Веденный - рефлекс Jarisch
Рефлекс Безолд -Джариша (также называемый рефлексом Бэзолда, рефлекс Джарша-Бизолд или фон-визиолд-Джариш Рефлекс [ 1 ] ) включает в себя различные сердечно -сосудистые и неврологические процессы, которые вызывают гипопноэ (чрезмерно мелкое дыхание или аномально низкую частоту дыхания ), гипотензию (аномально низкое кровяное давление) и брадикардия (аномально низкая частота сердечных сокращений ) в ответ на расслабленные стимулы, обнаруженные в кардиологических вентиляциях. Полем [ 2 ] Рефлекс назван в честь Альберта фон Уэйлд и Адольфа Джариша младшего. [ 3 ] Значение открытия заключается в том, что это было первое распознавание химического (немеханического) рефлекса.
История и физиология
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Фон Безольд и Хирт описали реакцию, включающую триаду брадикардии, гипотонии и апноэ (гипопнея), возникающей в результате внутривенной инъекции алкалоидного экстракта Veratrum viride или вице -альбома в 1867 году. [ 4 ] Это наблюдение сравнительно пренебрегали до тех пор, пока Джариш и Хензе не повторно рассмотрели его в 1937 году; Они идентифицировали реакцию как хеморефлекс, действующий через блуждающий нерв , который был передан в ядра Tractus solitarii (NTS) , и назвал ее рефлексом Bezold. [ 4 ] Сейчас его обычно называют рефлексом Безолда -Яриша; Однако брадикардия и гипопноя возникают из анатомически различных рецепторов в сердце и легких соответственно [ 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 have cell bodies in the nodose ganglion and the dorsal root ganglion. They manifest two types of nerve endings in the heart: complex unencapsulated endings located in the atrial and ventricular endocardium and an endocardial nerve network throughout the surface of the endocardium. The axons include myelinated fibers (A-fiber) and unmyelinated fibers (C-fibers) which travel with the vagus and sympathetic 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 the coronary 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 activity via the caudal ventrolateral medulla (CVLM) and possibly the rostral ventrolateral medulla (RVLM).[8][7][9] The sites of the chemoreflex and baroreflex input overlap and there is evidence that these reflexes modify each other, probably through the actions of excitatory and inhibitory neurotransmitters, such as serotonin and Gamma-Aminobutyric acid (GABA).[7][9]
Although the reflex was originally described in response to Veratrum alkaloids, it can be stimulated by many biologically active chemicals, including nicotine, capsaicin, bradykinin, atrial natriuretic peptide, prostanoids, nitrovasodilators, angiotensin II type 1 receptor (AT1) antagonists and serotonin agonists.[10][11][12] It may also contribute to various pathophysiological responses,[6] such as:
- Severe hemorrhage and hypovolemia: During severe hemorrhage or profound hypovolemia 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 the sinus bradycardia that commonly occurs within the first hour following a myocardial infarction,[13] and may explain the frequent occurrence of atrio-ventricular (AV) node block in acute posterior or inferior myocardial infarction.[14] Bradycardia in this setting may be treated with atropine.
- 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 after spinal anesthesia[16] and interscalene brachial plexus block.[17]
- Vaso-vagal syncope: the role of the Bezold–Jarisch reflex in vaso-vagal syncope is unclear. Upright posture results in pooling of blood in the lower extremities that diminishes venous return and results in a reduced cardiac output. The resultant lowering of blood pressure is sensed by carotid sinus baroreceptors, and stimulates the baroreflex to inhibit vagal activity and stimulate the sympathetic nervous system – this increases heart rate and contractility, induces vasoconstriction, and tends to restore blood pressure. However, if the Bezold–Jarisch reflex is activated due to the reduced ventricular volume this may trigger paradoxical bradycardia and arterial hypotension resulting in syncope. The importance of this mechanism is unclear since vaso-vagal syncope can be observed in cardiac transplant patients who are presumed to lack cardiac innervation.[6] If it operates this phenomenon would be expected to be exacerbated if the individual is dehydrated. It has also been proposed that this mechanism accounts for the increased susceptibility to orthostatic syncope of astronauts after space flights.[18]
References
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- ^ Salo LM, Woods RL, Anderson CR, McAllen RM (August 2007). "Nonuniformity in the von Bezold-Jarisch reflex". Am. J. Physiol. Regul. Integr. Comp. Physiol. 293 (2): R714–20. doi:10.1152/ajpregu.00099.2007. PMID 17567718. S2CID 7042569.
