| Serotonin neurons of the caudal raphe nuclei contribute to sympathetic recovery following hypotensive hemorrhage. | |
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MedLine Citation:
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PMID: 20130223 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Serotonin is thought to contribute to the syncopal-like response that develops during severe blood loss by inhibiting presympathetic neurons of the rostroventrolateral medulla (RVLM). Here, we tested whether serotonin cells activated during hypotensive hemorrhage, i.e., express the protein product of the immediate early gene c-Fos, are critical for the normal sympathetic response to blood loss in unanesthetized rats. Serotonin-immunoreactive cells of the raphe obscurus and raphe magnus, parapyramidal cells of the B3 region, subependymal cells of the ventral parapyramidal region, and cells of the ventrolateral periaqueductal gray region were activated by hypotensive hemorrhage, but not by hypotension alone. In contrast to findings in anesthetized animals, lesion of hindbrain serotonergic cells sufficient to produce >80% loss of serotonin nerve terminal immunoreactivity in the RVLM accelerated the sympatholytic response to blood loss, attenuated recovery of sympathetic activity after termination of hemorrhage, and exaggerated metabolic acidosis. Hindbrain serotonin lesion also attenuated ventilatory and sympathetic responses to stimulation of central chemoreceptors but increased spontaneous arterial baroreflex sensitivity and decreased blood pressure variability. A more global neurotoxic lesion that also eliminated tryptophan hydroxylase-immunoreactive cells of the ventrolateral periaqueductal gray region had no further effect on the sympatholytic response to blood loss. Together, the data indicate that serotonin cells of the caudal hindbrain contribute to compensatory responses following blood loss that help maintain oxygenation of peripheral tissue in the unanesthetized rat. This effect may be related to facilitation of chemoreflex responses to acidosis. |
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Authors:
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Ling-Hsuan Kung; Jaimee Glasgow; Anna Ruszaj; Thackery Gray; Karie E Scrogin |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-02-03 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 298 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-23 Completed Date: 2010-04-15 Revised Date: 2011-10-14 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R939-53 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Loyola University Stritch School of Medicine, Maywood, IL, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Baroreflex / physiology Blood Pressure Cerebral Hemorrhage / physiopathology* Heart Rate Hypotension / complications Male Medulla Oblongata / physiology Neurons / physiology* Neurotoxins / toxicity Pyramidal Cells / physiology Raphe Nuclei / physiology* Rats Rats, Sprague-Dawley Serotonin / physiology* Sympathetic Nervous System / physiology* Tryptophan Hydroxylase / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL-072354/HL/NHLBI NIH HHS; HL-076162/HL/NHLBI NIH HHS; R01 HL072354-07/HL/NHLBI NIH HHS; R01 HL072354-08/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Neurotoxins; 50-67-9/Serotonin; EC 1.14.16.4/Tryptophan Hydroxylase |
| Comments/Corrections | |
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