Study: Brain injuries can cause gut problems

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This study is in the process of publication. It shows that brain

injury can *cause* gut problems where there weren't any before. Makes

sense since the gut-brain connection is a two-way street. Gut

problems can result in behavior/thinking irregularities...and brain

differences can result in gut problems. Just I haven't seen it

spelled out and tested in this way.

.

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World J Gastroenterol. 2003 Dec;9(12):2776-81. Related Articles,

Links

Alterations of intestinal mucosa structure and barrier function

following traumatic brain injury in rats.

Hang CH, Shi JX, Li JS, Wu W, Yin HX.

Department of Neurosurgery, Jinling Hospital, 305 East Zhongshan

Road, Nanjing 210002, Jiangsu Province, China.

AIM: Gastrointestinal dysfunction is a common complication in

patients with traumatic brain injury (TBI). However, the effect of

traumatic brain injury on intestinal mucosa has not been studied

previously. The aim of the current study was to explore the

alterations of intestinal mucosa morphology and barrier function, and

to determine how rapidly the impairment of gut barrier function

occurs and how long it persists following traumatic brain injury.

METHODS: Male Wistar rats were randomly divided into six groups (6

rats each group) including controls without brain injury and

traumatic brain injury groups at hours 3, 12, 24, and 72, and on day

7. The intestinal mucosa structure was detected by histopathological

examination and electron microscopy. Gut barrier dysfunction was

evaluated by detecting serum endotoxin and intestinal permeability.

The level of serum endotoxin and intestinal permeability was measured

by using chromogenic limulus amebocyte lysate and lactulose/mannitol

(L/M) ratio, respectively.

RESULTS: After traumatic brain injury, the histopathological

alterations of gut mucosa occurred rapidly as early as 3 hours and

progressed to a serious state, including shedding of epithelial

cells, fracture of villi, focal ulcer, fusion of adjacent villi,

dilation of central chyle duct, mucosal atrophy, and vascular

dilation, congestion and edema in the villous interstitium and lamina

propria. Apoptosis of epithelial cells, fracture and sparseness of

microvilli, loss of tight junction between enterocytes, damage of

mitochondria and endoplasm, were found by electron microscopy. The

villous height, crypt depth and surface area in jejunum decreased

progressively with the time of brain injury. As compared with that of

control group (183.7+/-41.8 EU/L), serum endotoxin level was

significantly increased at 3, 12, and 24 hours following TBI (434.8+/-

54.9 EU/L, 324.2+/-61.7 EU/L and 303.3+/-60.2 EU/L, respectively),

and peaked at 72 hours (560.5+/-76.2 EU/L), then declined on day 7

(306.7+/-62.4 EU/L, P<0.01). Two peaks of serum endotoxin level were

found at hours 3 and 72 following TBI. L/M ratio was also

significantly higher in TBI groups than that in control group

(control, 0.0172+/-0.0009; 12 h, 0.0303+/-0.0013; 24 h, 0.0354+/-

0.0025; 72 h, 0.0736+/-0.0105; 7 d, 0.0588+/-0.0083; P<0.01).

CONCLUSION: Traumatic brain injury can induce significant damages of

gut structure and impairment of barrier function which occur rapidly

as early as 3 hours following brain injury and lasts for more than 7

days with marked mucosal atrophy.

PMID: 14669332 [PubMed - in process]