Effects Of Exercise And Drugs On Cardiovascular System Biology Essay

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The experiment was carried out in order to examine the effects of propanolol, salbutamol and GTN in subjects at rest and during exercise. This was done by taking recordings of SBP, DBP, MAP, PP, HR and PEFR at rest and during exercise for each drug. Using t-tests the results for each drug were compared at rest and during exercise in order to prove that changes were significant. However, only HR using propanolol was shown to have a significant decrease (two sample t-test, t=3.01, p=0.01). This was concluded to be because the subjects used were not medically unfit (in need of using the drugs).

Introduction.

Heart disease is an increasing cause of death in western countries due to unhealthy lifestyles smoking cigarettes, consuming alcohol, diets high in salt and fats as well as a lack of exercise. Because of this, a lot of medical research goes into developing drugs which lower the high blood pressure, brought about by an unhealthy lifestyle, as well as decrease heart rate in severe cases, provide acute relief of angina pectoris, reduce mortality following myocardial infarction and prevent recurrence 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 β-adrenoreceptor antagonistic drug (Geddes & Grosset 2006). It is used to treat angina pectoris, myocardial infarction, certain cardiac dysrhythmias and hypertension (Marcovitch 2007). Propanolol's mode of action works by depressing myocardium cellular cardiac membrane excitability. 'This membrane stabilising is thought to be effective against arrhythmias' (Craig & Stitzel 2004). It also decreases blood pressure, heart rate, myocardial contractility, cardiac output (and therefore arterial pressure) as well as conduction velocity in the heart (Craig & Stitzel 2004). The drug is administered orally as it is subject to a significant degree of first-pass metabolism as well as extensive absorption from the gastro-intestinal tract. Because of this, during the experiment, the subject had to wait 50 minutes after taking the drug before taking recordings as propanolol's peak therapeutic effect occurs between 1 and 1.5 hours after the drug is administered.

I expect no change in mean arterial pressure (MAP) at rest after propanolol is taken. However, during post-drug exercise I predict there to be 'a reduction in MAP as well as blood pressure' (Wheatley 1981).

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-1-Salbutamol is a short acting, selective β2-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 stimulation (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). Salbutamol's maximal effect is reached within 5 to 20 minutes of administration (Dale et al 2003). Because of this, readings could be taken straight away during the experiment.

For salbutamol I expect an increase in PEFR after the drug has been taken but no change in heart rate during post-drug exercise.

Glyceryl trinitrate (GTN) is a β-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 flow towards ischaemic areas via collaterals (collateral vessels that bypass narrowed coronary arteries' (Dale et al 2003). Angina is due to a lack of oxygen in myocardium (Naish et al 2009). GTN acts to relieve angina by decreasing circulating blood volume, thus reducing 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). GTN's onset of action occurs within 2 to 5 minutes, with it's 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 see 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 the 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 sound 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 licensed chemist.

All three subjects were seated comfortably at right angles to the lab bench. Using an electrical sphygmomanometer, each subject's resting systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded 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 formulas:

2PP = SBP - DBP

MAP = (PP/3) + DBP

Also, for the two 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 then took it in turn to use the cycle ergometer. The seat was adjusted to a comfortable height for cycling and a note of the seat height, for exercise after the drug was taken, was made. A load setting of 2 Kp was set and the subjects, in turn, were kept connected to the sphygmomanometer as they pedalled for 2 minutes at approximately 80 rpm. HR values were recorded every 15 seconds for both subject A and B.

After exercise and prior to taking the drug, subject A and B's 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 then 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 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.

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. The 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 µg 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 subject chewed the tablet and placed the debris 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 sample t-tests so that it could be seen 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 accurate 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.

 

Pre-Propanolol

Post-Propanolol

Group

HR at rest (BPM)

HR post-exercise (BPM)

HR at rest (BPM)

HR post-exercise (BPM)

1

91

142

81

112

2

74

79

67

120

3

92

126

76

112

4

72

125

59

95

5

82

137

55

115

6

74

150

72

152

7

79

133

72

102

8

73

132

60

118

4Table 1: the effect of propanolol on heart rate at rest and post-exercise.

At rest there was 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.

 

Pre-salbutamol

Post-salbutamol

Group

Mean PEFR at rest (LPM)

PEFR post-exercise (LPM)

Mean PEFR at rest(LPM)

PEFR post-exercise(LPM)

1

633

650

635

660

2

493

480

495

490

3

664

660

658

655

4

428

460

490

480

5

625

550

620

630

6

423

410

410

440

7

360

390

375

380

8

448

430

450

460

Table 2: the effect of salbutamol on PEFR at rest and post-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 difference (two sample t-test, t=-0.43, p=0.68).

5 minutes into exercise, there was an increase in HR of 5.71 bpm between 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).

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Finally, it was hypothesized that GTN would cause a decrease in systolic blood pressure (SBP) and a decrease in the heart rate.

 

Post-GTN

Group

Initial baseline Mean SBP (mmHg)

Mean SBP (mmHg) at 30 minutes

SBP (mmHg) at lowest MAP

1

125

119

116

2

119

109

120

3

102

102

84

4

124

118

128

5

105

107

93

6

129

114

114

7

117

108

109

8

110

117

108

Table 3: showing the effect of GTN on baseline SBP, SBP after 30 minutes and SBP at the lowest MAP.

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, during post-drug exercise I predicted there to be 'a reduction in MAP as well as blood pressure' (Wheatley 1981). The results have shown that there wasn't 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 neither 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.

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During 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 supply. When the oxygen supply is too low and pH too acidic (due to an accumulation 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 work 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.

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