Kristin Engelhard

ORCID: 0000-0003-3102-2627
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About
Contact & Profiles
Research Areas
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Anesthesia and Neurotoxicity Research
  • Anesthesia and Sedative Agents
  • Intensive Care Unit Cognitive Disorders
  • Cardiac Arrest and Resuscitation
  • Optical Imaging and Spectroscopy Techniques
  • Neuroscience and Neuropharmacology Research
  • Neurosurgical Procedures and Complications
  • Cardiac, Anesthesia and Surgical Outcomes
  • Hemodynamic Monitoring and Therapy
  • S100 Proteins and Annexins
  • Thermal Regulation in Medicine
  • Respiratory Support and Mechanisms
  • Acute Ischemic Stroke Management
  • Neurogenesis and neuroplasticity mechanisms
  • Intracranial Aneurysms: Treatment and Complications
  • Cardiac Ischemia and Reperfusion
  • Anesthesia and Pain Management
  • Intraoperative Neuromonitoring and Anesthetic Effects
  • Cerebrospinal fluid and hydrocephalus
  • Traumatic Brain Injury Research
  • Eicosanoids and Hypertension Pharmacology
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurological Disease Mechanisms and Treatments
  • Mitochondrial Function and Pathology

Johannes Gutenberg University Mainz
2015-2024

University Medical Center of the Johannes Gutenberg University Mainz
2014-2024

Klinik und Poliklinik für Psychosomatische Medizin und Psychotherapie
2015-2020

Focus (Germany)
2014-2015

Medical University of Vienna
2015

Society for Neuroscience in Anesthesiology and Critical Care
2014

Society for Neuroscience
2014

Deutsche Gesellschaft für Anästhesiologie und Intensivmedizin
2003-2010

Ophthalmology Associates (United States)
2006

American Association of Neuropathologists
2005-2006

In this study, we investigated whether the neuroprotection previously seen with dexmedetomidine or S(+)-ketamine involves regulation of proapoptotic (Bax and p53) antiapoptotic (Bcl-2 Mdm-2) proteins. Rats were anesthetized isoflurane. After surgical preparation isoflurane was discontinued, animals randomly assigned to receive fentanyl nitrous oxide (N(2)O)/oxygen plus 100 microg/kg intraperitoneally 30 min before ischemia (n = 8), 1 mg x kg(-1) min(-1) oxygen/air N(2)O/oxygen 8; control...

10.1097/00000539-200302000-00041 article EN Anesthesia & Analgesia 2003-02-01

Abstract Introduction Sepsis-associated delirium (SAD) increases morbidity in septic patients and, therefore, factors contributing to SAD should be further characterized. One possible mechanism might the impairment of cerebrovascular autoregulation (AR) by sepsis, leading cerebral hypo- or hyperperfusion these haemodynamically unstable patients. Therefore, present study investigates relationship between incidence and status AR during sepsis. Methods Cerebral blood flow velocity was measured...

10.1186/cc11665 article EN cc-by Critical Care 2012-10-04

Pain after craniotomy may be underdiagnosed, despite the fact that it can increase postoperative complications for example arterial hypertension and hemorrhage. This study investigates incidence intensity of pain characterizes influencing parameters. During a 1-year period 256 patients undergoing elective were prospectively included in study. Intensity was evaluated 1, 4, 24 hours extubation using verbal numerical rating scale (NRS) ranging from 0 (no pain) to 10 (maximal pain). Routine...

10.1097/ana.0b013e3181df0600 article EN Journal of Neurosurgical Anesthesiology 2010-05-18

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in animals. Aim of the present study was clarify whether age affects outcome, neuroinflammation secondary damage after trauma mice. Young (2 months) old (21 male C57Bl6N mice were anesthetized subjected a controlled cortical impact (CCI) on right parietal cortex. Animals both ages randomly...

10.1371/journal.pone.0043829 article EN cc-by PLoS ONE 2012-08-30

Disruption of the blood-brain barrier (BBB) results in cerebral edema formation, which is a major cause for high mortality after traumatic brain injury (TBI). As anesthetic care mandatory patients suffering from severe TBI it may be important to elucidate effect different anesthetics on formation. Tight junction proteins (TJ) such as zonula occludens-1 (ZO-1) and claudin-5 (cl5) play central role BBB stability. First, influence volatile sevoflurane isoflurane in-vitro integrity was...

