Sympathetic And Sympathetic Division Essay

Porges theory recognises his important discoveries on the vagus nerve which changed previous understanding and functioning of the autonomic nervous system. Prior to this discovery, it was understood that the system operated in a balanced sympathetic/parasympathetic way. Porges research changed the outlook and understanding on the system, firstly with the vagus nerve in mammals having two branches, and secondly that the newest branch is able to prevent other nervous system activity.

Alpha-blockers or alpha-adrenergic antagonist drugs help to decrease blood pressure and dilate blood vessels, allowing for blood to move more freely.Alpha-blockers accomplish this by either limiting or inhibiting the affects of norepinephrine, a stimulant hormone of the sympathetic nervous system. The term norepinephrine or noradrenaline works to constrict the muscles that line the interior of small veins and arteries in the body (Mayo Clinic, 2014). There are two types of alpha-receptors that are affected by norepinephrine, alpha-1 and alpha-2 receptors.Alpha-1 receptors are found throughout the body in: male reproductive organs, eyes, bladder, prostatic capsule, and more importantly blood vessels.Alpha-2 receptors exist in presynaptic nerve terminals. By blocking noradrenaline affects on alpha-1 receptors coronary arteries and veins will remain open, allowing for increased blood flow and in turn lowering blood pressure (Aschenbrenner & Venable, 2012).

In patients with symptomatic chronic HF who do not tolerate ACE inhibitors, angiotensin II type I receptor blockers (ARBs) can be used as an alternative to improve morbidity and mortality. However, the higher rate of hypotension, renal dysfunction, and hyperkalaemia with such a combination therapy warrants close monitoring of these parameters. As patients with end stage heart failure frequently show signs of fluid retention or have a history of such, inhibitors of the renin-angiotensin system should be co-administered with diuretics most commonly loop diuretics, which usually leads to rapid symptomatic improvement of dyspnea and exercise tolerance while lacking significant effects on survival. In addition to standard treatment with ACE inhibitors and diuretics, patients with symptomatic stable systolic heart failure should be treated with b-adrenergic receptor blockers unless there are contraindications. Additionally aldosterone receptor antagonists are recommended in addition to ACE inhibitors, b-adrenergic receptor blockers, and diuretics, unless contraindicated.

A patient in their 70s with documented systolic heart failure and hypertension would need pharmacologic therapeutic intervention along with some lifestyle changes. To reduce the patient’s mortality rate, an ACE inhibitor and beta blocker should be prescribed. The ACEI would be given to reduce the preload and afterload (McCance and Huether, 2014). The beta blocker will assist the client by improving the left ventricular ejection fraction, slow the progression of heart failure, and increase exercise tolerance (Burchum and Rosenthal,

The writing on the role of Beta-blockers in the treatment of heart failure is elaborative and absorbing. The brief explanation about the mechanism Beta blocker is illuminating. Beta blocker use can help to manage heart failure. Beta blockers blocks the effects of the epinephrine (adrenaline). When beta blockers are taken, then the heart rate gets slow and heart demand of oxygen decreases, consequently the blood pressure is reduced (Staff, 2016). Beta blockers have different kinds of with slight differences. Depending on the circumstances, different beta blockers are utilized. The beta blockers can vary in terms of side-effects, as well as in term of the amount that a patient need to take per day. Depending upon the patient condition and treatment

As the concentration of the drug was increased, clonidine blocked the effects of noradrenaline at prejunctional α₂adrenoceptors in the rate vas deferens. When the α₂ antagonist yohimbine was applied to the rat vas deferens, it binds to the receptors as it high affinity and results in blockage of prejunctional adrenoceptors leading to an increase in release of noradrenaline (NA). Figure 1 shows the yohimbine concentration-response curve of how higher concentrations of agonist are required to displace yohimbine from the receptors. Clonidine alone had an EC₅₀ of 2.02 x10⁻⁸ M, whereas in the presence of the antagonist yohimbine the EC₅₀ is 3.17 x10⁻⁷ M. the greater EC50 value represents a smaller concentration of a clonidine required to induce 50% inhibition of contractile activity. The dose response ratio of clonidine and yohimbine was 15.693. the nerve stimulation of rat vas deferens experiment only used a single agonist concentration therefore the Gaddum-Schild equation was used to calculate the KB value of 6 x 10⁻⁹ M, although it does not reflect the competitive nature of yohimbine it shows that the concentration of yohimbine produced a two-fold shift to the right of the clonidine

The question arises whether chronic long-term use of a beta-3 adrenoceptor agonist may be limited by beta-3 receptor desensitization. It is conceivable that like the beta-2 adrenoceptor in airway smooth muscle, continuous, prolonged administration of a beta-3 adrenoceptor agonist will elicit beta-3 adrenoceptor desensitization in bladder smooth muscle. Continuous exposure of a beta-3 adrenoceptor agonist may result in a decrease in the number of beta-3 adrenoceptors, a decrease binding affinity or diminished post-receptor signal transduction mechanisms and second messenger signaling, resulting in a diminished therapeutic response.

