Introduction
Mean arterial blood pressure is the average arterial pressure in a cardiac cycle. It is set by cardiac output and total peripheral resistance; it sets the average driving pressure and controls the flow. The pulse pressure is the difference between the highest and lowest pressure (systolic and diastolic blood pressure) readings during a subject’s cardiac cycle. Both mean arterial pressure and pulse pressure are detected by baroreceptors. The baroreceptors respond to stretching of the arterial wall so that if arterial pressure suddenly rises, the walls of these vessels passively expand, which stimulates the firing these receptors (Ottesen et. al., 2011). If arterial blood pressure suddenly falls, decreased stretch of the arterial walls lead to a decrease in receptor firing. Baroreceptors are found in the main arteries, the aortic arches and carotid arteries.

The addition of different chemicals into the bloodstream causes changes to occur in the heart rate, mean arterial pressure and pulse pressure. These changes are detected by the baroreceptors. Adrenaline and noradrenaline cause similar responses to the cardiovascular system. They have a sympathetic effect, causing an increase in the mean arterial pressure, pulse pressure and heart rate. Conversely, acetylcholine has a parasympathetic effect, the heart rate and blood pressure drops.

The aim of the experiment was to see the changes in the cardiovascular parameters of mean arterial pressure, pulse pressure and heart rate, when different chemicals, such as noradrenaline, adrenaline and acetylcholine were injected into the bloodstream and physical stimuli such as vagal stimulation and haemorrhage were performed on the rabbit.

Method
In this experiment, students were required to perform surgery on an anaesthetised rabbit. First, the rectal thermometer was to be inserted so the anaesthetist could monitor the rabbit’s main core body temperature.

The ear vein, at the head, was cannulated so that adrenalin and noradrenaline could be injected into the system. The vagus nerve was isolated for stimulation and the trachea was cannulated so respiratory measurements could be observed. The femoral artery at the leg was also cannulated, so that blood pressure and heart rate could be recorded.
After, the surgery was completed, a series of experiments were done on the rabbit. Between, each experiment, the resting values were recorded. First, noradrenaline was injected into the ear vein to see the response. The vagal nerve was then stimulated with a train of electrical pulses. Following the stimulation, adrenaline was injected into the rabbit to see the effects it had on the cardiovascular system. The effects of the changes in blood volume were also observed by withdrawing 10ml of blood from the rabbit and then returning the blood after a few minutes. Lastly acetylcholine was injected into the rabbit and changes were observed.

Students were required to monitor the rabbit’s anaesthesia and vital signs at all times.

Results
Adrenaline

Figure 1: The change in blood pressure after the addition of adrenaline in the bloodstream.
Noradrenaline

Figure 2: The change in blood pressure after the addition of noradrenaline into the bloodstream.
Figure 2: The change in blood pressure after the addition of noradrenaline into the bloodstream.

Vagal Stimulation

Figure 3: The change in blood pressure after vagal stimulation.

Withdrawal of Blood

Figure 4: The change in blood pressure after withdrawing 10ml of blood.
Acetylcholine

Figure 5: The change in blood pressure after the addition of acetylcholine into the bloodstream.
Figure 5: The change in blood pressure after the addition of acetylcholine into the bloodstream.

Discussion
The effect of injecting adrenaline is an increased cardiac output and a redistribution of the cardiac output to muscular and hepatic circulations with only a small change in mean arterial pressure. Although cardiac output is increased, arterial pressure does not change much because the systemic vascular resistance falls due to β2-adrenoceptor activation. At high plasma concentrations, epinephrine increases arterial pressure because of binding to α-adrenoceptors on blood vessels, which offsets the β2-adrenoceptor mediated vasodilation (Oliveira et. al., 2010).

Noradrenaline causes an increase in heart rate, pulse pressure and mean arterial blood pressure. The drug acts on cardiac muscle to increase cardiac contractility of the heart which results in increased heart rate, thus increasing cardiac output. It acts on the systemic arteries which causes vasoconstriction, therefore causing increased systemic vascular resistance. A rise in cardiac output and vascular resistance causes an increase in mean arterial pressure. The baroreceptors detect the change and works to bring the blood pressure back to baseline measurements (Treggiari et. al., 2002).

Vagal stimulation is known to have an inhibitory effect on the cardiovascular system, causing the slowing or even stopping of the heart. The response is mediated by muscarinic receptors that activate potassium channels in the supraventricular cells of the heart. In the sinoatrial node, activation of potassium efflux causes hyperpolarization and/or decreases the rate of diastolic depolarization (Oliveira et. al., 2010). Vagal stimulation causes a fall in blood pressure and heart rate. When the heart is stimulated at a frequency which is close to but not equal to the prevailing cardiac frequency, then each successive stimulus will occur at a progressively different time relative to the phase of the cardiac cycle. When the stimulus frequency exceeds the prevailing cardiac frequency, then successive stimuli will fall progressively earlier in the cardiac cycle. Conversely, when the stimulus frequency is less than the prevailing cardiac frequency then successive stimuli will fall progressively later in the cardiac cycle (Levy et. al. 1969).

With the withdrawal of blood in the rabbit, a huge drop in arterial blood pressure is observed, this in turn causes a drop in blood volume. This results in a decrease in cardiac output and pulse pressure, the reduced tension causes a stimulation of baroreceptors in the arteries. This instigates an increased sympathetic outflow to the heart which results in elevated sympathetic vascular resistance and contractility, which in turn causes a rise in right arterial pressure and stroke volume, thus increasing cardiac output and arterial pressure (Levy et. al., 1969).

Acetylcholine acts on the vascular system and plays a huge part in neurosynapses. This drug caused a huge drop in the heart rate and vasodilation which will then result in decreased blood pressure. Initiation on muscarinic cholinergic receptor resulted in an increased intercellular calcium and the production of nitric oxide. The production of nitric oxide results in the relaxation smooth muscle. However, in the actual experiment conducted on the rabbit, the expected drop in heart rate did not occur. As this part of the experiment was conducted last, the rabbit was already under a lot of stress, therefore it didn’t respond as expected (Masaki et. al., 1991).

References
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Matthew N. Levy, Paul J. M, Iano T and Zieske H, (1969), Paradoxical Effect of Vagus Nerve Stimulation on Heart Rate in Dogs, Journal of the American Heart Association, 25:303-314

Treggiari MM, Romand JA, Burgener D, Suter PM, Aneman A. (2002), Effect of increasing norepinephrine dosage on regional blood flow in a porcine model of endotoxin shock., Crit Care Med., (6):1334-9.

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