Experiment 12: Direct Blood Pressure Recording – Testing the Effects of the Vagus Nerve and Certain Chemicals on Blood Pressure

Experiment 12: Direct Blood Pressure Recording – Testing the Effects of the Vagus Nerve and Certain Chemicals on Blood Pressure

I. Introduction

Arterial blood pressure is the blood pressure in the arteries, reflecting the contractile force of the heart and the resistance of the vascular walls. It plays a vital role in ensuring the blood flow to the capillaries, providing oxygen and nutrients to the tissues.

II. Types of Blood Pressure

• Systolic Blood Pressure (SBP): The highest blood pressure during the cardiac cycle, occurring when the ventricles contract, reflecting the heart’s contractility. SBP typically ranges from 90-140 mmHg.

• Diastolic Blood Pressure (DBP): The lowest blood pressure during the cardiac cycle, occurring when the ventricles relax, reflecting the resistance of the blood vessels. DBP typically ranges from 50-90 mmHg.

• Pulse Pressure: The difference between SBP and DBP, a necessary condition for blood circulation. PP = SBP – DBP.

• Mean Arterial Pressure (MAP): The average of all blood pressure readings measured over a period of time. MAP = 1/3 SBP + 2/3 DBP = DBP + 1/3 Pulse Pressure. MAP is closer to DBP because the diastolic phase is longer than the systolic phase in a cardiac cycle. MAP represents the true working capacity of the heart.

III. Factors Influencing Blood Pressure

The most significant factor affecting blood pressure is the arterial radius. According to Poiseuille’s law, blood pressure is inversely proportional to the fourth power of the arterial radius (P = Q8ln/pi*r4). Therefore, vasodilation will decrease blood pressure.

Other factors influencing blood pressure include:

• Cardiac output

• Length of blood vessels

• Blood viscosity

IV. Principle of Direct Arterial Blood Pressure Recording

• Connect the carotid artery of the dog to a branch of the Ludwig manometer, the other branch with a float attached to a recording pen.

• Blood pressure fluctuations in a cardiac cycle cause the mercury column to oscillate, the recording pen will draw a recording line on the paper tape, which is the blood pressure graph.

V. Chemicals Used in Direct Arterial Blood Pressure Measurement

• Anesthetics: Morphine, thiopental.

• Anticoagulants: Heparin, 5% sodium citrate.

• Reagents:

• Atropine: Occupies all acetylcholine-binding receptors, blocking the effects of the parasympathetic nervous system.

• Adrenaline: A reagent to observe the effects on blood pressure.

• Acetylcholine: A reagent to observe the effects on blood pressure.

VI. Steps for Performing Direct Blood Pressure Measurement in Dogs

• Prepare the recording machine and manometer.

• Anesthetize the dog.

• Expose the carotid artery and the vagus nerve.

• Record the blood pressure graph.

VII. Types of Waves on the Direct Blood Pressure Graph

• α wave (small wave): Represents the contraction of the heart.

• β wave (large wave, collection of α wave peaks): Represents the influence of respiration on blood pressure.

• γ wave (largest wave, collection of β wave peaks): Represents the influence of the cardiovascular center in the medulla oblongata on blood pressure.

VIII. Blood Pressure Graph Analysis

• Increased Graph:

• Not significantly increased: Clamp the carotid artery at the root, stimulate the central end of the vagus nerve, cut the vagus nerve.

• Increased significantly: Inject Adrenaline 1st and 2nd time.

• Normal Graph: Inject a high dose of Atropine, stimulate the peripheral end of the vagus nerve 2nd time, inject Acetylcholine 2nd time.

• Decreased Graph:

• With a flat segment: Stimulate the vagus nerve, stimulate the peripheral end of the vagus nerve 1st time.

• Without a flat segment: Inject Acetylcholine 1st time.

IX. Phenomenon When Clamping the Carotid Artery

• The blood pressure graph goes up and then decreases to normal.

• Explanation: Clamping the carotid artery at the root reduces the blood pressure in the clamped carotid sinus, affecting the pressure receptors there, causing a sympathetic-mediated increase in pressure, making the heart beat faster, increasing the contractile force of the heart and causing vasoconstriction. This reflex also decreases vagal stimulation, contributing to an increased heart rate.

However, when blood pressure increases significantly, it affects the pressure receptors in the aortic arch and the carotid sinus on the other side, stimulating the vagus and IX nerves to the medulla oblongata, causing a vagus nerve-mediated decrease in pressure and inhibiting the vasoconstrictor region, causing vasodilation.

X. Analyzing the Experimental Steps:

• Injecting Adrenaline 1st time:

• The graph increases rapidly and significantly, the α wave increases both in amplitude and frequency, then gradually decreases.

• Explanation: Adrenaline is a sympathetic stimulant, binding to β1 receptors, increasing both the frequency and contractile force of the heart. Afterward, blood pressure returns to normal due to the pressure-reducing reflex and the rapid half-life of Adrenaline.

• Injecting Acetylcholine 1st time:

• The blood pressure graph decreases (without a flat segment).