Amiodarone is a potent antiarrhythmic agent which inhibits α- and β)-adrenergic neurons, increases PR and QT intervals, reduces sinus rhythm and peripheral vascular resistance. The rationale for using amiodarone is to decrease the ventricular rate and improve cardiac output. Heparin is an anticoagulant which prevents the activation of fibrin and thrombin by inhibiting thrombin III. The rationale is that anticoagulant agents prevent the formation of emboli that could result in a stroke or pulmonary embolus. Aspirin is an antiplatelet aggregation agent which is used for prophylaxis of thromboembolism. TEE is a test to identify the anatomical changes and whether a clot exists in the heart; it is a pretest for electrical

Thus, serotonergic innervation from the DRN greatly affects the modulation of a fear-like behavior. However, the 5-HT pathway from the DRN to the LC was critical only in pain modulation and not in the elaboration of defensive behavioral responses. It Both the non-selective and the selective serotonergic antagonists in the LC were found to impair the increase in the nociceptive threshold caused by the defensive reaction mediated by the DMH. It may be the case that the connective pathway between the DRN and the LC modulates the nociceptive

Lignocaine, a local anaesthetic, showed inhibition of peristalsis because it blocks sodium-ion protein channels in nerves. This prevented the initiation and proliferation of nerve action potentials; hence its use as a local anaesthetic (Nagy & Woolf, 1996). It acts on nociceptive neurons, which resulted in a diminished amplitude of contraction. This indicates that partial inhibition occurred. Partial inhibition of the peristaltic reflex was also

The rat phrenic nerve preparation is very useful as it teaches us not only a lot about neuro muscular and muscle physiology but also the pharmacodynamics of different drugs such as neuromuscular blocking agents and determining their potency at blocking the neuromuscular junction. This preparation was originally used for the bioassay of tubocurarine (Bülbring et al, 1997). However there are a few limitations to this prep, for example it is hard to differentiate between the different neuromuscular blockers, whether they are depolarizers or non-depolarizers because depolarizers fail to reverse the effects of non-depolarizers. As a result of this, another prep is preferred namely the chick sciatic nerve-tibialis anticus muscle (Vogel, 2013).

[Q3] The adrenergic receptors that are stimulated to improve consciousness include both alpha and beta receptors. This is due to epinephrine being a vasoactive adrenergic, and the affect on both receptors results in cardiac failure support. The alpha-1 receptor acts on the nerve

The onset, level and duration of sensory and motor blockade were recorded. The total sensory analgesia time, hemodynamic parameters and side-effects were also noted

The locus ceruleus is also the site of origin for the descending medullospinal adrenergic pathway, which is known to be a key mechanism in regulating nociceptive neurotransmission. The similar mechanisms of α-2 receptors and opioid receptors in this area of the brain have contributed to the thought that there must also be extra-spinal sites of action. When these sites are stimulated, they decrease the firing of nociceptor neurons stimulated by peripheral A and C fibers and also inhibit the release of their neurotransmitters. The analgesic effects are believed to be in the dorsal horn of the spinal cord. When a hypnotic dose of dexmedetomidine was administered to laboratory animals, norepinephrine release from the locus ceruleus was inhibited. The absence of inhibitory control over the ventrolateral preoptic nucleus (VLPO) resulted in the release of -aminobutyric acid (GABA) and galanin, which further inhibited the locus ceruleus and tuberomamillary nucleus (TMN). This inhibitory response also causes a decrease in the release of histamine, which results in a hypnotic response. This response is similar to that found in normal sleep in that the reduction of norepinephrine release by the locus ceruleus triggers the release of GABA and galanin by the VLPO. These neurotransmitters further inhibit norepinephrine release by the locus ceruleus and suppress histamine secretion by the TMN. The reduced occupancy of the histamine receptors on the cells of the subcortical areas induces a hypnotic state

Pharmacology is the branch of medicine and biology that seeks to understand drugs and how they affect the body. It involves the analysis of how drugs interact with the biological function of the body and how these drugs react with each other, their natures, and their properties. All drugs are considered chemicals and when ingested into the body an affect from the drug takes place. According to Doweiko (1999), “A drug is essentially a foreign chemical that is introduced into the individual’s body to bring about a specific desired response. There are many forms of drugs and how these drugs are administered in the body determines the kind of result that will take place. The Central Nervous System, (CNS) plays a major role in how these