Prognostic value of systemic immune-inflammation index and monocyte-to-HDL-cholesterol ratio in early cardio-cerebral complications in elderly patients with acute severe carbon monoxide poisoning.

To investigate how effectively systemic immune-inflammation index (SII) and Monocyte-to-HDL-cholesterol ratio (MHR) predict the development of early cardio-cerebral complications in elderly patients who have experienced acute severe carbon monoxide poisoning (ASCMP). A retrospective analysis was conducted on 77 elderly patients with ASCMP admitted to the emergency department of Harrison International Peace Hospital from November 2020 to March 2022. The prevalence of early-onset complications among the 77 individuals was 38.96%. Binary Logistics regression analysis showed that SII and MHR were independent influencing factors of early cardio-cerebral complications in elderly patients with ASCMP. The complication group had a longer length of stay, a greater mortality rate, and a higher incidence of delayed encephalopathy after acute carbon monoxide poisoning (p < .05) than the non-complication group. The area under the curve (AUC) of SII and MHR in predicting early cardio-cerebral complications in elderly patients with ASCMP were 0.724 and 0.796, respectively, with 80.0% and 63.3% sensitivity, and 61.7% and 87.2% specificity. The incidence of early cardio-cerebral complications in elderly patients who had ASCMP is high and the prognosis is poor. SII and MHR can be utilized as independent predictors of early cardio-cerebral complications in elderly patients with ASCMP, allowing doctors to diagnose and treat cardio-cerebral complications earlier and improve prognosis.

P2Y12 receptor-mediated microglia activation involved in delayed encephalopathy after acute carbon monoxide poisoning.

To investigate the role of P2Y12 receptor-mediated microglia activation in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), we used static inhalation carbon monoxide to build DEACMP rat model. DEACMP rats were randomly assigned into DEACMP group and intervention group. A control goup was also set. The rats in intervention group received intraperitoneal injection of 100uM suramin (a P2Y12 receptor antagonist). In control group, the escape latency, level of microglia activation and ATP content were similar between different time points. In both DEACMP group and intervention group, the escape latency, level of microglia activation and ATP content were significanlty increased at 21th and 28th day. The hippocampal cells in DEACMP group and intervention group were severely and moderately, respectively, damaged at 21th and 28th day. Meanwhile, compared to control group, both DEACMP group and intervention group had significanlty longer escape latency, higher level of microglia activation and ATP content at 21th and 28th day. Compared to DEACMP group, the intervention group had significantly shorter escape latency and lower level of microglia activation at 21th and 28th day. These results suggested that the microglia activation regulated by ATP through P2Y12 receptor pathway might be closely related to the development of DEACMP.

Microglia and Macrophages in the Pathological Central and Peripheral Nervous Systems.

Microglia, the immunocompetent cells in the central nervous system (CNS), have long been studied as pathologically deteriorating players in various CNS diseases. However, microglia exert ameliorating neuroprotective effects, which prompted us to reconsider their roles in CNS and peripheral nervous system (PNS) pathophysiology. Moreover, recent findings showed that microglia play critical roles even in the healthy CNS. The microglial functions that normally contribute to the maintenance of homeostasis in the CNS are modified by other cells, such as astrocytes and infiltrated myeloid cells; thus, the microglial actions on neurons are extremely complex. For a deeper understanding of the pathophysiology of various diseases, including those of the PNS, it is important to understand microglial functioning. In this review, we discuss both the favorable and unfavorable roles of microglia in neuronal survival in various CNS and PNS disorders. We also discuss the roles of blood-borne macrophages in the pathogenesis of CNS and PNS injuries because they cooperatively modify the pathological processes of resident microglia. Finally, metabolic changes in glycolysis and oxidative phosphorylation, with special reference to the pro-/anti-inflammatory activation of microglia, are intensively addressed, because they are profoundly correlated with the generation of reactive oxygen species and changes in pro-/anti-inflammatory phenotypes.

[Delayed neurological syndrome following carbon monoxide poisoning]. / Síndrome neurológico tardío tras intoxicación por monóxido de carbon.

