Blood pressure ephedrine effects

The main limitation to the clinical use of the MAOIs is due to their interaction with amine-containing foods such as cheeses, red wine, beers (including non-alcoholic beers), fermented and processed meat products, yeast products, soya and some vegetables. Some proprietary medicines such as cold cures contain phenylpropanolamine, ephedrine, etc. and will also interact with MAOIs. Such an interaction (termed the "cheese effect"), is attributed to the dramatic rise in blood pressure due to the sudden release of noradrenaline from peripheral sympathetic terminals, an event due to the displacement of noradrenaline from its mtraneuronal vesicles by the primary amine (usually tyramine). Under normal circumstances, any dietary amines would be metabolized by MAO in the wall of the gastrointestinal tract, in the liver, platelets, etc. The occurrence of hypertensive crises, and occasionally strokes, therefore limited the use of the MAOIs, despite their proven clinical efficacy, to the treatment of atypical depression and occasionally panic disorder. 

As drugs of mixed action, amphetamines activate adrenergic receptors and simultaneously release endogenic catecholamines (norepinephrine and dopamine) from neurons of the brain and periphery. Sympathomimetic effects on the periphery are very similar to those of ephedrine. Amphetamine elevates systolic and diastolic blood pressure and has weakly expressed, broncholytic action. These effects are more prolonged, yet less expressed, than with epinephrine. The distinctive feature of amphetamines is their psychostimulatory activity. Larger doses can cause hallucinations and mental conditions similar to paranoid schizophrenia. As a sympathomimetic, amphetamine is sometimes used for uterine inertia. Synonyms of amphetamine are phenamine and benzedrine. 

Ephedrine increases systolic and diastolic blood pressure heart rate is generally not increased. Contractile force of the heart and cardiac output are both increased. Ephedrine produces bronchial smooth muscle relaxation of prolonged duration when administered orally. Aside from pupillary dilation, ephedrine has little effect on the eye. 

Amphetamine is an indirectly acting adrenomimetic amine that depends for its action on the release of norepinephrine from noradrenergic nerves. Its pharmacological effects are similar to those of ephedrine however, its CNS stimulant activity is somewhat greater. Both systolic and diastolic blood pressures are increased by oral dosing with amphetamine. The heart rate is frequently slowed reflexively. Cardiac output may remain unchanged in the low- and moderate-dose range. 

A 77-year-old man is admitted to the hospital for a coronary artery bypass. He has been treated with a (3-blocker (Tenormin 100 mg per day), which he took every morning. He is induced with propofol 1 mg/kg, fentanyl 5 jjig/kg and vecuronium 8 mg for muscle relaxation. After 3 minutes a decreasing heart rate becomes a worry for the anesthesiologist. The heart rate continues to fall until it reaches 38 BPM. At this point the patient s blood pressure is 80/60 and the anesthesiologist gives atropine 0.4 mg and ephedrine 10 mg. This treatment results in a stable patient. What effects were most likely produced by the anesthesia procedure Could this have been avoided ... 

Ephedrine has positive inotropic and chronotropic effects and increases peripheral vascular resistance. It is preferable to methoxamine for maintaining blood pressure in elderly patients during spinal anaesthesia, possibly because it has less effect on coronary blood flow (less pronounced a activity). It is also less likely to impair placental blood flow than some other vasopressors, for the same reason. It is used as a bronchodilator because of its 32-agonist effects. 

Headaches, high blood pressure, and elevated body temperature were among noted side effects. Many reported side effects after 8-12 days. The body quickly adapts to clenbuterol so "on/off periods were a must for successful results. By alternating between E/C (Ephedrine and caffeine) stacks and Clenbuterol, the effective period was extended and results increased. Rotations weekly such as clenbuterol, week 1, ephedrine/ caffeine week 2, seem to have brought superior results. 

Ephedrine occurs in white, rosette, or needle crystals, or as an unctuous mass. It is soluble in water, alcohol, chloroform, ether, and in liquid petrolatum, the latter solution being turbid if the ephedrine is not dry. Ephedrine melts between 34 and 40°C, depending upon the amount of water it contains it contains not more than 0.1% of ash its solutions are alkaline to litmus it readily forms salts with acids and it responds to the usual tests for alkaloids. Ephedrine excites the sympathetic nervous system, depressing smooth and cardiac muscle action, and produces effects similar to those of epinephrine. It produces a rather long-lasting rise of blood pressure and mydriasis and diminishes hyperemia. The alkaloid may be used in 0.5 to 2% oil spray. 

