Physiological Effects Of The Vagus Nerve Biology Essay

The autonomic nervous system ( ANS ) plays an of import function in the care of homeostatic procedures in the organic structure. The cardiovascular system ( CVS ) which includes the bosom and the circulatory system is regulated by the ANS. Any alterations in bosom rate ( HR ) and blood force per unit area ( BP ) are homeostatically adjusted by the ANS via sympathetic or parasympathetic nervous system.

The primary cardiac control Centre ( cardioacceleratory, cardioinhibitory ) and vasomotor Centres ( big group of nerve cells for vasoconstriction and little group for vasodilation ) are located in the myelin oblongata. The cardioacceleratory Centre controls the sympathetic nervous system which responds by increasing HR and force of contraction. The cardioinhibitory Centre controls the bosom via parasympathetic nerve cells which in bend reduces HR. Vasoconstriction is brought approximately by the SNS and vasodilation by PNS. These Centres are influenced by automatic tracts and via input from higher Centres particularly from the intellectual cerebral mantle, bulbar reticulate country, upper spinal cord and hypothalamus ( Williams et al, 1981 ) . Ex-husband: Decrease in partial force per unit area of O ( POa‚‚ ) in the blood is detected by chemoreceptors which stimulate the cardioacceleratory Centre to increase cardiac activity and stimulate vasodilation.

The sympathetic ( SNS ) and parasympathetic ( PNS ) nervous system controls the bosom by agencies of the cardiac rete and both innervate the Sinoatrial Node ( SAN ) , Atrioventricular Node ( AVN ) and the myocardium. The ventricular myocardium preponderantly has SNS fibers compared to PNS fibers ( Martini and Nath, 2008 ) .

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The SNS preganglionic fibers synapse with postganglionic fibers in the cervical and superior thoracic ganglia ( t1-t4 ) and the postganglionic fibers innervate the bosom. Increased SNS activity releases

Noradrenaline ( NA ) which interacts with ? receptors in the nodes doing rapid depolarization which in bend consequences in increased HR. It besides interacts with ?

receptors in the blood vass advancing vasoconstriction. The terminal consequence is increase in blood force per unit area. SNS besides has a positive ionotropic consequence on the bosom, thereby increasing Stroke Volume ( SV ) . Increase in SV and HR contributes to increase Cardiac Output ( CO ) ( Williams et al, 1981 ) .

It is indispensable for the bosom to have this changeless autonomic tone. This is to forestall SNS from dramatically promoting HR and PNS cut downing HR. During the ‘rest and relaxation ‘ stage the PNS dominates keeping HR between 70-80 beats per minute and in the instance ‘flight or fight response ‘ it is the SNS. If SNS activity falls below normal it consequences in decreased HR and BP in major arterias lending to complications such as ischaemia. In the instance of blood vass the sympathetic vasoconstrictive nervousnesss are invariably active maintaining arteriolas partly constricted ( Martini and Nath, 2008 )

The pneumogastric nervus is the primary parasympathetic nervus fiber which controls the bosom. It releases Acetycholine ( Ach ) which interacts with Muscarinic receptors ( M2 ) in the bosom, decreasing rate of depolarization of the nodes and thereby cut downing HR. PNS does non hold any direct consequence on blood vas diameter ( Martini and Nath, 2008 ) . The PNS reduces force of contraction of the atria but has small consequence on the ventricular myocardium. Therefore PNS reduces HR, CO and BP.

The chief factors act uponing the cardiac Centre and vasomotor centre include chemoreceptors and baroreceptors which are innervated by the glossopharyngeal and vagus nervousnesss. Baroreceptors are chiefly located in the carotid arteria, carotid fistula, and aortal arch. They monitor acute alterations in BP via mensurating the grade of dilatation within walls of carotid arteria, fistula and aortal arch. The threshold for stimulation of receptors in carotid arteria and fistula is 60mmHg with peak activity at 175-200 mmHg. Aortal receptors have a higher threshold ( Williams et al, 1981 ) . Changes in BP affect the rate of fire of these receptors and fluctuation in O or C dioxide degrees in the plasma alters firing rate of chemoreceptors. When BP or plasma POa‚‚ additions or plasma PCOa‚‚ decreases, the receptors inhibit vasomotor and cardioaccelerator tone and addition activity in cardioinhibitory country, ensuing in reduced HR and BP. If BP or plasma PCOa‚‚ addition or plasma POa‚‚ lessening so the contrary is true.