INTRODUCTION: Poisoning by carbon monoxide is the most frequent form of intoxication in our milieu as a result of exposure to poisonous gases. The effects of carbon monoxide poisoning are not limited to acute exposure, since, following apparent recovery from the acute intoxication, neurological or behavioural disorders may appear. PATIENTS AND METHODS: A study was conducted to examine the cases of carbon monoxide poisoning that had occurred in a healthcare area of 80,000 inhabitants over a 10-year period. These patients were then submitted to a follow-up to appraise the appearance of delayed neurological syndrome (DNS) and its relationship with different variables in the initial exposure to the carbon monoxide, in the treatment that was administered or in the severity of the intoxication. RESULTS AND CONCLUSIONS: It was observed that around 9.1% of those intoxicated by carbon dioxide detected within the healthcare district of Salnés went on to develop DNS, which is more frequent in patients with severe analytical criteria and very unlikely in those who do not have them. Patients with DNS did not express any clinical or analytical manifestations that differed from those who did not have the syndrome; no differences were observed in relation to the oxygen therapy that was administered. The rate of DNS within the healthcare district of Salnés between 2002 and 2012 is 0.84 cases per 100,000 inhabitants per year.

TITLE: Sindrome neurologico tardio tras intoxicacion por monoxido de carbono.Introduccion. La intoxicacion por monoxido de carbono es la mas frecuente en nuestro medio a consecuencia de la exposicion a gases toxicos. Los efectos de la intoxicacion por monoxido de carbono no se limitan a la exposicion aguda porque, tras la aparente recuperacion de la intoxicacion, pueden aparecer alteraciones neurologicas o del comportamiento. Pacientes y metodos. Se realizo un estudio de las intoxicaciones por monoxido de carbono en un area sanitaria de 80.000 habitantes durante un periodo de 10 años. Posteriormente se hizo un seguimiento de estos pacientes y se valoro la aparicion de sindrome neurologico tardio (SNT) y su relacion con diferentes variables en la exposicion inicial al monoxido de carbono, en el tratamiento administrado o en la gravedad de la intoxicacion. Resultados y conclusiones. Se observo que el 9,1% de los intoxicados por monoxido de carbono detectados en el area sanitaria de Salnes desarrollan el SNT, que es mas frecuente en los pacientes con criterios analiticos de gravedad y muy poco probable en los que no los tienen. Los pacientes con SNT no expresaron manifestaciones clinicas ni analiticas diferentes a los que no presentaron el sindrome; tampoco se observaron diferencias en relacion con la terapia con oxigeno administrada. La tasa de SNT en el area sanitaria de Salnes entre 2002 y 2012 es de 0,84 casos por 100.000 habitantes y año.

Hydrogen rich saline reduces immune-mediated brain injury in rats with acute carbon monoxide poisoning.

OBJECTIVES: This experiment was designed to determine whether hydrogen (H(2)) rich saline can ameliorate brain abnormalities in a rat model with acute carbon monoxide (CO) poisoning. METHODS: Sprague-Dawley male rats were used for CO poisoning and H(2) rich saline treatment. Changes in neurons, microglias, and myelin sheath were observed by electron microscope. Neuron loss was assessed by Nissl staining. Antioxidant capacities were evaluated by studying superoxide dismutase activities and malondialdehyde concentration in the brain and serum. Infiltration of macrophages, expression of immune-associated cytokines (MIP-1-alpha and ICAM-1), and changes in myelin basic protein (MBP) were monitored by immunohistochemical staining and western blotting. RESULTS: CO-exposed rats showed the increase in neuron loss and the decrease in antioxidant capacities. And H(2) rich saline given after CO poisoning can prevent the alterations mentioned above. CO-mediated oxidative stress caused alterations in MBP, which initiated an adaptive immunological response that led to brain injury. MBP from H(2) rich saline-treated, CO-exposed rats was recognized normally by immunohistochemical staining and western blotting. Electron microscope observation from CO-exposed rats showed an apparent aggregation of microglias. Macrophages from CO-exposed rats were significantly more than those from H(2) rich saline-treated and control rats, and the immunofluorescence observation showed that macrophages were similar to microglias in type. Expression levels of MIP-1-alpha and ICAM-1 increased in the brains of CO-poisoned rats and H(2) rich saline treatment decreased the levels. DISCUSSION: The results indicate that H(2) rich saline prevents immune-mediated brain injury after CO poisoning.

