Exercise And Drugs On Cardiovascular System

Exercise And Drugs On Cardiovascular SystemThe experiment was carried come out of the closet in come in to examine the effects of propanolol, salsolelyamol and GTN in subjects at tarry and during exercise. This was done by taking recordings of SBP, DBP, lay out, PP, HR and PEFR at rest and during exercise for severally drug. apply t-tests the results for to each one drug were comp ard at rest and during exercise in rig to prove that changes were significant. However, only HR using propanolol was shown to flummox a significant come ( devil assay t-test, t=3.01, p=0.01). This was concluded to be because the subjects used were not medically uncollectible (in quest of using the drugs).Introduction.Heart disease is an increasing cause of death in western countries overdue to carbuncular lifestyles smoking cigarettes, consuming alcohol, diets high in salt and fats as substantially as a overleap of exercise. Because of this, a lot of medical research goes into developing d rugs which lower the high snag pressure, brought about by an unhealthy lifestyle, as well as simplification midpoint set up in severe cases, stand acute relief of angina pectoris, reduce mortality following myocardial infarction and prevent homecoming of tachyarrhythmias, as stated by Craig and Stitzel (2004). Three of these drugs, propanolol, salbutamol and glyceryl trinitrate (GTN), were used in the experiment.Propanolol is a non-selective -adrenoreceptor antagonistic drug (Geddes Grosset 2006). It is used to litigate angina pectoris, myocardial infarction, certain cardiac dysrhythmias and hypertension (Marcovitch 2007). Propanolols mode of action whole shebang by depressing myocardium cellular cardiac membrane excitability. This membrane stabilising is thought to be stiff against arrhythmias (Craig Stitzel 2004). It also decreases blood pressure, midriff rate, myocardial contractility, cardiac output (and in that locationfore arterial pressure) as well as conduction velocity in the nerve (Craig Stitzel 2004). The drug is administered viva vocely as it is subject to a significant degree of first-pass transfiguration as well as extensive absorption from the gastro-intestinal tract. Because of this, during the experiment, the subject had to bear 50 tenuouss by and by(prenominal) taking the drug before taking recordings as propanolols peak therapeutic effect occurs between 1 and 1.5 hours after the drug is administered.I brook no change in plastered arterial pressure (function) at rest after propanolol is interpreted. However, during post-drug exercise I harbinger there to be a reduction in MAP as well as blood pressure (Wheatley 1981).1-1-Salbutamol is a short acting, selective 2-adrenoreceptor agonist drug (Marcovitch 2007). Salbutamol treats bronchospasm associated with chronic obstructive pulmonary disease (COPD) (Naish et al 2009) by inducing bronchodilation. Although the drug has adrenergic effects, it has minimal cardiac stimulat ion (Craig Stitzel 2004). Salbutamol is inhaled as a spray using a metered dose in haler (MDI) (Marcovitch 2007). By inhaling the drug, it immediately enters the bronchi in the lungs (the source of the bronchospasm) and provides a rapid onset of action and acute relief (Craig Stitzel 2004). Salbutamols maximal effect is reached inwardly 5 to 20 transactions of administration (Dale et al 2003). Because of this, readings could be taken straight away during the experiment.For salbutamol I expect an sum up in PEFR after the drug has been taken but no change in heart rate during post-drug exercise.Glyceryl trinitrate (GTN) is a -adrenoreceptor antagonist and a potent vasodilator (Dale et al 2003). It is used to treat ischaemic heart disease, angina pectoris and coronary spasm (Marcovitch 2007). GTN relieves coronary spasm by redistributing coronary rate of flow towards ischaemic areas via collaterals (collateral vessels that bypass narrowed coronary arteries (Dale et al 2003). Angi na is due to a lack of oxygen in myocardium (Naish et al 2009). GTN acts to relieve angina by decreasing circulating blood volume, thus diminution the metabolic demand of the heart. It does this predominantly by dilating the veins, therefore decreasing preload and ventricular diastolic volume. GTN is administered sublingually as an oral tablet. Administration of GTN in this way allows it to pass straight into systemic circulation, thus avoiding the portal system and first-pass metabolism (Dale et el 2003). GTNs onset of action occurs within 2 to 5 transactions, with its maximal effects occurring between 3 and 10 minutes of administration (Craig Stitzel 2004). For these reasons, recordings were taken straight away (for 12 minutes) during the experiment.after GTN is taken, I expect to try out a decrease in systolic blood pressure and a decrease in the heart rate.The aim of the experiment was to improve understanding of how propanolol, salbutamol and GTN are useful in treating