Change and significance of serum levels of CRH, NOS and 5-HT in acute carbon monoxide poisoning patients with delayed encephalopathy
10.3760/cma.j.issn.1671-7368.2013.12.018
- VernacularTitle:急性一氧化碳中毒迟发性脑病患者血清肾上腺皮质激素释放激素、一氧化氮合成酶及5-羟色胺水平变化及意义
- Author:
Weilin LI
- Publication Type:Journal Article
- Keywords:
Carbon monoxide poisoning;
Hypoxia,brain
- From:
Chinese Journal of General Practitioners
2013;12(12):988-990
- CountryChina
- Language:Chinese
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Abstract:
To explore the change and significance of serum levels of corticotropin releasing hormone (CRH),nitric oxide synthase (NOS) and 5-hydroxytryptamine (5-HT) in the pathogenesis of acute carbon monoxide poisoning delayed encephalopathy (DEACMP).The groups of DEACMP (n =42),acute carbon monoxide poisoning (ACOP) (n =40) and normal control (n =40) were selected.The peripheral blood levels of CRH,NOS and 5-HT were measured for acute and convalescent phases of three groups.Information-memory-concentration test (IMCT),activities of daily living (ADL) and Hasegawa's dementia scale (HDS) were used to evaluate the intelligent state of acute and convalescent phases.When DEACMP and ACOP groups in acute phase were compared with normal control group,the serum levels of CRH and NOS significantly increased while the serum level of 5-HT decreased markedly (P ＜ 0.05).And statistically significant difference existed between DEACMP and ACOP groups (P ＜ 0.05).After treatment,the serum levels of CRH and NOS significantly decreased while the serum level of 5-HT increased markedly in DEACMP and ACOP groups in convalescent phase (P ＜ 0.05).The IMCT and HDS scores of acute phase DEACMP group were significantly lower than those of ACOP group while ADL was significantly higher (P ＜0.05).After treatment,the scores of IMCT and HDS increased and ADL decreased in DEACMP group in convalescence (P ＜ 0.05).CRH was correlated positively with NOS (P ＜ 0.05) and negatively with 5-HT (P ＜ 0.05).Hypothalamic-pituitary-adrenal cortical axis,NO-NOS system and the presence of 5-HT may be related with the pathogenesis of DEACMP.