• Explanation: Acetylcholine is the chemical mediator of the parasympathetic nervous system, binding to muscarinic receptors at the sinoatrial node, inhibiting the sinoatrial node, decreasing heart rate, thus decreasing blood pressure. Additionally, Acetylcholine also causes vasodilation in some areas, contributing to a decrease in blood pressure. Blood pressure returns to normal due to the pressure-increasing reflex and the short half-life of acetylcholine.

• Continuous Stimulation of the Vagus Nerve:

• The blood pressure graph decreases significantly, with a flat segment (heart stops beating), then increases back to normal.

• Explanation: When stimulating the vagus nerve, acetylcholine is released, binding to M receptors, inhibiting the sinoatrial node, decreasing heart rate, thus decreasing blood pressure. When stimulating continuously, blood pressure decreases significantly, possibly to 0, the heart stops beating, the graph is a flat line. However, blood pressure increases back to normal due to:

• Synaptic fatigue: The amount of chemical mediator in the nerve endings is limited, continuous stimulation, the mediator is completely released, not synthesized fast enough, no longer responding.

• When the sinoatrial node is inhibited, the bundle of His spontaneously fires impulses.

• Pressure-increasing reflex via the sympathetic nervous system.

• Heart-heart reflex.

• Cutting the Vagus Nerve on both sides:

• The blood pressure graph goes up, then returns to normal.

• Explanation: Cutting the vagus nerve is abolishing the parasympathetic nervous system, which is the pressure-reducing system. The autonomic nervous system is out of balance, only the sympathetic system is dominant, so the heart increases both frequency and contractile force, blood pressure increases. However, when blood pressure increases significantly, it affects the pressure receptors in the aortic arch and the carotid sinus on the other side, stimulating the vagus and IX nerves to the medulla oblongata, causing a pressure-reducing reflex via decreasing sympathetic activity.

• Stimulating the peripheral end of the vagus nerve:

• *Need to add information about the graph phenomenon and explanation*

• Stimulating the central end of the vagus nerve:

• The graph goes up and then gradually decreases back to normal.

• Explanation: When stimulating the central end, it affects the cerebral cortex, similar to creating a painful stress, increasing respiration, enhancing the sympathetic nervous system. Nerve impulses travel to the hypothalamus, down to the spinal cord, stimulating the adrenal medulla to release adrenaline and noradrenaline, increasing the frequency and contractile force of the heart, increasing blood pressure. However, when blood pressure increases significantly, it affects the pressure receptors in the aortic arch and the carotid sinus on the other side, stimulating the vagus and IX nerves to the medulla oblongata, causing a pressure-reducing reflex via decreasing sympathetic activity.

• Injecting Adrenaline 2nd time:

• Blood pressure increases significantly (higher than the 1st time), the α wave increases both in amplitude and frequency, then returns to normal more slowly than the 1st time.

• Explanation: Due to the loss of pressure-reducing reflex via the parasympathetic nervous system, even a small amount = 1/3 of the initial amount also causes a very significant increase in blood pressure. Then, it returns to normal due to:

• Pressure-reducing reflex via decreasing sympathetic activity.

• Increased blood pressure, pressure receptors in the carotid sinus receive changes through the IX nerve to the medulla oblongata, inhibiting the vasoconstrictor region, reducing the impulse to the periphery, causing vasodilation.

• Adrenaline is quickly broken down.

• Injecting Atropine and waiting 5-10 minutes: To give Atropine time to occupy all acetylcholine receptors.

• Stimulating the peripheral end 2nd time and injecting Acetylcholine 2nd time:

• The blood pressure graph does not change.

• Explanation: Because Atropine has occupied all acetylcholine receptors, so whether it is stimulating the peripheral end to release acetylcholine or injecting acetylcholine, it can no longer bind to receptors to exert its effect.

XI. Relationship Between Blood Pressure and Breathing Rate

• Breathing rate is the small line below the graph.

• The influence of respiration on blood pressure is reflected in the β wave.

• When inhaling, the chest cavity expands in all three dimensions, causing the parietal pleura to separate from the visceral pleura, increasing blood pressure as the intrathoracic pressure is more negative, more blood returns to the heart, the stroke volume increases, thus blood pressure increases. However, blood pressure changes during the respiratory cycle only fluctuate within a very small limit.

XII. Why does stimulating the vagus nerve cause blood pressure changes differently than injecting acetylcholine?

• The difference in the area of action:

• The vagus nerve mainly acts on the heart, stimulating the vagus nerve releases endogenous acetylcholine at the synaptic endings, inhibiting the sinoatrial node, the heart stops beating, so blood pressure only remains at a flat level (diastolic level).

• Exogenous acetylcholine not only acts on the sinoatrial node and atrioventricular node but also on the blood vessels of other organ systems. Therefore, its effect on the heart is less than when stimulating the vagus nerve, in addition, acetylcholine causes vasodilation, so diastolic blood pressure decreases.

XIII. Drawing a normal dog blood pressure graph

• *Need to add an image of a normal dog blood pressure graph*

XIV. Conclusion

This experiment helps us understand better arterial blood pressure, the factors influencing blood pressure, and the effects of the vagus nerve and certain chemicals on blood pressure. Recording direct arterial blood pressure is an essential technique in physiological and clinical research.