Erythrityl Tetranitrate

Indication	For the prevention of angina.
Pharmacodynamics	Erythrityl Tetranitrate is a vasodilator with general properties similar to nitroglycerin.
Mechanism of action	Similar to other nitrites and organic nitrates, erythrityl tetranitrate is converted to an active intermediate compound which activates the enzyme guanylate cyclase. This stimulates the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP) which then activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium ions results in the relaxation of the smooth muscle cells and vasodilation.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Symptoms of overdose include increased intracranial pressure, with any or all of persistent throbbing headache, confusion, and moderate fever; Vertigo; Palpitations; Visual disturbances; Nausea and vomiting (possibly with colic and even bloody diarrhea); Syncope (especially in the upright posture); Air hunger and dyspnea, later followed by reduced ventilatory effort; Diaphoresis, with the skin either flushed or cold and clammy; Heart block and bradycardia; Paralysis; Coma; Seizures; Death.

 Brand Names

Cardilate
Cardiloid
Cardivell
Cardiwell
Tetranitrin
Tetranitrol

  
Interactions

Drug Interactions	Drug Interaction Dihydroergotamine Possible antagonism of action Ergotamine Possible antagonism of action Methysergide Possible antagonism of action
Food Interactions	Avoid alcohol. Take on empty stomach: 1 hour before or 2 hours after meals.

Citation
Reference

Pharmacology Of Ergonovine

Indication	Used to treat postpartum haemorrhage and postabortion haemorrhage in patients with uterine atony.
Pharmacodynamics	Ergonovine belongs to the group of medicines known as ergot alkaloids. These medicines are usually given to stop excessive bleeding that sometimes occurs after abortion or a baby is delivered. They work by causing the muscle of the uterus to contract.
Mechanism of action	Ergonovine directly stimulates the uterine muscle to increase force and frequency of contractions. With usual doses, these contractions precede periods of relaxation; with larger doses, basal uterine tone is elevated and these relaxation periods will be decreased. Contraction of the uterine wall around bleeding vessels at the placental site produces hemostasis. Ergonovine also induces cervical contractions. The sensitivity of the uterus to the oxytocic effect is much greater toward the end of pregnancy. The oxytocic actions of ergonovine are greater than its vascular effects. Ergonovine, like other ergot alkaloids, produces arterial vasoconstriction by stimulation of alpha-adrenergic and serotonin receptors and inhibition of endothelial-derived relaxation factor release. It is a less potent vasoconstrictor than ergotamine. As a diagnostic aid (coronary vasospasm), ergonovine causes vasoconstriction of coronary arteries.
Absorption	Absorption is rapid and complete after oral or intramuscular administration.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Hepatic.
Route of elimination	Thought to be eliminated by non-renal mechanisms (i.e. hepatic metabolism, excretion in feces)
Half life	t1/2 α=10 minutes; t1/2 β=2 hours
Clearance	Not Available
Toxicity	The principal symptoms of overdose are convulsions and gangrene. Other symptoms include bradycardia, confusion, diarrhoea, dizziness, dyspnoea, drowsiness, fast and/or weak pulse, miosis, hypercoagulability, loss of consciousness, nausea and vomiting, numbness and coldness of the extremities, pain in the chest, peripheral vasoconstriction, respiratory depression, rise or fall in blood pressure, severe cramping of the uterus, tachycardia, tingling, and unusual thirst.

Pharmacology Of Enprofylline

Indication	Used in the management of symptoms of asthma. Also used in the treatment of peripheral vascular diseases and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy.
Pharmacodynamics	Enprofylline is a synthetic dimethylxanthine derivative structurally related to theophylline and caffeine. It antagonizes erythrocyte phosphodiesterase, increasing cAMP activity.
Mechanism of action	Enprofylline inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, enprofylline also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity.
Absorption	Rapidly absorbed from the digestive tract
Volume of distribution	Not Available
Protein binding	49%
Metabolism	Not Available
Route of elimination	Not Available
Half life	1.9 hours
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Edrophonium