This experiment was carried out to find the effects of NA on the CVS and set up whether atropine affects this response. The consequence of histamine on the CVS was besides investigated. Finally the consequence of an unknown drug on the bosom was examined and thereby established its individuality.

Method

Participants were told to entree a plan called ‘The practical cat v2.5.6 ‘ which is a computing machine simulation plan of an anesthetised cat readying, utilizing the computing machines available in the physiology suite. It was accessed utilizing the undermentioned tract:

Access My Computer displayed as 45000000 ( pupil figure ) on SCI 000000 ( PC figure ) . Then use the undermentioned tract

Gram: Strathclyde UniversityAnaesthetized Cat

They were ab initio told to entree and read the ‘contents ‘ subdivision utilizing the ‘Help ‘ check. Then they were told to snap the ‘Options ‘ check and uncheck nictitaing membrane and skeletal musculus so that lone bosom rate ( HR ) and blood force per unit area ( BP ) showed up on screen. They were besides told to uncheck the 3 boxes at the underside of the screen which included ‘stimulate pneumogastrics nervus ‘ , ‘stimulate spinal cord ganglion ‘ and ‘stimulate skeletal musculus ‘ .

There was a choice of ‘unknown drugs ‘ runing from A to Q and ‘standard drugs ‘ which include, Tubocurarine, NA, Acetylcholine, Neostigimine, Carbachol, Atropine, Histamine, Mepyramine, Hexamethonium, Gallamine, Verapamil, Morphin, Naloxone, and Adenosing 8-SPT.

In the initial portion of the experiment participants were told obtain a sample control informations by merely snaping the ‘Start ‘ button. After about 1 minute they were told to look into the ‘stimulate pneumogastric nervus ‘ option and observe and record any alterations in HR or intend BP for approximately 1 minute after which they stopped the hint. Average HR and BP were determined by traveling the pointer over the recording.

Afterwards, it was told to plot a dose-response curve for NA by shooting into a vena a get downing dosage of 0.1µg/kg and so duplicating each subsequent dosage making to a upper limit of 100µg/kg. For the response merely maximum HR and BP following disposal was recorded. Then standard dose 10mg/kg of Atropine was administered which was followed by disposal of increasing doses of NA. Changes in HR and BP were recorded.

On the 3rd stage of the experiment they were told to plot a dose-response curve for Histamine. The dose was similar as NA. They were so told to place a method that can be used to look into how histamine disposal altered HR and BP.

Finally from the list of unknown drugs, Drug A was chosen and participants were told to find its consequence on the sample readying and in making so place what type of drug it is.

Consequences

Dose-Response curves were plotted utilizing % of maximum response ( HR or BP ) as the dependent variable and Loga‚?a‚ˆ values of the several drug concentrations as the independent variable

% soap. response x 100

Blood force per unit area is given as ‘mean values ‘ and non in the signifier of systolic/diastolic.

Normal bosom rate was 108 beats per minute ( beats per minute ) and average blood force per unit area was 94.2 mmHg ( 133/75 mmHg ) .

Frequency of pneumogastric stimulation 0.03 stimulations/second ( 3 stimulations per 100 seconds ) . Immediately after each stimulation HR reduced to 61 beats per minute and average BP was reduced to 65 mmHg and after 19 seconds both HR and BP returned to normal.

