Purpose. The aim of the present study was to analyze the clinical characteristics of visual dysfunction in patients with carbon monoxide (CO) poisoning. Methods. A total of 436 patients with CO poisoning were enrolled in our hospital from October 2012 to December 2018, including 193 patients with moderate poisoning (MP group), 165 with severe poisoning (SP group), and 78 with delayed encephalopathy (DE group). The clinical characteristics of visual dysfunction in patients with CO poisoning were analyzed through the collection of medical history, regular physical examination, brain magnetic resonance imaging (MRI), ophthalmological examination, the National Eye Institute Visual Function Questionnaire (NEI-VFQ), and its influencing factors. Results. Some patients in the three groups had visual dysfunction. The main ocular symptoms were local pain, eye movement disorder, and visual field defect. The key pathological factors were keratopathy, retinal nerve cell damage, optic nerve damage, retinal vascular disease, macular disease, and occipital visual center damage. The clinical symptoms of visual dysfunction after CO poisoning lasted for a long time (>12 months) and were not completely consistent with the positive results of the ophthalmological examination. A few sequelae of ophthalmology were still left after the help of medicine. Conclusion. The incidence of visual dysfunction in patients with CO poisoning was high, the clinical symptoms were rich and diverse, the duration of disease was long, and the prognosis was poor. Thus, the relevant ophthalmological examination and intervention treatment should be perfected as soon as possible.

Oxidative stress has been considered as an important cause of neurocyte damage induced by carbon monoxide (CO) poisoning; however, the precise mechanisms are not fully understood. The study aimed to elucidate the molecular mechanism and the neuroprotective effect of targeted regulatory nuclear factor erythroid2‐related factor 2 (Nrf2) gene on acute brain injury in CO poisoning rats. An acute CO poisoning rat model was established by CO inhalation in hyperbaric oxygen chamber and followed by the administration of Nrf2 gene‐loaded lentivirus. Mitochondrial membrane potential (ΔΨM), the levels of Nrf2, glutamate‐cysteine ligase catalytic subunit (GCLC), catalase (CAT) and glutathione peroxidase (GSH‐Px), and cell apoptosis were determined in brain tissue in rats. We found that CO poisoning could decrease ΔΨm of cells, slightly increase the expressions of Nrf2 and GCLC at mRNA and protein levels, reduce CAT and GSH‐Px, and thus initiate apoptosis process. The Nrf2 gene treatment could obviously enhance the expressions of Nrf2 at mRNA and protein levels, and increase the concentrations of CAT and GSH‐Px, maintain the ΔΨm of cells in brain tissue, significantly inhibit cell apoptosis as compared with the CO poisoning group (p < .05). These findings suggest that CO poisoning could induce oxidative stress and impair mitochondrial function of cells in brain tissue. The administration of Nrf2 gene could notably strengthen the antioxidant capacity of cells through regulating the downstream genes of Nrf2/antioxidant responsive element signal pathway, and positively protect cells against brain injury induced by acute severe CO poisoning.

The pathogenesis of brain injury caused by carbon monoxide poisoning (COP) is very complex, and there is no exact and reliable treatment in clinic. In the present study, we screened the therapeutic target and related signal pathway of Salvia Miltiorrhiza for acute COP brain injury, and clarified the pharmacological mechanism of multicomponent, multitarget, and multisignal pathway in Salvia Miltiorrhiza by network pharmacology. To further verify the therapeutic effect of Salvia Miltiorrhiza on acute brain injury based on the results of network analysis, a total of 216 male healthy Sprague Dawley rats were collected in the present study and randomly assigned to a normal control group, a COP group and a Tanshinone IIA sulfonate treatment group (72 rats in each group). The rat model of acute severe COP was established by the secondary inhalation in a hyperbaric oxygen chamber. We found that Salvia Miltiorrhiza had multiple active components, and played a role in treating acute brain injury induced by COP through multiple targets and multiple pathways, among them, MAPK/ERK1/2 signaling pathway was one of the most important. COP can start apoptosis process, activate the MAPK/ERK1/2 signaling pathway, and promote the expression of VEGF‐A protein and the formation of brain edema. Tanshinone IIA can effectively inhibit apoptosis, up‐regulate the expressions of VEGF‐A, P‐MEK1/2 and P‐ERK1/2 proteins, thereby protect endothelial cells, promote angiogenesis and microcirculation, and finally alleviate brain edema.