The role of nitrous oxide in stroke

Abstract

Stroke that is caused by poor blood flow into the brain results in cell death, including ischemia stroke due to lack of blood into brain tissue, and hemorrhage due to bleeding. Both of them will give rise to the dysfunction of brain. In general, the signs and symptoms of stroke are the inability of feeling or moving on one side of body, sometimes loss of vision to one side. Above symptoms will appear soon after the stroke has happened. If the symptoms and signs happen in 1 or 2 hours, we often call them as transient ischemic attack. Moreover, hemorrhagic stroke often leads to severe headache. It is known that neuronal death can happen after stroke, and it depends upon the activation of N-methyl-D-aspartate (NMDA) excitatory glutamate receptor which is the goal for a lot of neuroprotective agents. Nitrous oxide was discovered by Joseph Priestley in 1772, and then he and his friends, including the poet Coleridge and Robert Sauce, experimented with the gas. They found this gas could make patients loss the sense of pain and still maintain consciousness after inhalation. Shortly the gas was used as an anesthetic, especially in the field of dentists. Now, accroding to theme of Helene N. David and other scientists, both of nitrous oxide at 75 vol% and xenon at 50 vol% could reduce ischemic neuronal death in the cortex by 70% and decrease NMDA-induced Ca2+ influx by 30%. Therefore, more clinical and experimental studies are important to illuminate the mechanisms of how nitrous oxide protects brain tissue and to explore the best protocol of this gas in stroke treatment.

Quantitative mass spectrometric analysis of the mouse cerebral cortex after ischemic stroke

“…Amongst down-regulated proteins, Nos1 produces nitric oxide (NO) in the brain, a molecule associated with both neurotoxic and neuroprotective abilities in stroke [20,21]. Though the true functional roles of these proteins have not been elucidated herein, future experiments may aim to explore their PAR-dependent roles in stroke and/or parthanatos.…”

Dysregulation of Serum MicroRNA after Intracerebral Hemorrhage in Aged Mice

“…ICH often causes severe brain damage that is categorized into primary and secondary brain injuries. The mass effect of the hematoma mostly contributes to primary brain damage, whereas the oxidative and inflammatory signaling pathways [ 7 , 8 ], induced by blood components such as thrombin, hemoglobin, hemin, and iron, are responsible for secondary brain damage [ 9 , 10 ]. In contrast to primary brain damage, secondary brain damage persists for a longer period of time, which could contribute to both acute and long-term neurological outcomes [ 11 ].…”

Effect of nitrous oxide on clinical outcome in patients undergoing cerebellopontine tumor surgery under sevoflurane anesthesia: a randomized controlled trial

“…N 2 O as an anesthetic agent has both advantages and disadvantages. 2 Major concerns with its use include its short duration of action, ability to expand air-filled spaces, postoperative nausea and vomiting (PONV), 3 bone marrow depression, 4 demyelination, 5 neuronal degeneration, 6 and neurotoxicity, 7 subacute combined degeneration of the spinal cord, 8 postoperative myocardial ischemia 9 and health risks to operating room personnel. 10 It also increases cerebral blood flow and cerebral metabolic rate, impairs cerebral autoregulation, and may increase intracranial pressure (ICP), 11 thus making its use in neurosurgical procedures further questionable.…”