Correct answer = D. Reserpine blocks the uptake of norepinephrine into intracellular storage vesicles, resulting in depletion of norepinephrine and gradual decline in blood pressure. Phenylephrine is a pure vasoconstrictor and raises systolic and diastolic blood pressures. Dopamine raises systolic and diastolic blood pressures by stimulating the heart and (at high doses) causing vasoconstriction. Ephedrine raises systolic and diastolic blood pressures by vasoconstriction and cardiac stimulation. Norepinephrine has a pressor effect. 

SAFETY PROFILE Poison by intravenous, intraperitoneal, and subcutaneous routes. Moderately toxic by ingestion. Human systemic effects by intravenous route increased pulse rate and blood pressure. When heated to decomposition it emits very toxic fumes of NOx and SOx. See also EPHEDRINE. 

The cardiovascular effects, subjective effects, and abuse potential of single intranasal doses of ephedrine 5 and 10 mg have been compared with oral doses of (—)ephe-drine 50 mg in 16 healthy Caucasian men with no drug/ alcohol/nicotine abuse or dependence (5). Intranasal ephedrine caused an increase in blood pressure but associated orthostatic hypotension. 

Scientists have conducted several studies and the totality of the available data showed little evidence of the effectiveness of ephedra except for modest, short-term weight loss without any clear health benefit, while confirming that the substance raises blood pressure and otherwise stresses the circulatory system. These effects are linked to significant adverse health outcomes, including heart attack and stroke. On Eebruary 6, 2004, the EDA issued a final rule prohibiting the sale of dietary supplements containing ephedrine alkaloids (ephedra) because such supplements present an unreasonable risk of illness or injury (Table 2). 

The basic pharmacological action of Ephedrine is that of a sympathomimetic. It does not contain a catechol moiety and is effective after oral administration. The drug stimulates heart rate and cardiac output and variably increases peripheral resistance as a result, ephedrine usually increases blood pressure. Stimulation of the a-adrenergic receptors of smooth muscle cells in the bladder base may increase resistance to the outflow of urine. Activation of S-adrenergic receptors in the lungs promotes bronchodilation. Ephedrine stimulates the cerebral cortex and subcortical centers to produce its effects in narcolepsy and depressive states. 

Preexisting medical conditions The likelihood of adverse effects of ephedrine is heightened in individuals with a history of high blood pressure, heart or thyroid disease, diabetes, kidney disease or difficulty urinating, glaucoma, a seizure disorder, depression, prostate enlargement, history of stress, or are involved in stressful activities. 

Receptor distribution probably explains why ephedrine has no effect on diastolic pressure, and only minimal effect on systolic. p2 Stimulation of vessels in peripheral muscles results in peripheral vasodilation and diastolic runoff, which more than cancels ephedrine s other inotropic effects (29). The absence of any significant effect on blood pressure was firmly established during the late 1970s and early 1980s in dozens of double-blind, placebo-controlled studies performed to compare the effectiveness of ephedrine with that of newly synthesized adrenergic agents (30-60). 

The ephedra alkaloids are all sympathomimetic amines, which means that a host of drug interactions are theoretically possible. In fact, only a handful of adverse drug interactions have been reported in the peer-reviewed literature. The most important of these involve the monoamine oxidase inhibitors (MAOI). Irreversible, nonselective MAOIs have been reported to adversely interact with indirectly acting sympathomimetic amines present in many cough and cold medicine. In controlled trials with individuals taking moclobemide, ephedrine s effects on pulse and blood pressure were potentiated, but only at higher doses than those currently provided in health supplements (137). Ephe-drine-MAOI interaction may, on occasion, be severe enough to mimic pheo-... 

Epinephrine (adrenaline) was one of the first hormones for which differential effects on blood pressure were reported for the two epimers in the early 20th century [58]. A reassessment of epinephrine activity was made by analyzing the effects of optical isomers of ephedrine and methylephedrine on the spontaneous beating rate of the isolated right atrium of normal and reserpinized rats by investigating direct and indirect actions on al-adrenoceptors. L-ephedrine, and to a lesser extent D-ephedrine, markedly increased the beating rate of rat right atrium [59]. 

As is the case with trifluoperazine, concomitant use of triflupromazine with sympathomimetics, including epinephrine, phenylephrine, phenylpropanolamine, ephedrine (often found in nasal sprays), and appetite snppressants may decrease their stimulatory and pressor effects. Using epinephrine as a pressor agent in patients taking triflupromazine may result in epinephrine reversal or further lowering of blood pressure. 

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