Effects of immune reaction in rats after acute carbon monoxide poisoning.

This study is designed to observe the immune reaction in rats after acute carbon monoxide (CO) poisoning. We observed brain injury, cognitive impairment, a variety of microglias and expression of immune factors, including major histocompatibility complex II (MHCII), CD4, vascular cell adhesion molecule-1 (VCAM-1) and interferon-gamma (IFN-gamma) in the brain tissues of CO-poisoned rats. Then relationships between cognitive impairment and immune factors were explored. We found that there were extensive neuronal degeneration and necrosis in the brains of CO-poisoned rats, and the escape latency of the CO Group in a Morris water maze became significantly longer than that of the Control Group (11.63 +/- 3.54s vs. 7.06 +/- 3.13s, p < 0.05) after six days of CO poisoning. Microglias, as immune effector cells, underwent activation and proliferation which reached 35.0 +/- 5.7 cells per five high-power fields (HPF) in the seventh day after CO poisoning, but 20.3 +/- 2.9 cells/5HPF in the Control Group (p < 0.05). Expression levels of immune factors increased in the brains of CO-poisoned rats. VCAM-1-positive cells peaked in quantity the first day, IFN-gamma-positive cells and MHCII-positive cells the third day and CD4-positive cells the seventh day. The results indicate that immune reaction plays an important role on CO-mediated neuropathology.

Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity.

The goal of this investigation was to determine whether exposure to hyperbaric oxygen (HBO(2)) would ameliorate biochemical and functional brain abnormalities in an animal model of carbon monoxide (CO) poisoning. In this model, CO-mediated oxidative stress causes chemical alterations in myelin basic protein (MBP), which initiates an adaptive immunological response that leads to a functional deficit. CO-exposed rats do not show improvements in task performance in a radial maze. We found that HBO(2) given after CO poisoning will prevent this deficit, but not eliminate all of the CO-mediated biochemical alterations in MBP. MBP from HBO(2) treated CO-exposed rats is recognized normally by a battery of antibodies, but exhibits an abnormal charge pattern. Lymphocytes from HBO(2)-treated and control rats do not become activated when incubated with MBP, immunohistological evidence of microglial activation is not apparent, and functional deficits did not occur, unlike untreated CO-exposed rats. The results indicate that HBO(2) prevents immune-mediated delayed neurological dysfunction following CO poisoning.

Delayed neuropathology after carbon monoxide poisoning is immune-mediated.

The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP.

[The changes of soluble interleukin-2 receptor in serum and cerebrospinal fluid of patients with delayed encephalopathy after acute carbon monoxide poisoning].

OBJECTIVE: To explore the changes of soluble interleukin-2 receptor(sIL-2R) in serum and cerebrospinal fluid (CSF) of patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). METHODS: There were 31 patients with DEACMP, 32 patients with other encephalopathy and 31 controls in this study. The levels of sIL-2R in serum and CSF were detected by ELISA. RESULTS: Serum sIL-2R in patients with DEACMP[(329.21 +/- 160.99)U/ml] was significantly higher than that in control[(115.67 +/- 89.58) U/ml, P < 0.05)], but not significantly different from that in the other encephalopathy group[(367.50 +/- 123.14) U/ml, P > 0.05)]. CSF sIL-2R in patients with DEACMP[(54.48 +/- 43.04) U/ml] measured a little before discharge was significantly lower than that in patients with the other encephalopathy[(110.24 +/- 76.56) U/ml, P < 0.05)], but not significantly different from that in the control group[(34.96 +/- 22.70)U/ml, P > 0.05)]. At the pre-discharged period, CSF sIL-2R in patients with DEACMP[(100.26 +/- 93.65) U/ml] was significantly higher than that at the early stage of hospitalization[(52.28 +/- 43.31) U/ml, P < 0.05)]. No significant difference in serum sIL-2R was found between early stage of hospitalization[(338.34 +/- 161.53) U/ml] and pre-discharge [(351.31 +/- 175.93) U/ml, P > 0.05)]. CONCLUSION: The occurrence of DEACMP may be related with immunopathological damage. The sIL-2R levels in serum and CSF may give information about the state of immunological function of the patients with DEACMP and may contribute to determining the patient's condition and prognosis.