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Objective To study the role of inflammation in white matter damage of spontaneously hypertensive rats (SHRs) through observing the pathology changes of tissues after white matter damage and detecting the levels of inflammation-related indicators.Methods Eighteen 40-week-old male SHRs were chosen as experimental group,and seven male Wistar-Kyoto (WKY) rats were used as control group.The animal brain tissues were taken for hematoxylin-eosin staining (HE staining) and immunohistochemical staining to observe the pathological changes,and the levels of myelin basic protein (MBP),neurofilament (NF) and glial fibrillary acidic protein (GFAP).Real-time PCR was employed to detect toll-like receptor 4 (TLR-4),monocyte chemotactic protein 1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) expression levels in the white matter tissues.Results The white matter of 40-week-old SHRs was apparently injured.HE staining displayed sponge-like changes in the white matter and immunohistochemical staining showed astrocyte activation,reduced number of axonal and demyelination in the white matter.As compared with those in the WKY rats,TLR-4,MCP-1 and VCAM-1 mRNA expressions in SHR white matter were significantly increased (P＜0.05); and TLR-4,MCP-1 and VCAM-1 expression levels in SHRs were positively related to the degree of white matter damage.Conclusion The white matter damage in 40-week-old SHRs is similar to that of LA;inflammation is involved in the pathophysiological process of white matter damage,being one of induced factors of white matter injury.
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Objective To investigate the incidences of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) in patients with acute cerebral infarction (ACI) and explore the role of serum superoxide dismutase (SOD) content in ACI-induced SIRS and its progression to MODS. Methods Sixty-eight ACI patients were in hospital and outpatient at the Heze Municipal Hospital from Jan.2006 to Jun.2008, including 36 with uncomplicated ACI (SACI group), 32 with ACl-induced SIRS (SIRS group), and 24 with ACI-induced MODS (MODS group) were enrolled in this study, with 28 healthy individuals from the hospital as the normal control group. Xanthine oxidase method was used to measure the serum SOD content in these subjects. Results SACI induced SIRS and MODS in 88.9% and 66.7% of these patients, respectively; in the ACI patients with SIRS, 75.0% had concurrent MODS, while all the patients with MODS showed the presence of SIRS. The serum SOD contents in patients with SACI, SIRS, and MODS were significantly lower than those in the normal control group (P<0.05). Patients with SIRS and MODS had significantly lower serum SOD contents than the SACI patients (P<0.05), and the MODS patients had significantly lower levels than the SIRS patients (P<0.05). The serum SOD content was significantly lower in patients with severe MODS (with a score no less than 9) than in those with milder MODS (with a score below 9) (P<0.05), and also significantly lower in fatal MODS cases than in surviving MODS cases (P<0.05). Conclusion ACI may initially trigger the occurrence of SIRS and then lead to MODS, and the abnormalities in serum SOD content in patients with ACI-induced SIRS can be a possible mechanism of MODS following ACI. The serum SOD levels may help estimate the severity of ACI-induced SIRS and MODS, and may serve as an indicator for predicting the prognosis and outcomes of the patients.
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Objective: To establish a rat model of multiple organ dysfunction syndrome (MODS) by subarachnoid hemorrhage (SAH), and to explore the pathogenesis of MODS occured in acute cerebrovascular diseases (ACVD). Methods: Model of SAH was induced in rats by injecting arterial blood around the Willis' circle. 48 Wister rats were randomly divided into three groups: normal control group (n = 6), sham-operative group (n = 6) and SAH group (n = 36). The SAH group was further divided into 6 groups according to the time points of 4h, 12h, 24h, 36h, 48h and 72h after SAH, each group has six rats. Changes of temperature, heart rate and respiratory rate of the rats in each group were recorded, the amount of white blood cell (WBC) and biochemical criteria were assayed. Pathological changes of lung, liver, intestines and kidney were observed under optical microscope. Systemic inflammatory response syndrome (SIRS) and MODS were diagnosed by their criteria. Results: 1 There were no significant differences of temperature, heart rate, respiratory rate and the levels of WBC, ALT, AST, BUN, Cr and CK between normal control group and sham-operative group (P > 0.05). The rats of SAH group had obviously higher temperature, heart rate, respiratory rate, WBC, ALT, AST, BUN, Cr and CK than that of the normal control group and sham-operative group (P < 0.01), the changes were most obvious at 24-36 hour point. 2 The vital organs of the rats showed inflammatory injuries in varying degree at each time point after SAH, and peaked on 24-36 h, alleviated after 48 h, and last to 72 h after SAH. 3 The incidences of SIRS, MODS and mortality were 100% (36/36), 69.4% (25/36) and 38.9% (14/36) respectively in the SAH group. Conclusion: 1 An experimental animal model of MODS can be established successfully by injecting arterial blood around the Willis' circle in rats. 2 SAH can cause inflammatory changes in lung, liver, intestines, kidney as well as SIRS, and SIRS may be the pathological basal of MODS after SAH.