- ^ synd/3165 at Who Named It?
- ^ Jump up to: a b Aviado, Domingo M.; Aviado, Domingo Guevara (2001). "The Bezold-Jarisch Reflex". Annals of the New York Academy of Sciences. 940 (1): 48–58. Bibcode:2001NYASA.940...48A. doi:10.1111/j.1749-6632.2001.tb03666.x. ISSN 1749-6632. S2CID 70636612.
- ^ Jump up to: a b c Aviado, D. M.; Guevara Aviado, D. (June 2001). "The Bezold-Jarisch reflex. A historical perspective of cardiopulmonary reflexes". Annals of the New York Academy of Sciences. 940: 48–58. doi:10.1111/j.1749-6632.2001.tb03666.x. ISSN 0077-8923. PMID 11458703. S2CID 70636612.
- ^ Jump up to: a b c d Campagna, Jason A.; Carter, Christopher (May 2003). "Clinical relevance of the Bezold-Jarisch reflex". Anesthesiology. 98 (5): 1250–1260. doi:10.1097/00000542-200305000-00030. ISSN 0003-3022. PMID 12717149. S2CID 6790577.
- ^ Jump up to: a b c Kashihara, Koji (November 2009). "Roles of arterial baroreceptor reflex during bezold-jarisch reflex". Current Cardiology Reviews. 5 (4): 263–267. doi:10.2174/157340309789317805. ISSN 1875-6557. PMC 2842957. PMID 21037842.
- ^ Jump up to: a b Grimm, D. R. (May 1997). "Neurally mediated syncope: a review of cardiac and arterial receptors". Journal of Clinical Neurophysiology. 14 (3): 170–182. doi:10.1097/00004691-199705000-00002. ISSN 0736-0258. PMID 9244157.
- ^ Jump up to: a b Vasquez, E. C.; Meyrelles, S. S.; Mauad, H.; Cabral, A. M. (April 1997). "Neural reflex regulation of arterial pressure in pathophysiological conditions: interplay among the baroreflex, the cardiopulmonary reflexes and the chemoreflex". Brazilian Journal of Medical and Biological Research. 30 (4): 521–532. doi:10.1590/s0100-879x1997000400014. ISSN 0100-879X. PMID 9251774.
- ^ Koji Kashihara (Nov 2009). "Roles of Arterial Baroreceptor Reflex During Bezold-Jarisch Reflex". Curr Cardiol Rev. 5 (4): 263–267. doi:10.2174/157340309789317805. PMC 2842957. PMID 21037842.
- ^ Sever, P. S.; Hughes, A. (June 2001). "Angiotensin receptor antagonists and vaso-vagal attacks due to sensitisation of the Bezold-Jarisch reflex?". Journal of Human Hypertension. 15 (6): 437–438. doi:10.1038/sj.jhh.1001190. ISSN 0950-9240. PMID 11439322.
- ^ eMedicine - Syncope : Article by M Silvana Horenstein, MD
- ^ Голдман, Ли; Андерсон, Джеффри Л. (2012-01-01). «Острая инфаркт миокарда и осложнения инфаркта инфаркта миокарда». Голдман: Сесил Медицина Голдмана (24 -е изд.). Сондерс, отпечаток Elsevier Inc. с. 444. ISBN 978-1-4377-1604-7 .
- ^ Кац, Арнольд М. (2001). Физиология сердца (3 -е изд.). Филадельфия [UA]: Липпинкотт Уильямс и Уилкинс. п. 595. ISBN 978-0-7817-1548-5 .
- ^ Марк, Аллин Л. (1983-01-01). «Рефлекс Bezold-Jarisch Reflex Reflex: клинические последствия ингибирующих рефлексов, происходящих в сердце» . Журнал Американского колледжа кардиологии . 1 (1): 90–102. doi : 10.1016/s0735-1097 (83) 80014-x . ISSN 0735-1097 . PMID 6826948 .
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