Hemoglobin and cerebral hypoxic vasodilation in humans: Evidence for nitric oxide-dependent and <i>S</i>-nitrosothiol mediated signal transduction

Hoiland, Ryan L.; MacLeod, David B.; Stacey, Benjamin S.; Caldwell, Hannah G.; Howe, Connor A.; Nowak‐Flück, Daniela; Carr, Jay M J R; Tymko, Michael M.; Coombs, Geoff B.; Patrician, Alexander; Tremblay, Joshua C.; Mierlo, Michelle van; Gasho, Chris; Stembridge, Mike; Sekhon, Mypinder S.; Bailey, Damian Miles; Ainslie, Philip N.

doi:10.1177/0271678x231169579

Cited by 15 publications

(6 citation statements)

References 51 publications

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“…There is evidence that hypoxia-induced increases in cerebral blood flow are mediated by NO. 6 , 14 We found that in our experimental conditions, hypoxia-induced dilations of cortical arterioles in response to 10% inspired O 2 were unaffected by systemic NO synthase (NOS) blockade with N(ω)-nitro-L-arginine methyl ester (L-NAME) ( Figures 1 E and S2 ), which is consistent with the results of some human 15 and experimental animal studies. 16 However, blockade of cGMP signaling was reported to inhibit the cerebrovascular response to hypoxia, 17 and NO can also be produced by reduction of the nitrite anion (NO 2 − ), an alternative mechanism of NO generation by some heme- or molybdenum-cofactor-containing metalloproteins that can transfer an electron and facilitate proton donation.…”

Section: Resultssupporting

confidence: 90%

Astrocytes produce nitric oxide via nitrite reduction in mitochondria to regulate cerebral blood flow during brain hypoxia

Christie,

Theparambil,

Braga

et al. 2023

Cell Reports

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Section: Resultssupporting

confidence: 90%

Astrocytes produce nitric oxide via nitrite reduction in mitochondria to regulate cerebral blood flow during brain hypoxia

Christie,

Theparambil,

Braga

et al. 2023

Cell Reports

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“…Indeed, in hyperoxia [ 81 , 82 , 83 ], hypoxia [ 81 , 82 ], and hypercapnia [ 84 ], it was found to be an essential mediator of CBF in animal models. Moreover, NO also plays a leading role in coupling CBF and neuronal activity [ 85 ].…”

Section: Reactive Nitrogen Speciesmentioning

confidence: 99%

Oxidative Stress and Cerebral Vascular Tone: The Role of Reactive Oxygen and Nitrogen Species

Salvagno,

Sterchele,

Zaccarelli

et al. 2024

IJMS

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The brain’s unique characteristics make it exceptionally susceptible to oxidative stress, which arises from an imbalance between reactive oxygen species (ROS) production, reactive nitrogen species (RNS) production, and antioxidant defense mechanisms. This review explores the factors contributing to the brain’s vascular tone’s vulnerability in the presence of oxidative damage, which can be of clinical interest in critically ill patients or those presenting acute brain injuries. The brain’s high metabolic rate and inefficient electron transport chain in mitochondria lead to significant ROS generation. Moreover, non-replicating neuronal cells and low repair capacity increase susceptibility to oxidative insult. ROS can influence cerebral vascular tone and permeability, potentially impacting cerebral autoregulation. Different ROS species, including superoxide and hydrogen peroxide, exhibit vasodilatory or vasoconstrictive effects on cerebral blood vessels. RNS, particularly NO and peroxynitrite, also exert vasoactive effects. This review further investigates the neuroprotective effects of antioxidants, including superoxide dismutase (SOD), vitamin C, vitamin E, and the glutathione redox system. Various studies suggest that these antioxidants could be used as adjunct therapies to protect the cerebral vascular tone under conditions of high oxidative stress. Nevertheless, more extensive research is required to comprehensively grasp the relationship between oxidative stress and cerebrovascular tone, and explore the potential benefits of antioxidants as adjunctive therapies in critical illnesses and acute brain injuries.

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“…Vasodilatory peptides include NO and acetylcholine. Vasoconstrictive peptides include the neuropeptide Y and serotonin[ 51 , 52 ].…”

Section: Autoregulation Of Cbfmentioning

confidence: 99%

Future of neurocritical care: Integrating neurophysics, multimodal monitoring, and machine learning

Srichawla

2024

World J Crit Care Med

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Multimodal monitoring (MMM) in the intensive care unit (ICU) has become increasingly sophisticated with the integration of neurophysical principles. However, the challenge remains to select and interpret the most appropriate combination of neuromonitoring modalities to optimize patient outcomes. This manuscript reviewed current neuromonitoring tools, focusing on intracranial pressure, cerebral electrical activity, metabolism, and invasive and noninvasive autoregulation monitoring. In addition, the integration of advanced machine learning and data science tools within the ICU were discussed. Invasive monitoring includes analysis of intracranial pressure waveforms, jugular venous oximetry, monitoring of brain tissue oxygenation, thermal diffusion flowmetry, electrocorticography, depth electroencephalography, and cerebral microdialysis. Noninvasive measures include transcranial Doppler, tympanic membrane displacement, near-infrared spectroscopy, optic nerve sheath diameter, positron emission tomography, and systemic hemodynamic monitoring including heart rate variability analysis. The neurophysical basis and clinical relevance of each method within the ICU setting were examined. Machine learning algorithms have shown promise by helping to analyze and interpret data in real time from continuous MMM tools, helping clinicians make more accurate and timely decisions. These algorithms can integrate diverse data streams to generate predictive models for patient outcomes and optimize treatment strategies. MMM, grounded in neurophysics, offers a more nuanced understanding of cerebral physiology and disease in the ICU. Although each modality has its strengths and limitations, its integrated use, especially in combination with machine learning algorithms, can offer invaluable information for individualized patient care.

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Hemoglobin and cerebral hypoxic vasodilation in humans: Evidence for nitric oxide-dependent and S-nitrosothiol mediated signal transduction

Cited by 15 publications

References 51 publications

Astrocytes produce nitric oxide via nitrite reduction in mitochondria to regulate cerebral blood flow during brain hypoxia

Astrocytes produce nitric oxide via nitrite reduction in mitochondria to regulate cerebral blood flow during brain hypoxia

Oxidative Stress and Cerebral Vascular Tone: The Role of Reactive Oxygen and Nitrogen Species

Future of neurocritical care: Integrating neurophysics, multimodal monitoring, and machine learning

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