Introduction: Carbon monoxide (CO) poisoning can cause serious neurological sequelae. However, there is neither effective treatment strategy nor reliable indicators to determine the prognosis of patients with CO poisoning. The present study aimed to observe the changes of neurological function score, disease severity score, cerebral oxygen utilization (OUCc), bispectral (BIS) index and neuron-specific enolase (NSE) concentration, and to elucidate the clinical significance of these potential indicators and the neuroprotective effect of mild hypothermia on brain injury in patients with severe acute CO poisoning.
View Article and Find Full Text PDFPurpose: 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.
Purpose: We aim to analyze the feasibility of external application of Xiao-Shuan-Santo prevent peripherally inserted central catheter (PICC) -related thrombosis.
Methods: A total of 218 patients with PICC catheterization were randomly divided into a control group (n = 103) and a treatment group (n = 115). Patients in the treatment group received additional external application of Xiao-Shuan-San.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
December 2017
Objective: To investigate the effects of N-butylphthalide (NBP) on cognitive function in acute severe carbon monoxide (CO) poisoning rats and its mechanism.
Methods: 120 health Sprague-Dawley (SD) rats were randomly divided into three groups (n = 40): normal control group (NC group), CO poisoning group (CO group) and NBP treatment group (NBP group). The acute severe CO poisoning model was established in a hyperbaric oxygen chamber by intoxicated with 1 000 ×10 CO for 40 minutes, followed with 3 000 ×10 CO for another 20 minutes, and then received hyperbaric oxygen therapy 1.
Basic Clin Pharmacol Toxicol
June 2017
Carbon monoxide (CO) poisoning is one of the leading causes of toxicity-related mortality and morbidity worldwide, primarily manifested by acute and delayed central nervous system (CNS) injuries and other organ damages. However, its definite pathogenesis is poorly understood. The aim of this study was to explore the pathogenesis of the ultrastructural and functional impairment of mitochondria and the protection of sulphoraphane (SFP) at different dosages on hippocampus neurons in rats after exposure to CO.
View Article and Find Full Text PDFCarbon monoxide (CO) poisoning is one of the most important health concerns and may result in neuropathologic changes and neurologic sequelae. However, few studies have addressed the correlation between CO poisoning and blood-brain barrier (BBB) impairment. In this study, we investigated the effects of -butylphthalide (NBP) on the expressions of zonula occludens-1 (ZO-1), claudin-5 and aquaporin-4 (AQP-4) proteins in a CO poisoning rat model.
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