ArticleMolecular neurobiology2017
Vasopressin Impairment During Sepsis Is Associated with Hypothalamic Intrinsic Apoptotic Pathway and Microglial Activation.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Vasopressin and its analogues in patients with septic shock: holy Grail or unfulfilled promise?Critical care (London, England) · 2025Review
- Article
- Review
- Autonomic Disbalance During Systemic Inflammation is Associated with Oxidative Stress Changes in Sepsis Survivor Rats.Inflammation · 2022Article
- The biological alterations of synapse/synapse formation in sepsis-associated encephalopathy.Frontiers in synaptic neuroscience · 2022Review
- Microglial Activation Modulates Neuroendocrine Secretion During Experimental Sepsis.Molecular neurobiology · 2021Article
- Article
- Vagus Nerve Stimulation: A Potential Adjunct Therapy for COVID-19.Frontiers in medicine · 2021Article
- Simvastatin Prevents Long-Term Cognitive Deficits in Sepsis Survivor Rats by Reducing Neuroinflammation and Neurodegeneration.Neurotoxicity research · 2020Article
- Baroreceptor denervation reduces inflammatory status but worsens cardiovascular collapse during systemic inflammation.Scientific reports · 2020Article
- Exploring the Mechanism on the Medullary Visceral Zone Inhibiting the Cholinergic Anti-inflammatory Pathway Induced by Sepsis.Mediators of inflammation · 2020Article
- Neuroinflammation in the NTS is associated with changes in cardiovascular reflexes during systemic inflammation.Journal of neuroinflammation · 2019Article
- Impairment of osmotic challenge-induced neurohypophyseal hormones secretion in sepsis survivor rats.Pituitary · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that in the early phase of sepsis, the plasma concentration of arginine vasopressin (AVP) is increased, but in the late phase, its levels remain inadequately low, despite of persistent hypotension. One hypothesis suggested for this relative deficiency is apoptosis of vasopressinergic neurons. Here, we investigated apoptosis pathways in the hypothalamus during sepsis, as well as mechanisms underlying this process. Male Wistar rats were submitted to sepsis by cecal ligation and puncture (CLP) or nonmanipulated (naive) as control. After 6 and 24 h, the animals were decapitated and brain and blood were collected to assess hypothalamic apoptotic markers, IFN-γ plasma levels, and evidence for breakdown of the blood-brain barrier (BBB). Sepsis caused a decrease in mitochondrial antiapoptotic proteins (Bcl-2, Bcl-xL) in the hypothalamus, but had no effect on markers of cell death mediated by death receptors or immune cells. In the supraoptic nuclei of these animals, microglia morphology was consistent with activation, associated with an increase in plasma IFN-γ. A transitory breakdown of BBB in the hypothalamus was seen at 6 h following CLP. The results indicate that the intrinsic but not extrinsic apoptosis pathway is involved in the cell death observed in vasopressinergic neurons, and that this condition is temporally associated with microglial activation and BBB leaking.
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