th e various forms of heart disease and how their physiology in the cardiovascular system operates.Method.3 subjects, 2 female and 1 male, were deemed medically sizeable by a medical supervisor to take one of the following drugs, propanolol, salbutamol and glyceryl trinitrate (GTN). Each of these drugs was obtained from a accredited chemist.All three subjects were seated comfortably at right angles to the research lab bench. Using an electrical sphygmomanometer, each subjects resting systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were enter at 3 minute intervals for 9 minutes. From the SBP and DBP values, the pulse pressure (PP) and mean arterial pressure (MAP) were calculated at each interval using the following formulas2PP = SBP DBPMAP = (PP/3) + DBPAlso, for the deuce subjects chosen to take propanolol (subject A) and salbutamol (subject B), a Wright peak flow mini-meter was used to measure peak expiratory flow rate (PEFR) at each interval. A mean of each recorded value across all subjects was calculated and recorded.Subjects A and B and so took it in turn to use the cycle ergometer. The seat was adjusted to a comfortable aggrandisement for cycling and a note of the seat height, for exercise after the drug was taken, was made. A load background signal of 2 Kp was set and the subjects, in turn, were kept connected to the sphygmomanometer as they pedalled for 2 minutes at almost 80 rev. HR values were recorded any 15 seconds for both subject A and B.After exercise and prior to taking the drug, subject A and Bs HR, SBP, DBP and PEFR were recorded (HR every 15 seconds, SBP, DBP and PEFR every minute) for five minutes. PP and MAP were also calculated where possible (i.e. at the minute intervals). Subject A whence took four 10 mg tablets (i.e. 40 mg) of propanolol and waited for 50 minutes to allow absorption of the drug.Using a sphygmomanometer, the first stage of the experiment was repeated with SBP, DBP, PP, MAP, HR and PEFR, as well as a mean value for each, were calculated and recorded at 3 minute intervals for 9 minutes. The subject then repeated exercise on the cycle ergometer, ensuring that the same height was used, a 2 Kp load ground was again used and a cycling average of 80 rpm was maintained. During this post-drug exercise HR was taken at 15 second intervals for 2 minutes.After post-drug exercise, HR, SBP, DBP and PEFR were recorded, PP and MAP were also calculated and recorded. HR was recorded every 15 seconds, SBP, DBP and PEFR were recorded every minute. These recordings were taken for 5 minutes.Subject B then took two doses of 0.1 mg (in separate inspirations) of salbutamol using a metered dose inhaler (MDI). The same steps as taken for subject B (post drug) were repeated.Using a sphygmomanometer, the first stage of the experiment was repeated with SBP, DBP, PP, MAP, HR and PEFR, as well as a mean value for each, were calculated and recorded at 3 minute intervals for 9 minutes. Th e subject then repeated exercise on the cycle ergometer, ensuring that the same height was used, a 2 Kp load setting was again used and a cycling average of 80 rpm was maintained. During this post-drug exercise HR was taken at 15 second intervals for 2 minutes.3 After post-drug exercise, HR, SBP, DBP and PEFR were recorded, PP and MAP were also calculated and recorded. HR was recorded every 15 seconds, SBP, DBP and PEFR were recorded every minute. These recordings were taken for 5 minutes.Finally, subject C (glyceryl trinitrate) was administered 500 g of glyceryl trinitrate (oral tablet form) sublingually whilst comfortably sat at right angles to the lab desk. By sitting down, tachycardia and postural hypotension due to venous pooling in the legs was minimised). Subject C was also connected to the sphygmomanometer. Readings of SBP, DBP, PP, MAP and HR were then calculated and recorded at 3 minute intervals for 30 minutes.At 12 minutes, the tablet had still not dissolved and so the s ubject chewed the tablet and placed the dust back under the tongue. It was also noted that subject C suffered from a slight headache due to decreased blood pressure.Statistics.To examine the results, the relevant data was used in statistical paired two example t-tests so that it could be percolaten whether or not an increase or decrease across the data was of significance. Data was represented in the text with a standard error of the mean to show how finished the data was by showing how much of the data in a sample was close to the mean value.Results.For propanolol, it was predicted that there would be no change in mean arterial pressure (MAP) at rest after propanolol is taken and that there would be a reduction in heart rate (HR) as well as blood pressure (BP).There was an increase in mean MAP at rest pre-propanolol (89.3 15.3 mmHg, n=8) to post-propanolol (90.3 20.3 mmHg, n=8) of 1 mmHg (two sample t-test, t=-0.21, p=0.84). This was an insignificant increase.At rest there w as a decrease in mean HR