Table 1. Comparison between the Effect of NA ( NA – µg/kg ) and the Effect of

10mg/kg dosage of Atropine on Heart Rate ( beats per minute )

Dose ( µg/kg )

Heart Rate with NA ( beats per minute )

Heart Rate with NA + Atropine ( beats per minute )

0.1

106.5

121.7

0.2

107.6

128.3

0.5

114.4

130.0

1

117.4

130.0

2

126.1

131.0

5

134.8

132.0

10

144.6

142.4

20

159.8

153.3

50

138.0

156.5

100

121.7

167.4

Graph 1. Dose Response Curve for the consequence of NA ( Loga‚?a‚ˆ [ NA ] ) and 10mg/kg dosage of Atropine on Heart Rate ( % maximum HR )

Dose ( µg/kg )

Mean BP with NA ( mmHg )

Mean BP with NA + Atropine ( mmHg )

0.1

92.0

105.1

0.2

94.2

108.0

0.5

97.8

108.3

1

105.8

115.2

2

113.0

123.2

5

129.0

131.0

10

137.0

160.1

20

162.3

182.6

50

187.7

200.2

100

197.8

220.6 Table 2. Comparison between the Effect of NA ( NA – µg/kg ) and the Consequence

of 10mg/kg dosage of Atropine on Mean Blood Pressure ( BP – mmHg )

Graph 2. Dose Response Curve for the consequence of NA ( Loga‚?a‚ˆ [ NA ] ) and 10mg/kg dosage of Atropine on Mean Blood Pressure ( % maximum BP )

Table 3. Changes in Heart Rate ( beats per minute ) and Mean Blood Pressure ( mmHg ) in response to Histamine ( mg/kg )

Histamine Dose

( mg/kg )

Heart Rate

( beats per minute )

Mean Blood Pressure ( mmHg )

0.1

108.0

82.6

0.2

108.0

68.8

0.5

107.0

57.2

1

107.0

47.1

2

108.0

38.4

5

107.0

34.1

10

108.0

30.4

20

107.0

29.7

50

108.0

29.0

100

108.0

28.5

Graph 3. Dose Response Curve for the consequence of Histamine ( Loga‚?a‚ˆ [ Histamine ] ) on Heart Rate ( HR ) and Blood Pressure ( BP ) – in the signifier of % of maximum response

Table 4. Changes in Heart Rate ( beats per minute ) and Mean Blood Pressure ( mmHg ) in response to Drug A ( mg/kg )

Drug A Dosage ( mg/kg )

Heart Rate ( beats per minute )

Mean Blood Pressure ( mmHg )

0.1

112.0

95.0

0.2

113.0

96.0

0.5

114.0

97.0

1

117.0

98.0

2

121.0

99.0

5

124.0

105.0

10

126.0

105.0

20

126.0

105.0

50

128.0

105.0

100

128.0

105.0

Graph 4. Dose Response Curve for the consequence of Drug A ( Loga‚?a‚ˆ [ Drug A ] ) on Heart Rate ( HR ) and Blood Pressure ( BP ) – in the signifier of % of maximum response

Discussion

It was found that stimulation of the pneumogastric nervus ( VN ) reduced HR by 42.6 % and BP by 30.9 % .

The tenth cranial nervus, which is portion of the parasympathetic nervous system, reduced the force of contraction of the myocardium with a characteristic decrease in figure of action potencies. The left pneumogastric nervus innervates the AVN and the right pneumogastric nervus innervates the SAN. Ach released from VN interacted with M2 receptors in the nodes which increased conductance of K+ and inhibited Ca?+ channels by increasing K+ permeableness and cut downing Ca?+ permeableness in pacesetter cells thereby hyperpolarised the sinoatrial cells. This drawn-out period of repolarisation and reduced self-generated depolarization and thereby reduced the overall clip it took for the SAN to make threshold potency and eventually resulted in decreased HR ( Martini and Nath, 2008 ) . The Ach released by the pneumogastric nervus interacted with M3 receptors in the blood vass which resulted in the release of azotic oxide ( NO ) from endothelial cells. No fake vasodilation which resulted in decreased BP ( Patel et al, 2006 ) .

Vagal tone can be inhibited by a muscarinic adversary. Ex-husband: Atropine – used in the intervention of Sinus bradycardia and AVN block. Atropine ( competitory muscarinic adversary ) prevents binding of Ach to M2 receptors in the bosom and M3 receptors in blood vass ( Walch et al, 2001 ) thereby forestalling consequence of pneumogastric stimulation ensuing in tachycardia ( Rang and Dale, 2007 ) and vasoconstriction. However atropine ‘s consequence on blood force per unit area is non strikingly important ( Rees et al, 1989 ) .

