TheBezold–Jarisch reflex (also called theBezold reflex, theJarisch-Bezold reflex or Von Bezold–Jarisch reflex^[1]) involves a variety of cardiovascular and neurological processes which causehypopnea (excessively shallow breathing or an abnormally lowrespiratory rate),hypotension (abnormally low blood pressure) andbradycardia (abnormally low restingheart rate) in response to noxious stimuli detected in the cardiac ventricles.^[2] The reflex is named afterAlbert von Bezold and Adolf Jarisch Junior.^[3] The significance of the discovery is that it was the first recognition of a chemical (non-mechanical) reflex.

von Bezold and Hirt described a reaction comprising a triad of bradycardia, hypotension, and apnea (hypopnea) resulting from an intravenous injection of an alkaloidal extract ofVeratrum viride orViscum album in 1867.^[4] This observation was comparatively neglected until Jarisch and Henze re-examined it in 1937; they identified the reaction as a chemoreflex actingvia thevagus nerve that was relayed in thenucleus tractus solitarii (NTS), and termed it the Bezold reflex.^[4] It is now usually called the Bezold–Jarisch reflex; however the bradycardia and hypopnea arise from anatomically distinct receptors in the heart and lung respectively^[5] and whether hypopnea should be regarded as part of the reflex is disputed.^[6][7] The afferent cardiac neurons relevant to the Bezold–Jarisch reflex havecell bodies in thenodose ganglion and thedorsal root ganglion. They manifest two types of nerve endings in the heart: complex unencapsulated endings located in theatrial andventricularendocardium and an endocardial nerve network throughout the surface of the endocardium. The axons includemyelinated fibers (A-fiber) andunmyelinated fibers (C-fibers) which travel with the vagus andsympathetic nerves. The myelinated afferents originating in the atria are attached to discrete receptor endings, whereas most of the unmyelinated fibers are located in the ventricles and the walls of thecoronary vessels.^[8] Vagal afferent C fibers originating in the heart and lungs terminate in the NTS, while axons from the heart also inhibit sympathetic nervous activityvia thecaudal ventrolateral medulla (CVLM) and possibly therostral ventrolateral medulla (RVLM).^[8][7][9] The sites of the chemoreflex andbaroreflex input overlap and there is evidence that these reflexes modify each other, probably through the actions of excitatory and inhibitory neurotransmitters, such asserotonin andGamma-Aminobutyric acid (GABA).^[7][9]

Although the reflex was originally described in response toVeratrum alkaloids, it can be stimulated by many biologically active chemicals, includingnicotine,capsaicin,bradykinin,atrial natriuretic peptide,prostanoids,nitrovasodilators,angiotensin II type 1 receptor (AT1) antagonists andserotoninagonists.^[10][11][12] It may also contribute to various pathophysiological responses,^[6] such as:

• Severe hemorrhage and hypovolemia: During severehemorrhage or profoundhypovolemia the ventricle can become relatively empty and trigger cardiac vagal afferent fibers to elicit the Bezold–Jarisch reflex resulting in paradoxical bradycardia, vasodilation, and hypotension.^[6]
• Myocardial ischemia: Chemoreceptors located in the ventricles respond to myocardial ischemia, resulting in an increase in blood flow to the myocardium and a decrease in the work of the heart. This appears to be a cardioprotective reflex, as coronary vasodilation occurs. The pathway for this cardioprotective reflex begins with receptors in the ventricles of the heart, which detect mechanical and chemical stimuli. Afferent unmyelinated C-fibers travel through the vagus to enhance the baroreceptor reflex mechanisms, inhibit sympathetic output, and inhibit vasomotor tone, leading to peripheral vasodilation. The Bezold–Jarisch reflex is thought to be responsible for thesinus bradycardia that commonly occurs within the first hour following amyocardial infarction,^[13] and may explain the frequent occurrence ofatrio-ventricular (AV) node block in acute posterior or inferior myocardial infarction.^[14] Bradycardia in this setting may be treated withatropine.
• Hypotension during coronary reperfusion^[5]
• Hypotension following injection of contrast media during coronary angiography^[5]
• Exertional syncope in aortic stenosis: in severe aortic stenosis exercise may cause a rise in left ventricular pressure which stimulates the Bezold–Jarisch reflex and results in reflex vasodilation and syncope.^[15]
• Spinal anesthesia: The Bezold–Jarisch reflex has been suggested as a possible cause of profound bradycardia and circulatory collapse afterspinal anesthesia^[16] and interscalenebrachial plexus block.^[17]
• Vaso-vagal syncope: the role of the Bezold–Jarisch reflex in vaso-vagalsyncope is unclear. Upright posture results in pooling of blood in thelower extremities that diminishesvenous return and results in a reducedcardiac output. The resultant lowering of blood pressure is sensed bycarotid sinusbaroreceptors, and stimulates thebaroreflex to inhibit vagal activity and stimulate the sympathetic nervous system – this increases heart rate andcontractility, inducesvasoconstriction, and tends to restore blood pressure. However, if the Bezold–Jarisch reflex is activated due to the reduced ventricular volume this may trigger paradoxicalbradycardia and arterialhypotension resulting in syncope. The importance of this mechanism is unclear since vaso-vagal syncope can be observed incardiac transplant patients who are presumed to lack cardiacinnervation.^[6] If it operates this phenomenon would be expected to be exacerbated if the individual isdehydrated. It has also been proposed that this mechanism accounts for the increased susceptibility toorthostatic syncope of astronauts after space flights.^[18]

• Cardiovascular diseases
• Reflexes

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