ArticleJournal of neurotrauma2019
Inhaled Nitric Oxide Protects Cerebral Autoregulation and Reduces Hippocampal Neuronal Cell Necrosis after Traumatic Brain Injury in Newborn and Juvenile Pigs.
Article in Journal of neurotrauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Inhalational Gases for Neuroprotection in Traumatic Brain Injury.Journal of neurotrauma · 2021Pooled it
- Inhaled nitric oxide: role in the pathophysiology of cardio-cerebrovascular and respiratory diseases.Intensive care medicine experimental · 2022Review
- Article
- Article
- Inhaled Nitric Oxide Treatment for Aneurysmal SAH Patients With Delayed Cerebral Ischemia.Frontiers in neurology · 2022Article
- Regulation of the Cerebral Circulation During Development.Comprehensive Physiology · 2021Article
- Inhaled nitric oxide reduces injury and microglia activation in porcine hippocampus after deep hypothermic circulatory arrest.The Journal of thoracic and cardiovascular surgery · 2021Article
- Effects of Remote Ischemic Conditioning on Cerebral Hemodynamics in Ischemic Stroke.Neuropsychiatric disease and treatment · 2020Review
- Propranolol protects cerebral autoregulation and reduces hippocampal neuronal cell death through inhibition of interleukin-6 upregulation after traumatic brain injury in pigs.British journal of anaesthesia · 2019Article
- Translational approach towards determining the role of cerebral autoregulation in outcome after traumatic brain injury.Experimental neurology · 2019Review
- Inhaled Nitric Oxide Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis After Traumatic Brain Injury Through Inhibition of ET-1, ERK MAPK and IL-6 Upregulation in Pigs.Neurocritical care · 2019Article
Corrections and comments
- Retraction · 2022-04-29Author Unresponsive · Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · · this notice lists three articles as being retracted; William Armstead has ORI finding of misconduct; see https://ori.hhs.gov/content/case-summary-armstead-william-m
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Cerebral blood flow (CBF) is reduced and autoregulation is impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). In prior studies of male and female newborn and juvenile pigs, we observed that phenylephrine, norepinephrine, epinephrine, and dopamine demonstrated different sex- and age-dependent abilities to prevent impairment of cerebral autoregulation and limit histopathology after TBI, despite equivalent CPP values. This observation complicated treatment choice. Alternatively, administration of a cerebral vasodilator may improve cerebral hemodynamics after TBI by increasing CBF. In prior studies, intravenous sodium nitroprusside, a nitric oxide (NO) releaser, elevated CBF after TBI but failed to prevent impairment of cerebral autoregulation due to a confounding decrease in MAP, which lowered CPP. We presently test the hypothesis that inhaled NO (iNO) will protect cerebral autoregulation and prevent hippocampal histopathology after TBI. Results show that iNO administered at 30 min or 2 h after TBI protected cerebral autoregulation and prevented neuronal cell necrosis in CA1 and CA3 hippocampus equivalently in male and female newborn and juvenile pigs without change in MAP. Protection lasted for at least 2 h after iNO administration was stopped. Papaverine-induced dilation was unchanged by TBI and iNO. These data indicate that iNO offers the opportunity to have a single therapeutic that uniformly protects autoregulation and limits hippocampal neuronal cell necrosis across both ages and sexes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.