NA elevated HR by 51.8 beats per minutes and BP by 103.6 mmHg. HR reached a upper limit of 159.8 beats per minute for a dosage of 20 µg/kg and BP was elevated to 197 mmHg for a dosage of 100 µg/kg. This confirms that NA released by the SNS, is extremely effectual during a ‘flight-or-fight ‘ response and fixing the organic structure for vigorous activity by promoting HR and advancing vasoconstriction ( Craig and Stitzel, 2003 ) .

When dosage was increased to 50 and 100 µg/kg HR reduced to 138 and 121.7 beats per minute severally. This decrease in HR was due to reflex bradycardia which was achieved via stimulation of baroreceptors in response to elevated degrees of BP.

Bradycardia was achieved by increased pneumogastric stimulation and this restored homeostasis.

When atropine was added it resulted in tachycardia making a upper limit of 167.4 beats per minute for a dose 100 µg/kg NA. Atropine blocks the consequence of bradycardia physiological reaction by suppressing pneumogastric stimulation. Since it is a muscariinc adversary it does non affect responses of NA ( Craig and Stitzel, 2003 ) . Atropine did non hold a important consequence on blood force per unit area which supports the findings of Rees et Al ( 1989 )

The chief adrenoreceptors that mediate the consequence of NA in cardiac and vascular smooth musculus include ; ?1, ?2, ?1, and ?2. All these receptors involve 2nd courier systems. The features of these receptors are discussed in item in table 5.

Histamine had no important consequence on HR but reduced blood force per unit area by 65.7 mmHg making a lower limit of 28.5 mmHg for a dosage of 100 mg/kg. Therefore histamine was effectual as a vasodilative and the grade of vasodilation depends on the concentration of histamine and the grade of baroreceptor automatic compensation ( Craig and Spitzel, 2003 ) .

The chief receptors involved here are H1 ( rapid abruptly lived response ) and H2 ( slow and sustained response ) receptors. Activation of H1 ( bosom and endothelium ) lead to activation of Gqa‚?a‚? protein taking to activation of Phospholipase C ensuing in lift of IP3 and Ca?+ degrees. H2 ( bosom ) activation in bend activated Gs protein taking to increased camp degrees thereby increasing intracellular Ca?+ degrees. To a lesser grade H3 ( in some endothelia ) receptors are excessively involved ( Craig and Stitzel, 2003 ) . They act by suppressing release of NA from SNS thereby forestalling vasoconstriction. Once H3 is activated this in bend activates Gi/o protein ensuing in reduced Ca?+ inflow via G protein coupled N-type Ca?+ channels.

From the list of standard drugs Mepyramine which is a first coevals antihistamine ( h1 receptor adversary ) , can be used to look into the consequence of histamine by administrating the drug to a sample readying with histamine and building a dose response curve. When comparing this ( histamine + mepryamine ) to a dose response curve of histamine it should demo a parallel displacement to the right. This determination is supported by Cardell and Edvinson ( 1994 )

Receptor Type

Location with respects to the Cardiovascular system

2nd Messenger

Consequence on Cardiovascular System

Protagonist

Adversary

?1

Blood vass ( arterias and venas )

Activates G protein ( Gq ) which in bend activates Phospholipase C ensuing in the production of 2nd couriers inositol triphosphate ( IP3 ) , Ca?+ and Diacylglycerol

Ca?+ will adhere to calmodulin which in bend activates assorted proteins

Vasoconstriction

Methoxamine – used in the bar and intervention of acute hypotension happening with spinal anaesthesia

Prazosin – used in intervention of high blood pressure and bosom failure ( Wishart, 2009 )

?2

Blood vass ( arterias and venas )

Activates Gi protein which inhibits adenyl cyclase lending to decrease in the formation of cyclic AMP ( camp ) from ATP ensuing in protein kinase A ( PKA ) being unable to phosphorylate other proteins.

There is besides suppression of Ca?+ channels and stimulation of K+ channels.

Vasoconstriction ( via station junctional ?2a receptor ) of arterias and venas

Vasodilation ( via pre-junctional and endothelial ?2b receptor ) of arterias ( Craig and Stitzel, 2003 )

Clonidine – used in the intervention of high blood pressure and intoxicant backdown.