from pre-propanolol (78 13 bpm, n=8) to post-propanolol (65.86 15.14 bpm, n=8) of 12.14 bpm, a significant decrease (two sample t-test, t=3.01, p=0.01).Blood pressure of the subjects immediately after beginning post-propanolol exercise (60.4 40.4 mmHg, n=8) showed an average decrease of 19 mmHg compared to the subjects at pre-propanolol exercise (79.4 28.6 mmHg, n=8) (two sample t-test, t=1.28, p=0.23). The t-test shows that this was not a significant decrease.For salbutamol it was hypothesized that there would be an increase in PEFR after the drug has been taken but no change in heart rate during post-drug exercise.PEFR of the subjects 5 minutes into exercise, post-salbutamol (505 155 lpm, n=8) averaged 22.14 lpm higher than the subjects 5 minutes into exercise, pre-salbutamol (482.86 177.14, n=8). However, this was not a significant dissimilitude (two sample t-test, t=-0.43, p=0.68).5 minutes into exercise, there was an increase in HR of 5.71 bpm be tween pre-salbutamol (84.43 22.57 bpm, n=8) and post-salbutamol (90.14 15.14 bpm, n=8). However, the t-test showed this to be an insignificant increase (two sample t-test, t=-0.81, p=0.43).5Finally, it was hypothesized that GTN would cause a decrease in systolic blood pressure (SBP) and a decrease in the heart rate.SBP showed an average decrease of 4.43 mmHg between an initial baseline of 115.14 10 mmHg, n=8, and 30 minutes after the drug had been taken, 110.71 8.29, n=8. This was shown not to be a significant decrease in SBP by a t-test (two sample t-test, t=1.02, p=0.33).The HR during the GTN experiment was seen to increase from 72.57 15.43 bpm, n=8, to 75.86 14.86 bpm, n=8. This was a total increase of 3.29 bpm. Again, this was not a significant increase as shown by the t-test carried out (two sample t-test, t=-0.61, p=0.56).Discussion.My hypotheses for propanolol were that I expected no change in mean arterial pressure (MAP) at rest after propanolol was taken. However, dur ing post-drug exercise I predicted there to be a reduction in MAP as well as blood pressure (Wheatley 1981). The results set out shown that there wasnt a significant increase in MAP at rest (two sample t-test, t=-0.21, p=0.84). However, the p-value shows that there is a large chance of error. On the other hand, there was a significant decrease in heart rate at rest (two sample t-test, t=3.01, p=0.01) with less than 1% chance of error.For salbutamol it was expected that there would be an increase in PEFR after the drug had been taken but no change in heart rate during post-drug exercise. There was an increase in PEFR of 22.14 lpm 5 minutes into exercise after taking salbutamol. However, the t-test showed that this was not a significant increase.After GTN was taken, I expected to see a decrease in systolic blood pressure and a decrease in the heart rate. The experiment showed that n all of these hypotheses was correct as although there was a decrease in SBP of 4.43 mmHg, there was an increase in HR of 3.29 bpm. Neither of these changes was shown to be significant.6During the experiment, the subjects chosen to take the drug were required to have a certain standard of medical fitness, with regards to blood pressure, in order to participate and take either propanolol, salbutamol or GTN. This was biased as the drugs are normally prescribed to patients with hypertension or who suffer from heart diseases such as angina. Therefore, the lack of significance in changes in the majority of the results could be because the subjects did not have a high blood pressure or heart disease, they were deemed medically fit and so antihypertensive drugs such as propanolol and GTN did not have many significant effects.Therefore in order to improve the experiment, I would use a wide range of both male and female subjects deemed medically fit (normal) as well as medical subjects deemed medically unfit. I would also carry out more t-tests comparing all aspects measured (SBP, DBP, PEFR, MAP, PP and HR). In such an experiment I would expect to see a significant change in recordings such as SBP and HR in the medically unfit patients after they had taken the drugs (propanolol, GTN or salbutamol).The physiological mechanisms which control HR and ventilation with respect to exercise are pH and oxygen total. When the oxygen supply is too low and pH too acidic (due to an hookup of carbonic acid in the blood) HR increases and smooth muscle in the bronchi dilates to increase oxygen supply and blood flow to the muscles.However, in subjects with an already high heart rate, it is dangerous to increase it further and so when exercising it is necessary to take drugs developed to decrease blood pressure so that the heart has to arrive at less to deliver blood around the body and thus HR is decreased.The salbutamol had little effect in the subjects because although the drug has adrenergic effects, it has minimal cardiac stimulation (Craig Stitzel 2004). Therefore only a change in PEFR would be expected.7