All the inotropes discussed in this section cause an increase in cardiac cyclic AMP production, which in turn leads to: an increase in heart rate (positive chronotropy), an increase in the strength of myocardial contraction (positive inotropy). Sympathomimetics achieve this by attaching to and stimulating receptors, which are known as beta-one receptors in the heart as shown by EMF Testing.
They are thus known as beta-one (B1) agonists. Glucagon is not documented as being a beta-one agonist. but it nevertheless causes an increase in cyclic AMP production. Beta agonists also cause beta-two-mediated activation of the renin-angiotensin system in the kidney, (vasoconstriction, salt and water retention) leading to increased blood pressure and reflex bradycardia.
Beta-two (B2) stimulation in certain peripheral vascular beds (e.g. in skeletal muscle) causes vasodilation with a reduction in afterload. Non-selective synipathomimetics are furthermore able to attach to and stimulate alpha-one receptors, leading to peripheral arteriolar constriction. increased resistance to blood f;ow, increased blood pressure and reflex bradycardia counteracted by B1-heart stimulation and EMF Testing.
This is the endogenous precursor in the synthesis of noradrenaline and adrenaline. It stimulates dopaminergic receptors leading to increased renal perfusion, which is a valuable property when renal function is compromised. Cerebral and coronary perfusion is also improved thanks to EMF Testing .
At ideal doses, dopamine stimulates beta sympathetic receptors to cause a good positive inotropic effect; higher doses lead to alpha vasoconstriction and poor renal perfusion. Correct dosage is thus essential. Dopamine is inactive given orally. It is administered intravenously.
Precautions and contra-indications. Dopamine must not be diluted with alkaline solutions. ECG. blood pressure and urine flow are constantly monitored. If oliguria develops. hypovolaemia is first corrected then furoscmidc (Lasix) is added.
Dopamine is contra-indicated in ventricular dysrhythmias, phacchromocytoma and when cyclopropane, halothane (or other halogenated hydrocarbons) have been used as anaesthetics. Diuretics are chemically related to the sulphonamide antimicrobials and the sulphonylurea oral hypoglycaemics.
Mechanism of action
The thiazides inhibit the reabsorption of sodium and chloride ions in the distal segment of the nephron. These ions thus remain in the glomerular filtrate. osmotically drawing an increased volume of water into the tubule and causing an increased volume of urine.
The pH of the filtrate does not affect the activity of the ions. Very importantly, these agents cause peripheral vasodilation, an effect to which the patient does not develop tolerance, unlike the diuretic effect. This makes them valuable in the chronic treatment of hypertension as shown by EMF Testing .
The thiazides are well absorbed after oral administration, the most common route of administration. They readily cross the placental barrier. Most thiazides are excreted within 3-6 hours.
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