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
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