10.1371/journal.pone.0050752 article EN cc-by PLoS ONE 2012-12-10

The purpose of this study was to assess the incidence and risk factors postoperative nausea vomiting (PONV) after craniotomy because most available data about PONV in neurosurgical patients are retrospective nature or derive from small prospective studies.Postoperative prospectively assessed within 24 hours surgery 229 requiring supratentorial infratentorial craniotomy. To rule out relevance procedure itself development PONV, observed compared with rate predicted a surgery-independent score...

10.3171/2010.9.jns10151 article EN Journal of neurosurgery 2010-10-29

To determine the neuroprotective efficacy of inert gas xenon following traumatic brain injury and to whether application has a clinically relevant therapeutic time window.Controlled animal study.University research laboratory.Male C57BL/6N mice (n = 196).Seventy-five percent xenon, 50% or 30% with 25% oxygen (balance nitrogen) treatment mechanical lesion by controlled cortical impact.Outcome trauma was measured using 1) functional neurologic outcome score, 2) histological measurement...

10.1097/ccm.0000000000000624 article EN Critical Care Medicine 2014-09-05

In this study, we investigated whether the neuroprotection previously seen with dexmedetomidine or S(+)-ketamine involves regulation of proapoptotic (Bax and p53) antiapoptotic (Bcl-2 Mdm-2) proteins. Rats were anesthetized isoflurane. After surgical preparation isoflurane was discontinued, animals randomly assigned to receive fentanyl nitrous oxide (N2O)/oxygen plus 100 μg/kg intraperitoneally 30 min before ischemia (n = 8), 1 mg · kg−1 min−1 oxygen/air N2O/oxygen 8; control group). all...

10.1213/00000539-200302000-00041 article EN Anesthesia & Analgesia 2003-02-01

This study investigates whether neuroprotection seen with dexmedetomidine is associated suppression of peripheral or central sympathetic tone.Thirty fasted male Sprague-Dawley rats were intubated and ventilated isoflurane N2O/O2 (fraction inspired oxygen = 0.33). Catheters inserted into the right femoral artery vein jugular vein. Cerebral blood flow was measured using laser Doppler flowmetry. Bilateral microdialysis probes placed cortex dorsal hippocampus. At end preparation, administration...

10.1097/00000542-200202000-00034 article EN Anesthesiology 2002-02-01

Propofol reduces neuronal damage from cerebral ischemia when investigated for less than 8 postischemic days. This study investigates the long-term effects of propofol on and apoptosis-related proteins after reperfusion.Male Sprague-Dawley rats were randomly assigned as follows: group 1 (n = 32, control): fentanyl nitrous oxide-oxygen; 2 propofol): oxygen-air. Ischemia (45 min) was induced by carotid artery occlusion hemorrhagic hypotension. Pericranial temperature arterial blood gases...

10.1097/00000542-200410000-00016 article EN Anesthesiology 2004-09-21

Quantitative measurements of gene expression require correction for tissue sample size, RNA quantity, and reverse transcription efficiency. This can be achieved by normalization with control genes. The study was designed to identify candidates not altered after brain trauma. Male C57Bl/6 mice were anesthetized isoflurane, a pneumatic trauma induced controlled cortical impact (CCI) on the right parietal cortex. Brains removed at 15 min, 3, 6, 12 24 h CCI from naive animals (n = 6 each)....

10.1089/neu.2007.0497 article EN Journal of Neurotrauma 2008-07-01

Inflammatory and ischemic processes contribute to the development of secondary brain damage after mechanical injury. Recent data suggest that thiazolidinediones (TZDs), a class drugs approved for treatment non-insulin-dependent diabetes mellitus, effectively reduces inflammation lesion by stimulation peroxisome proliferator-activated receptor-γ (PPAR-γ). The present study investigates influence TZD pioglitazone rosiglitazone on experimental traumatic injury (TBI). A controlled cortical...

10.1089/neu.2010.1685 article EN Journal of Neurotrauma 2011-04-18

HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects 2-methoxyestradiol (2ME2), involved HIF-1α-dependent response, alternative splicing exon 14 (HIF-1α∆Ex14) after traumatic injury (TBI) mice. Intraperitoneal 2ME2 administration 30 min TBI...

