Vagal reflexes

Atropine may be given to prevent cardiac arrest resulting from vagal reflex activation, incident to anesthetic in-ductioa gastric lavage, or endoscopic procedures. 

The reflex nature of the bradycardia induced by parenterally administered norepinephrine can readily be demonstrated by administration of atropine, a choli-noreceptor antagonist. Atropine abolishes the compensatory vagal reflexes. Under conditions of vagal blockade, the direct cardiac stimulatory effects of norepinephrine are unmasked. There is marked tachycardia, an increase in stroke volume, and as a consequence, a marked increase in cardiac output (Fig. 10.4). 

The Hi Receptor and its ligands. The 11, receptor mediates most uf the important histamine effects in allergic diseases. These include smooth muscle contraclion. increased vascular permeability, pruritus, prostaglandin generation, decreased atrioventricular node conduction time with resultant tachycardia, activation of vagal reflexes, and increased cyclic guant sine monophosphate tcGMP) production. 

Norepinephrine (levarterenol, noradrenaline) and epinephrine have similar effects on Bi receptors in the heart and similar potency at receptors. Norepinephrine has relatively little effect on B2 receptors. Consequently, norepinephrine increases peripheral resistance and both diastolic and systolic blood pressure. Compensatory vagal reflexes tend to overcome the direct positive chronotropic effects of norepinephrine however, the positive inotropic effects on the heart are maintained (Table 9-4). 

Capsaicin, like the other irritant RCAs, also causes bronchoconstriction, but the mechanism is uncertain. Capsaicin releases substance P that can cause bronchoconstriction directly by activation of specific receptors or by release of histamine or other mediators. It may also cause reflex bronchoconstriction by stimulating C fibers in both pulmonary and bronchial circulation. Therefore, bronchoconstriction may be secondary to substance P release, or to a vagal reflex. The altered neurophysiology of sensory neurons in the airway mucosa induces the release of tachykinins and neurokinin A, which causes neuro-mediated inflammation of the epithelium, airway, blood vessels, glands, and smooth muscles. This leads to bronchoconstriction, mucus secretion, enhanced vascular permeability, and neutrophil chemotaxis. 

Goehler LE, Finger TE (1992) Functional organization of vagal reflex systems in the brain stem of the goldfish, Carassius auratus. 1 Comp Neurol 319 463—478 Haffter P, NUsslein-Volhard C (1996) Large scale genetics in a small vertebrate, the zebrafish. Int 1 Dev Biol 40 221-227... 

Methoxamine (a,) use in paroxysmal atrial tachycardia—elicits vagal reflex. 

Figure II-4-13 Block of tachycardia due to Drug P by hexamethonium is indicative of a sympathetic reflex that follows a decrease in BP due to a vasodilator (choice B). Reversal of bradycardia due to Drug Q by hexamethonium indicates a vagal reflex elicited by vasoconstriction (e.g., alpha activation) masking cardiac stimulation (e.g., beta activation) typical of norepinephrine (choice C). Tachycardia due to Drug R is unaffected by any antagonist, indicative of a beta activator (choice D). Reversal of tachycardia due to Drug S by hexamethonium indicates a sympathetic reflex masking a vagotomimetic action typical of a muscarinic activator (choice A) this is confirmed by the effect of atropine.

In addition to inhibition of mediator release, cromoglycate has the property of inhibiting vagal reflex-mediated bronchoconstriction in dogs, which results from the stimulation of irritant nerve fibers with substances such as histamine and prostaglandins (Dixon et al., 1980). The importance of this latter mechanism in the therapeutic actions of cromoglycate is unclear. 

CNS Atropine to prevent vagal reflexes induced by manipulation of visceral organs. Scopolamine to prevent motion sickness... 

Because of its rapid vasoconstrictor activity, the drug produces a marked reflex bradycardia, due to stimulation of vagal reflexes. The increase in vagal tone increases the threshold for firing of the sinoatrial (SA) node and atrial tissue, resulting in a slower rate of firing and atrial conduction. 

Methoxamine paroxysmal atrial tachycardia through vagal reflex... 

Drug X causes slowing of heart rate, but this is converted into tachycardia by hexamethonium and atropine—ie, the bradycardia is caused by reflex vagal discharge. Phenoxybenzamine also reverses the bradycardia to tachycardia, suggesting that alpha receptors are needed to induce the reflex bradycardia and that X has direct beta-agonist actions. The choices that evoke a vagal reflex bradycardia but can also cause direct tachycardia are limited the answer is (E). 

Reduction of secretions and vagal reflexes Muscarinic antagonists, usually hyoscine, are used to prevent salivation and bronchial secretions and, more importantly, to proteci the heart from arrhythmias, particularly bradycardia caused by halothane, propofol, suxamethonium and neostigmine. Hyoscine is also iiniiemeiic and produces some amnesia. 

C. Vomiting may stimulate vagal reflex, resulting in bradycardia or atrioventricu-iar biock. 

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