title: Hypovolemic hemorrhage induces Fos expression in the rat hypothalamus: Evidence for involvement of the lateral hypothalamus in the decompensatory phase of hemorrhage.
abstract: 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/100g 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 μl or 0.3 μl) or cobalt chloride (5mM; 0.3 μl) 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.
authors.affiliation: Department of Medical Pharmacology, Uludag University, Faculty of Medicine, Bursa, Turkey.
authors.forename: G
authors.initials: G
authors.lastname: Göktalay
authors.affiliation: Department of Pharmaceutical Sciences, Albany College of Pharmacy and Health Sciences, Albany, NY, United States. Electronic address: william.millington@acphs.edu.
authors.forename: W R
authors.initials: WR
authors.lastname: Millington
mesh_terms: D000818:Animals; D001919:Bradycardia / Q000473:pathology / Q000503:physiopathology; D003035:Cobalt / Q000494:pharmacology; D004195:Disease Models, Animal; D006470:Hemorrhage / Q000473:pathology / Q000503:physiopathology*; D006490:Hemostatics / Q000494:pharmacology; D007031:Hypothalamus / Q000378:metabolism* / Q000473:pathology; D020896:Hypovolemia / Q000473:pathology / Q000503:physiopathology*; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D017207:Rats, Sprague-Dawley
chemical_list: D006490:Hemostatics; D016760:Proto-Oncogene Proteins c-fos; D003035:Cobalt; D008012:Lidocaine; C018021:cobaltous chloride
keywords: Fos immunoreactivity; arcuate nucleus; hemorrhage; hemorrhagic shock; lateral hypothalamus; ventromedial hypothalamus