Indication	For the differential diagnosis of myasthenia gravis and as an adjunct in the evaluation of treatment requirements in this disease. It may also be used for evaluating emergency treatment in myasthenic crises.
Pharmacodynamics	Edrophonium is a short and rapid-acting anticholinesterase drug. Its effect is manifest within 30 to 60 seconds after injection and lasts an average of 10 minutes. Edrophonium's pharmacologic action is due primarily to the inhibition or inactivation of acetylcholinesterase at sites of cholinergic transmission. Muscarinic receptors are found throughout the body, especially on muscle. Stimulation of these receptors causes to muscle contraction. In myasthenia gravis the body's immune system destroys many of the muscarinic receptors, so that the muscle becomes less responsive to nervous stimulation. Edrophonium chloride increases the amount of acetylcholine at the nerve endings. Increased levels of acetyl choline allow the remaining receptors to function more efficiently.
Mechanism of action	Edrophonium works by prolonging the action acetylcholine, which is found naturally in the body. It does this by inhibiting the action of the enzyme acetylcholinesterase. Acetylcholine stimulates nicotinic and muscarinic receptors. When stimulated, these receptors have a range of effects.
Absorption	Rapidly absorbed.
Volume of distribution	1.6±0.4 L/kg [Adults] 2.2±1.5 L/kg [Children (0.08-10 yrs)] 1.8±1.2 L/kg [Elderly (65-75 yrs)]
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Edrophonium is primarily renally excreted with 67% of the dose appearing in the urine. Hepatic metabolism and biliary excretion have also been demonstrated in animals
Half life	Distribution half-life is 7 to 12 minutes. Elimination half-life is 33 to 110 minutes.
Clearance	6.8 +/- 2. mL/kg/min [Adults] 6.4 +/- 3.9 mL/kg/min [Children (0.08-10 yrs)] 2.9 +/- 1.9 mL/kg/min [Elderly (65-75 yrs)]
Toxicity	With drugs of this type, muscarine-like symptoms (nausea, vomiting, diarrhea, sweating, increased bronchial and salivary secretions and bradycardia) often appear with overdosage (cholinergic crisis).

Pharmacology Of Echothiophate

Indication	For use in the treatment of subacute or chronic angle-closure glaucoma after iridectomy or where surgery is refused or contraindicated.
Pharmacodynamics	Echothiophate Iodide is a potent, long-acting cholinesterase inhibitor used as a miotic in the treatment of glaucoma. Echothiophate iodide will depress both plasma and erythrocyte cholinesterase levels in most patients after a few weeks of eyedrop therapy.
Mechanism of action	Echothiophate Iodide is a long-acting cholinesterase inhibitor for topical use which enhances the effect of endogenously liberated acetylcholine in iris, ciliary muscle, and other parasympathetically innervated structures of the eye. Echothiophate iodide binds irreversibly to cholinesterase, and is long acting due to the slow rate of hydrolysis by cholinesterase. It causes miosis, increase in facility of outflow of aqueous humor, fall in intraocular pressure, and potentiation of accommodation.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Side effects include blurred vision or change in near or distant vision and eye pain.

Pharmacology Of Drospirenone

Indication	For the prevention of pregnancy in women who elect an oral contraceptive.
Pharmacodynamics	Drospirenone differs from other synthetic progestins in that its pharmacological profile in preclinical studies shows it to be closer to the natural progesterone. As such it has anti-mineralocorticoid properties, counteracts the estrogen-stimulated activity of the renin-angiotensin-aldosterone system, and is not androgenic.
Mechanism of action	Progestins such as drospirenone diffuse freely into target cells in the female reproductive tract, mammary gland, hypothalamus, and the pituitary and bind to the progesterone receptor. Once bound to the receptor, progestins slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH surge.
Absorption	Oral bioavailability is approximately 76%.
Volume of distribution	Not Available
Protein binding	97%
Metabolism	Extensively metabolized following oral or intravenous administration. The two major metabolites are inactive and are formed independent of the CYP450 enzyme system. The metabolites are the acid form of drospirenone formed by opening of the lactone ring and the 4,5-dihydro-drospirenone-3-sulfate.
Route of elimination	Not Available
Half life	30 hours
Clearance	Not Available
Toxicity	Not Available

Pharmacology Of Drostanolone

Indication	For use in females, for palliation of androgenresponsive recurrent mammary cancer in women who are more than one year but less than five years postmenopausal.
Pharmacodynamics	Dromostanolone is a synthetic androgen, or male hormone, similar to testosterone. Dromostanolone works by attaching itself to androgen receptors; this causes it to interact with the parts of the cell involved in the making of proteins. It may cause an increase in the synthesis of some proteins or a decrease in the synthesis of others. These proteins have a variety of effects, including blocking the growth of some types of breast cancer cells, stimulating cells that cause male sexual characteristics, and stimulating the production of red blood cells.
Mechanism of action	Dromostanolone is a synthetic androgenic anabolic steroid and is approximately 5 times as potent as natural methyltestosterone. Like testosterone and other androgenic hormones, dromostanolone binds to the androgen receptor. This causes downstream genetic transcriptional changes. This ultimately causes retention of nitrogen, potassium, and phosphorus; increases protein anabolism; and decreases amino acid catabolism. The antitumour activity of dromostanolone appears related to reduction or competitive inhibition of prolactin receptors or estrogen receptors or production.
Absorption	Well absorbed following parenteral administration.
Volume of distribution	Not Available
Protein binding	Not Available
Metabolism	Not Available
Route of elimination	Not Available
Half life	Not Available
Clearance	Not Available
Toxicity	Side effects include virilization (masculine traits in women), acne, fluid retention, and hypercalcemia.