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Table of Contents
This coursework investigates the literature on the effect of drugs on blood pressure of a rabbit heart. It establishes the differential responses noted when different concentration of saline is added to the experimental heart. In addition, it elucidates the changes in blood pressure characteristic of different concentrations of various catecholamines. Further, the coursework examines the effects of using alpha adrenoceptor blockers when administered concurrently with various types of catecholamine. According to the literature, blood pressure as well as the heart rate increases with the administration of a catecholamine, while they considerably reduce when alpha adrenoceptor blockers like prazosin are administered solely or concurrently with a catecholamine (Mannfred 2003).
The experiment set up for the determination of heart rate and blood pressure of a rabbit heart worked on the basis of the pulsating activity of the experimental heart. This rate of these pulsations was determined by connecting the experimental heart through a thin wire to a counting device. As such, it is possible to determine the number of pulsations made in every minute. This was determined for a number of minutes and the average value obtained as the heart rate. On the other side, the blood pressure of the experimental heart was determined by the use of a fluid column. For instance, the normal height of the fluid column was noted and any changes on addition of each drug recorded as variances in blood pressure (Maehle & Halliwell 2002).
The experimental heart was injected with saline to provide an ideal physiological condition for the normal heart functions. This stems from the fact that 0.9% normal saline is hypotonic to blood plasma. This is a proved fact from the study of colligative properties of liquids where addition of solutes alters physical properties of solutions. As such, saline can be used conventionally to provide physiological conditions that are exactly similar to those of the body plasma. In fact, this is why there was no fundamental difference in the heart’s activity on saline injection. For instance, the heart rate increases from 339 to 343 beats per minute. This was clearly notable from changes in the blood pressure as well. Essentially, it formed the reference point from which changes were determined in the activity of the experimental heart. For instance, blood pressure would be said to increase on addition of a drug, if a rise in the level of a fluid column was noted relative to that under saline injection (Mannfred 2003).
The three types of catecholamines generally caused an increase in both the heart rate and blood pressure. However, the magnitude of observed changes was directly proportional to the concentration of the catecholamine. For instance, 1 milliliter/kg of adrenaline caused a change in heart rate by 21 units, while 10 milliliters/kg of the same drug caused a change of 83. This explains the pharmacological principle of occupation of receptors. For instance, 1 milliliter/kg of adrenaline was only able to act on a limited number of adrenergic receptors and as such only produced a little effect. This was comparatively different from injection of 10 milliliters of the same drug where a relatively greater number of adrenergic receptors were occupied. According to the pharmacological theory of receptor occupation, pharmacological activity elicited by an agonist is directly proportional to the extent of receptor occupation. However, there was a notable difference in the effects caused by adrenaline, isoprenaline and nor-adrenaline. For instance, while 10 milliliter/kg of adrenaline caused a change in heart rate by 86 units, 20 milliliter/kg of nor-adrenaline only caused a change by 33 units. This showed that adrenaline exhibits a greater activity on adrenergic receptors than does nor-adrenaline. This is due to the difference in their structure-activity relations. For example, adrenaline has a bulky methyl group that gives it a greater affinity for beta adrenergic receptors that are responsible for determination of the heart rate. In fact, it is the same principle that caused a huge increase of 75 units in the heart rate with only 1 milliliter/kg isoprenaline. Essentially, isoprenaline has the bulkiest isopropyl group that gives it an exaggerated affinity for the beta receptors. These dozes have been chosen to elucidate the different characteristic activities noted with different drugs. Ideally, this serves to reveal the significance of structure-activity relations as regards the pharmacological activities of individual drugs of the same class (Maehle & Halliwell 2002).
Blockers of alpha adrenoceptors have the effect of significantly reducing the blood pressure. This is because they cause relaxation of peripheral muscles thus help in keeping small blood vessel open. Ideally, catecholamines cause vasoconstriction of peripheral blood vessels thereby putting a train to a smooth flow of blood. This results in a rise in blood pressure as the heart has to pump harder to supply the same amount of blood required for adequate tissue perfusion. As such, injection of prazosin would cause a considerable fall in the blood pressure of the experimental heart as it blocks the catecholamine activity on alpha adrenoceptors. Administering 100 milliliters of prazosin alone would cause a greater reduction in blood pressure because its action is based on competitive inhibition of adrenergic drugs at the alpha receptors. As such, its concentration would be higher relative to the concentration of the adrenergic drugs hence the effect is more inhibitory than a stimulatory (Maehle & Halliwell 2002).
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In conclusion, normal saline was used in this experimental procedure to provide ideal physiological conditions for the rabbit heart. As such, it made it possible to notice differences in heart rate or blood pressure when various drugs are added. Besides, it enabled the determination of the inhibitory effects of alpha adrenergic blockers.