ORCID Profile
0000-0001-5794-3307
Current Organisation
UCL Institute of Ophthalmology, University College London
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Publisher: Wiley
Date: 24-01-2022
Abstract: Blue light (~400‐470 nm) is considered potentially detrimental to the retina but is present in natural environmental light. Mitochondrial density is highest in the retina, and they exhibit a prominent optical absorption around 420 nm arising from the Soret band of their porphyrins, including in cytochrome‐c‐oxidase in their respiratory chain. We examine the impact of continuous 420 nm at environmental energy levels on retinal mitochondrial metabolism and haemodynamics in vivo in real time using broadband near‐infrared spectroscopy. One hour environmental exposure to 420 nm induces significant metabolic instability in retinal mitochondria and blood signals, which continues for up to 1 h post blue exposure. Porphyrins are important in mitochondrial adenosine triphosphate (ATP) production and cytochrome‐c‐oxidase is a key part of the electron transport chain through which this is achieved. Hence, environmental 420 nm likely restricts respiration and ATP production that may impact on retinal function.
Publisher: S. Karger AG
Date: 2017
DOI: 10.1159/000458438
Abstract: The selective α sub /sub -adrenoreceptor agonist dexmedetomidine has shown neuroprotective, analgesic, anti-inflammatory, and sympatholytic properties that may be beneficial in neonatal encephalopathy (NE). As therapeutic hypothermia is only partially effective, adjunct therapies are needed to optimize outcomes. The aim was to assess whether hypothermia + dexmedetomidine treatment augments neuroprotection compared to routine treatment (hypothermia + fentanyl sedation) in a piglet model of NE using magnetic resonance spectroscopy (MRS) biomarkers, which predict outcomes in babies with NE, and immunohistochemistry. After hypoxia-ischaemia (HI), 20 large White male piglets were randomized to: (i) hypothermia + fentanyl with cooling to 33.5°C from 2 to 26 h, or (ii) hypothermia + dexmedetomidine (a loading dose of 2 μg/kg at 10 min followed by 0.028 μg/kg/h for 48 h). Whole-brain phosphorus-31 and regional proton MRS biomarkers were assessed at baseline, 24, and 48 h after HI. At 48 h, cell death was evaluated over 7 brain regions by means of transferase-mediated d-UTP nick end labeling (TUNEL). Dexmedetomidine plasma levels were mainly within the target sedative range of 1 μg/L. In the hypothermia + dexmedetomidine group, there were 6 cardiac arrests (3 fatal) versus 2 (non-fatal) in the hypothermia + fentanyl group. The hypothermia + dexmedetomidine group required more saline ( i /i = 0.005) to maintain blood pressure. Thalamic and white-matter lactate/N-acetylaspartate did not differ between groups ( i /i = 0.66 and i /i = 0.21, respectively) the whole-brain nucleotide triphosphate/exchangeable phosphate pool was similar ( i /i = 0.73) over 48 h. Cell death (TUNEL-positive cells/mm sup /sup ) was higher in the hypothermia + dexmedetomidine group than in the hypothermia + fentanyl group (mean 5.1 vs. 2.3, difference 2.8 [95% CI 0.6-4.9], i /i = 0.036). Hypothermia + dexmedetomidine treatment was associated with adverse cardiovascular events, even within the recommended clinical sedative plasma level these may have been exacerbated by an interaction with either isoflurane or low body temperature. Hypothermia + dexmedetomidine treatment was neurotoxic following HI in our piglet NE model, suggesting that caution is vital if dexmedetomidine is combined with cooling following NE.
Location: No location found
Location: Iran (Islamic Republic of)
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Pardis Kaynezhad.