ABSTRACT
Objective:To observe the relationship between inducible carbon monoxide synthase (iNOS) and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and explore its mechanism of action in DEACMP.Methods:This study was designed as prospective cohort study. Patients with acute carbon monoxide poisoning who met the diagnostic criteria and were admitted to Emergency Intensive Care Unit(EICU) of our hospital from June 2019 to June 2021 were selected as subjects. Patients were divided into the DEACMP group and non-DEACMP group according to the occurrence of DEACMP. Serum samples were collected on the first 24 h after admission and on day 7 and 14 after admission, and the serum nitric oxide (NO), neuronal nitric oxide synthase (nNOS), inducible carbon monoxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) level were measured by enzyme-linked immunosorbent assay. The generalized estimating equation was used to estimate the difference of NO, nNOS, iNOS and eNOS between DEACMP and non-DEACMP patients.Results:A total of 78 patients with carbon monoxide poisoning were included in our study finally, including 49 (62.82%) males and 29 (37.18%) females, with an average age of (53.96±14.95) years, 20 (25.64%) patients with DEACMP, and 1 (1.28%) death. Univariate analysis showed that patients with DEACMP had an average increase of 3 h (95% CI: 1.00, 5.00) in carbon monoxide exposure time and a 5-point decrease in GCS score (95% CI: 1.00, 6.00) than the patients without DEACMP, and the proportion of patients with severe carbon monoxide poisoning in the DEACMP group was higher than that of the non-DEACMP group (90.00% vs. 32.76%). According to the analysis of generalized estimation equation, on day 7 and 14 after admission, Compared with non-DEACMP patients, neither by performing unadjusted nor adjusted analysis with the iNOS of DEACMP patients was significantly higher than that in non-DEACMP patients regardless of whether exposure time, GCS score, coma time or severity of carbon monoxide poisoning were adjusted or not ( P <0.01 or P <0.05). Except for the level of nNOS in the GEE model adjusted with carbon monoxide exposure time, the levels of NO, nNOS and eNOS showed no significant difference between DEACMP and non-DEACMP patients ( P >0.05). Conclusions:The expression of iNOS level is increased in DEACMP patients, and its continuous expression may be involved in the pathogenesis of DEACMP.
ABSTRACT
Objective:To explore the effect of different hemoperfusion times on the recovery of serum cholinesterase (ChE) in patients with severe acute oral organophosphorus pesticide poisoning (AOPP).Methods:This was a retrospective case-control study. Patients with severe AOPP admitted to our hospital were identified between January 2010 and December 2019. The clinical information of patients with severe AOPP was collected between January 2010 and December 2019, the patient's ChE vitality levels were collected on admission, at 1, 3 and 5 days after admission, and the sex, age, oral poison volume, and related treatments were recorded as well. The relationship between ChE, different HP treatment times and patients without HP treatment was analyzed by generalized estimation equations and multiple comparisons afterward.Results:A total of 159 patients with severe AOPP were included in our study. Among them, 60 (37.74%) patients were male and 99 (62.26%) were female, with a median age of 33 years old (range 13-75 years old). The median oral dose of OPs was 75 mL (range 15-500 mL). Multivariate analysis results showed that in the unadjusted generalized estimation equation, compared with patients without HP treatment, the average ChE value of patients with single HP treatment was 745.6 U/L higher (95% CI: 467.09 - 1024.1; P<0.01), the average ChE value of patients with 2 times HP treatment was 565.81 U/L higher (95% CI: 384.25-747.36; P<0.01), and the average ChE value of patients with 3 times HP treatment was 43.86 U/L higher (95% CI: 420.71-1 067.01; P<0.01), the differences were all statistically significant. After adjusting the amount of oral OPs at admission, age and PSS score in the multiple generalized estimation equations, the results showed that whatever single HP treatment or multiple HP treatment, the recovery rate of ChE was significantly faster than those without HP treatment. And the multiple comparison results of multiple models showed that the difference between 3 times HP treatment and 1 to 2 times HP treatment was not statistically significant, and the average difference between 2 times HP treatment and single HP treatment was also not statistically significant. Conclusions:Hemoperfusion therapy can accelerate the recovery rate of ChE in AOPP patients; Whatever single HP treatment or multiple HP treatments, the recovery rate of ChE in AOPP patients has no significant difference.
ABSTRACT
Objective To investigate the potential effect of glucagon-like peptide-1 (GLP-1) analogue exendin-4 (Ex-4) on immune function of T lymphocytes via neuroendocrine modulation mechanism in mice following severe burns.Methods Male BALB/C mice were randomly (ramdam number) divided into thermal injury group (n =50) and sham-thermal group (n =30).The thermal injury model was made by exposing the back skin of 15％ total body surface area (TBSA) to 95 ℃ water for 7 seconds,while in sham-thermal model the mice were immersed in 37 ℃ water instead.The expression of GLP-1 receptor (GLP-1 R) was determined in sorted CM + T cells from normal mice by immunofluorescence method.In ex vivo experiment,the mice were sacrificed at 24 h post-bum,then the mononuclear cells (MNC) from spleen were separated from both groups and cultured in RMPI 1640 with 10％ FCS (fetal calf serum) in presence of ConA (concanavalin A,5 μg/mL).Cells were pretreated with catecholamine receptor antagonist propranolol (prop) for 1 hour,followed by consecutive dose of Ex-4 for another 48 h.In in vivo experiment,prop (30 mg/kg) was i.p.injected 30 minutes before thermal injury,then Ex-4 (2.4 nmol/kg) was injected i.p.immediately after scalding.Mice were sacrificed at 6 h and 24 h after thermal injury,then the serum and the spleens were collected.Results GLP-1R was expressed on splenic CD4 + T cells from normal micc.Ex-4 exerted no marked effect on the functions of T cells in terms of proliferation and IL-2 secretion at all doses examined ex vivo,which was not affected by pretreatment with prop.In vivo,T cell functions were suppressed by Ex-4 in thermal mice (P ＜ 0.05),but was restored by pretreatment with prop.Regardless of ex vivo or in vivo,Ex-4 could induce T cells switched to Th2 response (P ＜ 0.05).Moreover,the Th2 switch by Ex-4 was greatly potentiated by prop intervention in thermal mice in vivo other than ex vivo.Norepinephrine level was increased and epinephrine was decreased by Ex-4 in thermal mice.Both norepinephrine and epinephrine levels were obviously enhanced by pretreatment with prop.Conclusions Ex-4 can inhibit the proliferation and IL-2 secretion of splenic T lymphocytes through the sympathetic nervous system,however,it might induce Th2 switch from Th cells by acting directly on GLP-1R.