/24 h PO qid -1- in renal insuff Caution [C, +] Contra Poorly controlled HTN or CAD, w/MAOIs Disp Tabs, caps, Liq SE HTN, insomnia, tach, arrhythmias, nervousness, tremor Interactions T Risk of HTN crisis W/ MAOIs T effects W/BBs, sympathomimetics X effects W/TCAs -1- effect OF methyldopa, reserpine EMS Found in many OTC cough/cold pr >arations use sympathomimetics w/ caution, may T adverse effects OD May cause N/V, HTN, arrhythmias, and Szs symptomatic and supportive... 

Mechanism of Action A direct-acting sympathomimetic amine that acts on alpha-adrenergic receptors in arterioles of the nasal mucosa to produce constriction. Therapeutic Effect Causes vasoconstriction resulting in decreased blood flow and decreased nasal congestion. 

SYMPATHOMIMETICS LINEZOLID Risk of t BP when linezolid is co-ingested with either direct or indirect sympathomimetics Linezolid causes accumulation of norepinephrine at the nerve ends sympathomimetics stimulate the release of these T reserves of norepinephrine, which in turn causes vasoconstriction and a rise in BP Monitor BP closely watch for t BP. Warn patients taking linezolid not to take OTC remedies containing sympathomimetics... 

SYMPATHOMIMETICS ACE INHIBITORS, ADRENERGIC NEURONE BLOCKERS 1 hypotensive effect. Note there is a risk of interactions even with topical sympathomimetics (eye and nose drops) Adrenergic neurone blockers act mainly by preventing release of norepinephrine. Sympathomimetics t cardiac output and/or cause vasoconstriction Monitor BP at least weekly until stable... 

Beta-blockers with intrinsic sympathomimetic (ISA) properties are not pure antagonists. These agents partially stimulate the beta-receptors as well. Theoretically, these agents are less likely to cause bradycardia and bronchospasm, increase lipids, decrease cardiac output, and cause peripheral vasoconstriction. However, these agents can still cause bronchospasm or exacerbate heart failure. 

Uncertain. Simple additive hypertensive effects would seem to be part of the explanation. The effects of caffeine may compound the effects of these sympathomimetic drugs on the cardiovascular and central nervous systems by blocking adenosine receptors (causing vasoconstriction) and also augmenting the release of catecholamines. ... 

Ephedrine is a sympathomimetic or central nervous system stimulant. It is a potent stimulator of a, pi and p2 adrenergic receptors. The effects include vasoconstriction, raised blood pressure and pulse, bronchodilation and diuresis. Ephedrine-based drugs are used as nasal decongestants, bronchodilators and in anaphylactic shock. In excess they cause insomnia, tachycardia and dizziness. 

The adrenergic effects caused by ephedrine occur mainly due to its capacity to be a sympathomimetic agonist at both a- and (3-adrenergic receptors. As consequence of these stimulations, an increase in cardiac rate and contractility, peripheral vasoconstriction, bronchodilation, and CNS stimulation can be observed as general effects caused by the use of this amine [62, 65]. 

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