Yohimbine – used in intervention of erectile disfunction ( Wishart, 2009 ) .

?1

Heart ( SAN, AVN, atrial and ventricular myocardium )

Activates Gs protein which in bend elevates degrees of camp and increased activity of PKA

Increased HR, BP, CO and force of contraction

Dobuatmine – used in intervention of bosom failure and cardiogenic daze.

Metoprolol – used for handling high blood pressure and angina ( Wishart, 2009 ) .

?2

Blood vas ( artery – to skeletal musculus ) and Heart ( Rang and Dale, 2003 )

Lapp as ?1

Vasodilation, minor addition in HR and force of contraction ( Rang and Dale, 2003 ) .

Formoteroll – used in direction of asthma and chronic clogging pneumonic disease

There is no clinical usage for adversaries. Ex-husband: Butoxamine ( Wishart, 2009 ) .

Table 5. Features of Adrenoreceptors involved in the Cardiovascular System

2- ( 3-trifluoromethyl ) phenyl histamine is a H1 receptor agonist and its usage is still being researched

( Craig and Stitzel, 2003 ) . Diphenhydramine ( antihistamine ) is a H1 adversary used as an antiemetic, ataractic and provides impermanent alleviation of allergic symptoms ex: coryza. Antihistamines are normally classified as first coevals or 2nd coevals substances. Second coevals is less powerful than first coevals and is less able to traverse the blood encephalon barrier thereby bring forthing less sedation ( Craig and Stitzel, 2003 ) .

Betazole is H2 receptor agonist used to prove for stomachic secretory map. Cimetidine is a H2 anatagonist used in intervention of bosom burn and peptic ulcers. Imetit is a H3 agonist used for research intents and Ciproxifan is a powerful H3 adversary ( Wishart, 2009 ) .

Drug A elevated HR and BP by 20 beats per minutes and 10.8 mmHg making a upper limit of 128 beats per minute and 105 mmHg severally after which BP remained dead. The elevated HR, the superficial consequence on BP and the absence of bradycardia physiological reaction indicate that Drug A was a muscarinic adversary, viz. Atropine. Besides it merely caused little tachycardia and vasoconstriction compared to NA ( Valentin, 1985 ) .

Restrictions

One of import restriction is that there was no direct interaction with life tissue and the plan used prefixed doses – so there is no fluctuation in consequences and it was hard to analyze any alone observations since the computing machine simulated plan ( CSP ) frequently produced the same consequences ( responses ) every clip. Some expertness was required to manage the package ; for an perceiver it is more likely for him/her to bury the methods used and there was deficiency of cognition of how to really transport out a existent life experiment. ( Baby, 2009 )

Advantages

The chief benefit was that there was no demand to utilize existent animate beings. This saved clip required to transport out the experiment ; minimised troubles in managing animate beings ( populating or dead ) which is labor-intensive and dearly-won ; eliminated jobs with handiness of animate beings and alleviated any emotional jobs that might impact the perceiver. It besides eliminates possible ethical issues ( babe, 2009 )

With the usage of CSP many pupils can transport out their ain experiment and observe consequences and there are fewer opportunities of any experimental mistakes happening and the experiment can be visualised clearly.

In a ‘real life ‘ experiment a spinalized cat is used. The cat is ab initio anesthetized and a column is inserted into the spinal cord. It hence destroys CNS control of HR and BP, which in bend amendss the blood force per unit area physiological reaction and baroreceptor reflex arising from carotid arteria, carotid fistula and aortal arch ( Kitagawa and Walland, 1982 ) thereby impacting consequences ( bradycardia physiological reaction ) . However, usage of spinalized cats is effectual in measuring consequence of drugs on spinal physiological reactions and it is possible to detect merely the drug ‘s effects on the organic structure without any intervention from the organic structure ‘s natural biological responses ( Kehne, 1985 ) .

Decision

The parasympathetic nervous system reduced HR and BP via stimulation of pneumogastric nervus and it was found that the muscarinic adversary, Atropine abolishes this response. However its consequence on BP was non profound. This was confirmed when tested with NA where it merely caused profound tachycardia. Histamine had no important consequence on HR but was responsible for vasodilation ensuing in important decrease in BP. Drug A was identified as atropine.

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