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May slow clotting; contraindicated for people with bleeding disorders and before and after surgery. May induce uterine contractions; contraindicated when pregnant or nursing. [21] Pyrrolizidine alkaloids (contained in comfrey, borage, senecio, coltsfoot, and others) Liver damage [5] Reserpine: Rauvolfia serpentina
Slow acting substances would hold the danger of ischaemia due to an uncontrollably low blood pressure and are therefore contraindicated. Depending on the circumstances, even fast acting substances can be contraindicated – for example, glyceryl trinitrate in patients with obstructive heart failure.
The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
Modified-release dosage is a mechanism that (in contrast to immediate-release dosage) delivers a drug with a delay after its administration (delayed-release dosage) or for a prolonged period of time (extended-release [ER, XR, XL] dosage) or to a specific target in the body (targeted-release dosage).
Low blood pressure caused by phenothiazines, hypertension, and pheochromocytoma. [citation needed]Patients receiving monoamine oxidase inhibitors. [citation needed]For shock due to loss of blood or fluid, give fluid replacement therapy primarily, cardiovascular disease, hypertension, hyperthyroidism, chronic illnesses, lactation, pregnancy, skin dryness. headache.
The M 2 muscarinic receptors are located in the heart and lungs. In the heart, they act to slow the heart rate down below the normal baseline sinus rhythm, by slowing the speed of depolarization. In humans, under resting conditions, vagal activity dominates over sympathetic activity.
They are a class of sympathomimetic agents, each acting upon the beta adrenoceptors. [2] In general, pure beta-adrenergic agonists have the opposite function of beta blockers : beta-adrenoreceptor agonist ligands mimic the actions of both epinephrine - and norepinephrine - signaling, in the heart and lungs, and in smooth muscle tissue ...
Reverse use dependent drugs that slow heart rate (such as quinidine) can be less effective at high heart rates. [11] The refractoriness of the ventricular myocyte increases at lower heart rates . [ citation needed ] This increases the susceptibility of the myocardium to early Afterdepolarizations (EADs) at low heart rates.