10.1111/jnc.12708 article EN Journal of Neurochemistry 2014-03-07

Tissue sampling for gene expression analysis is usually performed under general anesthesia. Anesthetics are known to modulate hemodynamics, receptor-mediated signaling cascades, and outcome parameters. The present study determined the influence of anesthetic paradigms typically used euthanization tissue on cerebral mRNA in mice. Naïve mice animals with acute traumatic brain injury induced by controlled cortical impact (CCI) were randomized following euthanasia protocols (n=10-11/group): no...

10.1089/neu.2013.3243 article EN Journal of Neurotrauma 2014-05-15

Following traumatic brain injury (TBI) neuroinflammatory processes promote neuronal cell loss. Alpha-melanocyte-stimulating hormone (α-MSH) is a neuropeptide with immunomodulatory properties, which may offer neuroprotection. Due to short half-life and pigmentary side-effects of α-MSH, the C-terminal tripeptide α-MSH(11-13) be an anti-inflammatory alternative. The present study investigated mRNA concentrations precursor proopiomelanocortin (POMC) melanocortin receptors 1 4 (MC1R/MC4R) in...

10.1371/journal.pone.0071056 article EN cc-by PLoS ONE 2013-08-05

Summary Trendelenburg positioning in combination with pneumoperitoneum during robotic‐assisted prostatic surgery possibly impairs cerebrovascular autoregulation. If autoregulation is disturbed, arterial hypertension might induce cerebral hyperaemia and brain oedema, while low blood pressure can ischaemia. The time course of was investigated use the position a for using transcranial Doppler ultrasound. Cerebral flow velocity correlated index (Mx) calculated. In 23 male patients, Mx assessed...

10.1111/anae.12477 article EN Anaesthesia 2013-11-20

Traumatic brain injury (TBI) is a major cause of death and disability. The underlying pathophysiology characterized by secondary processes including neuronal gliosis. To elucidate the role NG2 proteoglycan we investigated response NG2‐knockout mice (NG2‐KO) to TBI. Seven days after TBI behavioral analysis, damage volumetry assessment blood barrier integrity demonstrated an exacerbated NG2‐KO compared wild‐type (WT) mice. Reactive astrocytes expression reactive astrocyte neurotoxicity marker...

10.1002/glia.22944 article EN Glia 2015-12-06

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl N2O/O2; control) 2 (2.0 vol% O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals killed after 1, 3, 7, 28 days. In hematoxylin eosin-stained brain...

10.1213/01.ane.0000222634.51192.a4 article EN Anesthesia & Analgesia 2006-06-16

It is unclear whether a single, brief, 15-minute episode of background anesthesia already modulates delayed secondary processes after experimental brain injury. Therefore, this study was designed to characterize three protocols for their effect on molecular and histological endpoints. Mice were randomly separated into groups that received sevoflurane (sevo), isoflurane (iso) or an intraperitoneal anesthetic combination (midazolam, fentanyl medetomidine; comb) prior traumatic injury...

10.1371/journal.pone.0019948 article EN cc-by PLoS ONE 2011-05-19

J. Neurochem. (2009) 112 , 1015–1025. Abstract The role of the endothelial contractile apparatus in process brain edema formation after trauma is not characterized. Phosphorylation myosin light chains by chain kinases (MLCK) activates elements and results a rearrangement cytoskeleton. This may enhance post‐traumatic blood‐brain barrier dysfunction. In order to investigate MLCK on permeability injury, mice were anesthetized subjected controlled cortical impact (CCI). expression significantly...

10.1111/j.1471-4159.2009.06514.x article EN Journal of Neurochemistry 2009-11-28

To establish the molecular background for glucocorticoid insensitivity, that is, failure to reduce edema formation and protect blood-brain barrier integrity after acute traumatic brain injury.Controlled animal study.University research laboratory.Male C57Bl/6N mice.Mechanical lesion by controlled cortical impact.Our study demonstrates 1) proteasomal receptor degradation is established in endothelial cells injury as a form of posttranslational modification; 2) inhibition pathway with...

10.1097/ccm.0b013e31827ca494 article EN Critical Care Medicine 2013-03-08
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