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Objective To investigate the protective effects of 3-n-butylphthalide (dl-NBP) on the cognitive dysfunction of chronic cerebral ischemic rats and its mechanism.Methods Old chronic cerebral ischemic rats (15 months) were modelized with ligating bilateral common carotid arteries for three months.Model rats were divided into four groups:sham,model,NBP 30 and 120 mg · kg-1 groups.The former and the latter two groups were administered vegetable oil and NBP for 45 days,respectively.Then,the cognitive function was measured in rats with Morris water maze.Meanwhile,the activities of superoxide dismutase (SOD),choline acetyltransferase (ChAT),true choline esterase (TChE),and the malondialdehyde (MDA) levels in brain cortex and hippocampus were detected with biochemical methods.Results During the five days of Morris water maze,the change of escape latency was from (57.7±3.8) s to (30.5±17.1) s in low dose of NBP group,and from (58.4±1.8) s to (28.9±11.3) s in high dose of NBP group as compared with no change from 60s to 60s in model group.Significant differences were found in escape latency between NBP's and model groups(P＜0.05 or 0.01).In spatial exploratory test,the time percentages spent in the platformquadrant were increased obviously in low and high doses of NBP [(26.0±6.9) ％ and (27.3±5.3) ％,respectively,P＜0.05],compared with that of model group.The SOD activity was obviously reduced in cortices of high dose of NBP group [(112.3 ± 7.6) U/mg protein] compared with that (134.6 ± 13.9) U/mg protein of model group (P＜0.01).The MDA contents were significantly reduced in cortices of low and high doses of NBP (2.39±0.31) nmol/mg protein and (1.56±0.19) nmol/mg protein,compared with that of model group (P＜0.01).The MDA contents in hippocampi of low and high doses of NBP [(0.71±0.10) nmol/mg protein and (0.83±0.05) nmol/mg protein] were also decreased significantly,compared with that of model group (P＜0.01).The ChAT level in cortex of high dose of NBP was increased significantly [(1615 ± 100) U/g protein,P＜0.05].The ChAT level in hippocampi of two doses of NBP also increased significantly [(1746±204) U/g protein and (1697± 117) U/g protein,P＜0.05].Conclusions NBP may improve cognition damage of chronic cerebral ischemic rats by ameliorating oxidative stress lesion and enhancing the activity of cholinergic nerve in brain tissue.
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Objective To explore association between the changes of myenteric nerve plexus and the delayed gastrointestinal transit in acute necrotic pancreatitis (ANP) rat complicated with hyperlipemia. Methods Atotal of 40 male Sprague-Dawley (SD) rats were randomly divided into 4 groups (normal control group, ANP group, hyperlipemia (HL) control group and HL with ANP group). HL rat model was established by fed with high-fat diet for 4 weeks, and ANP rat model was induced by retrograde injection of 3.5% sodium taurocholate into pancreatic duct. Gastrointestina1 transit distance was measured by ink gavage method. The histological changes of cholinergic and nitriergic nerves in myenteric plexus were observed by Karnovsky-Root method and NADPH histochemistry method. Results Pathological injuries were more severe in HL with ANP group than in ANP group (12.8±0.63 vs. 10.8±1.93,P<0.01), gastrointestinal transit was obviously delayed (transmission rate was 27%±5% vs. 38%±6%,P<0.01), the density of cholinergic neurons decreased (4.80±1.23 vs. 5.80±0.79, P<0.05), and the density of nitriergic neurons significantly increased (8.70±0.75 vs. 6.80±1.48, P<0.01). There was a linear regression between changes of cholinergic and nitrievgic nerves in myenteric nerve plexus and gastrointestinal transit (R2=0.531, P<0.01). Conclusion There was significant gastrointestinal motility disorder in the ANP rat complicated with hyperlipemia, which may be closely related with the changes of myenteric nerve plexus.
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Objective To investigate the relationship between white matter lesions (WML) within the cholinergic pathway and vascular cognitive impairment.Method Middle-aged and elderly stroke patients underwent brain MRI examination and Montreal Cognitive Assessment (MoCA).Cholinergic Pathways Hyperintensities Scale (CHIPS) scores and the overall WML burden by Schelten on fluidattenuated inversion recovery MRI images were determined and compared with MoCA scores.Spearman partial rank correlation coefficients and standardized regression coefficients were calculated.Results Thirty four patients were included ( mean age ( 62.2 ± 8.8 ) years, 45-82 years).MoCA scores negatively correlated with WML burdens by Schelten scores ( β = - 0.357, P = 0.042) and CHIPS scores ( β =-0.382,P=0.026).CHIPS scores were negatively associated with visuospatial and executive function (r = - 0.290, P = 0.048 ), naming function ( r = - 0.486, P = 0.002 ), attention ( r = - 0.311, P =0.037) and abstraction ( r = - 0.344, P = 0.023).Schelten scores were negatively associated with naming function (r = - 0.492, P = 0.002), attention ( r = - 0.364, P = 0.017) and abstraction ( r = - 0.390,P=0.011).Conclusion WML lesions within the cholinergic pathyway play a possible role in vascular cognitive impairment especially in visuospatial and executive function.
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Background: About 120 years ago, Roy and Sherrington hypothesized that the cerebral blood flow (CBF) is closely coupled to metabolism, and metabolism is closely coupled to function. This concept has colored all subsequent inquiries. However, recent studies have revealed a temporal and spatial mismatch between changes in CBF and metabolism. Objective: This article aims to reappraise the nature of functional hyperemia in response to somatosensory stimuli. Method: Firstly, the author discusses what is known and unknown about the control of CBF, reviewing the traditional concepts of autoregulation, neurogenic control, metabolic control and the role of endothelial cells. Secondly, recent papers showing a mismatch or uncoupling between function, metabolism and flow are considered. Thirdly, the reviewer uses his own published and unpublished data to point out the intrinsic and largely unrecognized limitations of spectroscopic techniques for evaluation of oxygen metabolism. Finally, a novel hypothesis is presented concerning the nature of functional hyperemia. Results and conclusion: The reviewer deduces that the initial flow increase in functional hyperemia is elicited by central neural systems, since it is reported that the central cholinergic pathway increases CBF immediately after the onset of somatosensory stimuli. The flow increase occurs concurrently with neuronal activation, but is much faster than the increase of neuronal metabolism. The novel hypothesis is proposed that functional hyperemia is biphasic: an initial flow increase under central neural control and a delayed increase is under traditional metabolic control. The metabolic phase may supply more blood than is needed, and may last even after discontinuation of the stimulation (overcompensation). These two phases of hyperemia are suggested to be well mixed, presumably in glial processes, which coordinate blood redistribution in the surrounding microvascular network. Many stimuli from the environment might be managed simply by the neurogenic control of functional hyperemia, without the metabolic change.
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With 58 of New Zeeland rabbits, following experiments were carried out: (1) the dose-response relationship of MSG which decreased the body temperat ure; (2) the effects of the propranolol and the anisodamine (654-2) on the action of decreasing body temperature by MSG. The results indicated: following intravenous administration of MSG at a dose of 0.5g/kg. w and 1.0g/kg. w, the body temperature of rabbits were decreased significantly, but at a dose of 0.1g/kg.w, the change of temperature was insignificant.Pretreatment with propranolol did not affect the effect of MSG decreasing body temperature which was blocked significantly by anisodamine, one of blocker of the cholinergic nerve. The authors suggest that the effect of MSG decreasing body temperature may depend on the cholinergic nerve.