Hypovolemic hemorrhage induces Fos expression in the rat hypothalamus: Evidence for involvement of the lateral hypothalamus in the decompensatory phase of hemorrhage
Autor: | William R. Millington, Gökhan Göktalay |
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Přispěvatelé: | Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı., Göktalay, Gökhan, AAH-1448-2021 |
Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Male Lateral hypothalamus Lidocaine Rats sprague-dawley Protein c fos Nucleus-tractus-solitarius Hypovolemia Anterior hypothalamus Ventrolateral periaqueductal gray Brain function Pathogenesis Disease models animal Hemostatics Animal tissue 0302 clinical medicine Immunoreactivity Dorso medial hypothalamus Pathology Premovement neuronal activity Arterial pressure Priority journal Brain-stem Neurons Arc (protein) General Neuroscience Proto-oncogene proteins c-fos Cobalt Arcuate nucleus Synapse Nerve cell Hypovolemic hemorrhage Zona incerta Sprague dawley rat Posterior hypothalamus Hypothalamus Hemorrhagic shock Vulgaris-leukoagglutinin L-glutamate medicine.symptom Hypotension Animal cell hormones hormone substitutes and hormone antagonists medicine.drug Excitatory projections Bradycardia endocrine system medicine.medical_specialty Efferent connections Cardiovascular-responses Heart rate Hemorrhage Neurosciences & neurology Periaqueductal Gray Animals Escape Reaction Pathophysiology Article 03 medical and health sciences Protein fos Internal medicine medicine Animal model Animal experiment Delta-opioid receptors Fos immunoreactivity Disease duration Evoked response business.industry Animal Disease model Ventromedial hypothalamus Bleeding Neurosciences Body weight Hemostatic agent Nonhuman Cobalt chloride 030104 developmental biology Blood pressure Endocrinology Metabolism nervous system Medial preoptic area Protein expression Rat business Hypothalamic paraventricular nucleus Controlled study 030217 neurology & neurosurgery |
Popis: | This study tested the hypothesis that the hypothalamus participates in the decompensatory phase of hemorrhage by measuring Fos immunoreactivity and by inhibiting neuronal activity in selected hypothalamic nuclei with lidocaine or cobalt chloride. Previously, we reported that inactivation of the arcuate nucleus inhibited, but did not fully prevent, the fall in arterial pressure evoked by hypotensive hemorrhage. Here, we report that hemorrhage (2.2 ml/100 g body weight over 20 min) induced Fos expression in a high percentage of cells in the paraventricular, supraoptic and arcuate nuclei of the hypothalamus as shown previously. Lower densities of Fos immunoreactive cells were also found in the medial preoptic area (mPOA), anterior hypothalamus, lateral hypothalamus (LH), dorsomedial hypothalamus, ventromedial hypothalamus (VMH) and posterior hypothalamus. Bilateral injection of lidocaine (2%; 0.1 mu l or 0.3 mu l) or cobalt chloride (5 mM; 0.3 mu l) into the tuberal portion of the LH immediately before hemorrhage was initiated reduced the magnitude of hemorrhagic hypotension and bradycardia significantly. Lidocaine injection into the VMH also attenuated the fall in arterial pressure and heart rate evoked by hemorrhage although inactivation of the mPOA or rostral LH was ineffective. These findings indicate that hemorrhage activates neurons throughout much of the hypothalamus and that a relatively broad area of the hypothalamus, extending from the arcuate nucleus laterally through the caudal VMH and tuberal LH, plays an important role in the decompensatory phase of hemorrhage. Office of Naval Research - N00014-00-1-0056 |
Databáze: | OpenAIRE |
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