Amiloride, an antikaliuretic-diuretic agent, is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known antikaliuretic or diuretic agents. It is an antihypertensive, potassium-sparing diuretic that was first approved for use in 1967 and helps to treat hypertension and congestive heart failure. The drug is often used in conjunction with thiazide or loop diuretics. Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) are occasionally observed in patients taking amiloride. Amiloride works by inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys by binding to the amiloride-sensitive sodium channels. This promotes the loss of sodium and water from the body, but without depleting potassium. It is used for as adjunctive treatment with thiazide diuretics or other kaliuretic-diuretic agents in congestive heart failure or hypertension.

Atenolol is a Beta-1 cardio-selective adreno-receptor blocking agent discovered and developed by ICI in 1976. Atenolol was launched in the market under the trade name Tenormin in 1976, and became the best-selling Beta-blocker in the world in the 1980s and 1990s. TENORMIN is indicated for the treatment of hypertension, to lower blood pressure; also for the long-term management of patients with angina pectoris and also is indicated in the management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality. Like metoprolol, atenolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension. Higher doses of atenolol also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles. Hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.

Amiloride, an antikaliuretic-diuretic agent, is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known antikaliuretic or diuretic agents. It is an antihypertensive, potassium-sparing diuretic that was first approved for use in 1967 and helps to treat hypertension and congestive heart failure. The drug is often used in conjunction with thiazide or loop diuretics. Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) are occasionally observed in patients taking amiloride. Amiloride works by inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys by binding to the amiloride-sensitive sodium channels. This promotes the loss of sodium and water from the body, but without depleting potassium. It is used for as adjunctive treatment with thiazide diuretics or other kaliuretic-diuretic agents in congestive heart failure or hypertension.

Disopyramide is an antiarrhythmic drug indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia that are life-threatening. In man, Disopyramide at therapeutic plasma levels shortens the sinus node recovery time, lengthens the effective refractory period of the atrium, and has a minimal effect on the effective refractory period of the AV node. Little effect has been shown on AV-nodal and His-Purkinje conduction times or QRS duration. However, prolongation of conduction in accessory pathways occurs. Disopyramide is a Type 1A antiarrhythmic drug (ie, similar to procainamide and quinidine). It inhibits the fast sodium channels. In animal studies Disopyramide decreases the rate of diastolic depolarization (phase 4) in cells with augmented automaticity, decreases the upstroke velocity (phase 0) and increases the action potential duration of normal cardiac cells, decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium, and has no effect on alpha- or beta-adrenergic receptors. It is used for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, ventricular pre-excitation and cardiac dysrhythmias. It is a Class Ia antiarrhythmic drug.

Oxybutynin is an antispasmodic, anticholinergic agent indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency. Oxybutynin relaxes bladder smooth muscle. Oxybutynin exhibits only one-fifth of the anticholinergic activity of atropine on the rabbit detrusor muscle, but four to ten times the antispasmodic activity. Antimuscarinic activity resides predominantly in the R-isomer. Oxybutynin exerts a direct antispasmodic effect on smooth muscle and inhibits the muscarinic action of acetylcholine on smooth muscle. No blocking effects occur at skeletal neuromuscular junctions or autonomic ganglia (antinicotinic effects). By inhibiting particularily the M1 and M2 receptors of the bladder, detrusor activity is markedly decreased.

Oxybutynin is an antispasmodic, anticholinergic agent indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency. Oxybutynin relaxes bladder smooth muscle. Oxybutynin exhibits only one-fifth of the anticholinergic activity of atropine on the rabbit detrusor muscle, but four to ten times the antispasmodic activity. Antimuscarinic activity resides predominantly in the R-isomer. Oxybutynin exerts a direct antispasmodic effect on smooth muscle and inhibits the muscarinic action of acetylcholine on smooth muscle. No blocking effects occur at skeletal neuromuscular junctions or autonomic ganglia (antinicotinic effects). By inhibiting particularily the M1 and M2 receptors of the bladder, detrusor activity is markedly decreased.

Metaproterenol, also known as Orciprenaline, is a brochodilator that is FDA approved for the treatment of bronchial asthma and for reversible bronchospasm which may occur in association with bronchitis and emphysema. Metaproterenol Sulfate is a potent beta-adrenergic stimulator with a rapid onset of action. It is postulated that beta-adrenergic stimulants produce many of their pharmacological effects by activation of adenyl cyclase, the enzyme which catalyzes the conversion of adrenosine triphosphate to cyclic adenosine monosphosphate. Metaproterenol is a moderately selective beta(2)-adrenergic agonist that stimulates receptors of the smooth muscle in the lungs, uterus, and vasculature supplying skeletal muscle, with minimal or no effect on alpha-adrenergic receptors.

Amoxicillin is one of the widely prescribed antibacterial agents, which was discovered by scientists at Beecham Research Laboratories in 1972. In the US GlaxoSmithKline markets it under the original brand name Amoxil. It is the first line treatment for middle ear infections. It is also used for strep throat, pneumonia, skin infections, and urinary tract infections it is taken by mouth. Amoxicillin inhibits the third and final stage of bacterial cell wall synthesis by preferentially binding to specific penicillin-binding proteins (PBPs) that are located inside the bacterial cell wall. This results in a formation of defective cell wall and a cell death. Common side effects include nausea and rash. It may also increase the risk of yeast infections and, when used in combination with clavulanic acid, diarrhea. It should not be used in those who are allergic to penicillin.

Amoxicillin is one of the widely prescribed antibacterial agents, which was discovered by scientists at Beecham Research Laboratories in 1972. In the US GlaxoSmithKline markets it under the original brand name Amoxil. It is the first line treatment for middle ear infections. It is also used for strep throat, pneumonia, skin infections, and urinary tract infections it is taken by mouth. Amoxicillin inhibits the third and final stage of bacterial cell wall synthesis by preferentially binding to specific penicillin-binding proteins (PBPs) that are located inside the bacterial cell wall. This results in a formation of defective cell wall and a cell death. Common side effects include nausea and rash. It may also increase the risk of yeast infections and, when used in combination with clavulanic acid, diarrhea. It should not be used in those who are allergic to penicillin.

Pancuronium (trademarked as Pavulon) is an aminosteroid muscle relaxant with various medical uses. Pancuronium is a typical non-depolarizing curare-mimetic muscle relaxant. It competitively inhibits the nicotinic acetylcholine receptor at the neuromuscular junction by blocking the binding of acetylcholine. It has slight vagolytic activity, causing an increase in heart rate, but no ganglioplegic (i.e., blocking ganglions) activity. It is a very potent muscle relaxant drug, with an ED95 of only 60 µg/kg body weight. The onset of action is relatively slow compared to other similar drugs, in part due to its low dose - an intubating dose takes 3–6 minutes for full effect. Clinical effects (muscle activity lower than 25% of physiological) last for about 100 minutes. The time needed for full (over 90% muscle activity) recovery after single administration is about 120–180 minutes in healthy adults. Pancuronium is used with general anesthesia in surgery for muscle relaxation and as an aid to intubation or ventilation. It does not have sedative or analgesic effects. Side-effects include moderately raised heart rate and thereby arterial pressure and cardiac output, excessive salivation, apnea and respiratory depression, rashes, flushing, and sweating. The muscular relaxation can be dangerous for the seriously ill and it can accumulate leading to extended weakness. Pancuronium is not preferable to long-term use in ICU-ventilated patients. Pancuronium is also used as one component of a lethal injection in the administration of the death penalty in some parts of the United States.