Vagal stimulation

Paroxysmal (re-entry) supraventricular tachycardia (recurrent/ refractory to vagal stimulation or adenosine)... 

Digoxin Inhibits AV nodal conduction by 1. Vagal stimulation 2. Directly slowing AV nodal conduction and prolonging AV nodal refractoriness 0.25 mg every 2 hours up to 1.5 mg 0.125-0.25 mg PO once daily Amiodarone, verapamil, quinidine inhibit digoxin elimination... 

Gastrin G cells in pyloric region of the stomach Protein in stomach vagal stimulation Stimulates parietal cells (HC1) and chief cells (pepsinogen) in stomach enhances gastric motility... 

The answer is a. (Katzung, p 240.) Older therapies—all designed to favor parasympathetic control of rhythm—include digoxin, propranolol, edrophonium, and vasoconstrictors. The vasoconstrictor phenylephrine (given by intravenous bolus) causes stimulation of the carotid sinus and reflex vagal stimulation of the atria. More recently, adenosine has been favored over verapamil, which is also very effective but slower acting... 

The actions of anticholinesterase agents on the cardiovascular system are complex. The primary effect produced by potentiation of vagal stimulation is bradycardia with a consequent decrease in cardiac output and blood pressure. However, potentiation of both parasympathetic and sympathetic ganglionic transmis-... 

Transmembrane action potential of a sinoatrial node cell. In contrast to other cardiac cells, there is no phase 2 or plateau. The threshold potential (TP) is -40 mV. The maximum diastolic potential (MDP) is achieved as a result of a gradual decline in the potassium conductance (gK+). Spontaneous phase 4 or diastolic depolarization permits the cell to achieve the TR thereby initiating an action potential (g = transmembrane ion conductance). Stimulation of pacemaker cells within the sinoatrial node decreases the time required to achieve the TR whereas vagal stimulation and the release of acetylcholine decrease the slope of diastolic depolarization. Thus, the positive and negative chronotropic actions of sympathetic and parasympathetic nerve stimulation can be attributed to the effects of the respective neurotransmitters on ion conductance in pacemaker cells of the sinuatrial node. gNa+ = Na+ conductance. 

Cardiovascular effects are related to both central and peripheral sympathetic stimulation. Initial bradycardia appears to be related to vagal stimulation this is followed by tachycardia and hypertension. Larger doses are directly depressant to the myocardium, and death results from cardiac failure. 

Muscarinic Receptor Interactions. Excitatory muscarinic effects, such as temporary stimulation of salivation and stimulation of intestinal peristalsis, were seen with 2-PAM. Atropine-like actions were seen at high concentrations (15-20 mg/kg or more), and, when injected rapidly, 2-PAM caused temporary diplopia (nicotinic block) and loss of accommodation in the eye.Both TMB-4 and 2-PAM blocked bradycardia induced by vagal stimulation. At low concentrations, neither compound affected normal intestinal peristalsis, but they did block peristalsis caused by increased vagal stimulation. TMB-4, 2-PAM, and toxogonin antagonized the effect of acetylcholine, acetyl- -methyl-choline, and other agonists on Isolated guinea pig ileum.62... 

Doses of 2-PAM larger than 40 mg/kg, as well as TMB-4 and toxogonin, produced a temporary block of the cardiac response to vagal stimulation and of the nictitating membrane response to preganglionic, but not postganglionic, stimulation. There was transient hypotension due to block of ganglionic transmission.9,63,71... 

To suppress respiratory and other secretions and vagal stimulation caused by anaesthetics. 

Atracurium causes minimal cardiovascular effects except those associated with some histamine release if the drug is given rapidly or in high doses. As with vecuronium, it produces little increase in heart rate in fact, decreases in heart rate have been reported. This is once again thought to be due to the effects of other agents, such as the opiates, or as a result of vagal stimulation. The incidence of histamine release with atracurium is about one-third of that observed after tubocurarine administration. 

Neural vagal stimulation reieases acetylcholine, which acts on muscarinic M3 receptors, leading to increased cytosoiic Ca2+. 

Inhaled anesthetics change heart rate either directly by altering the rate of sinus node depolarization or indirectly by shifting the balance of autonomic nervous system activity. Bradycardia can be seen with halothane, probably because of direct vagal stimulation. In contrast, enflurane, and sevoflurane have little effect, and both desflurane and isoflurane increase heart rate. In the case of desflurane, transient sympathetic activation with elevations in catecholamine levels can lead to marked increases in heart rate and blood pressure when high inspired gas concentrations are administered. 

Aconitum laciniatum Stapf. A. kusnezoffii Reichenbach A. chineme Paxt. A. vilmorinianum Kom. A. pariculigerum Nakai Cao Wu (root) Hypaconitine, aconitine, aconine, mesaconitine, talatisamine. This herb is highly toxic.33 Analgesic, sedative, vagal-stimulation, local anesthetic effect. 

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