ABSTRACT
0.05);After one month,thrombus could not be seen in the ovaries of all four groups.No injury could be seen in all kinds of cells in the four groups. Conclusion:Rabbit ovarian angiogenesis was not affected by low power ultrasound.
ABSTRACT
Objectives: The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly 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, 72 and days 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 were 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, and damage of mitochondria and endoplasm were found by electron microscope. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. The level of serum endotoxin and L/M ratio were significantly higher in traumatic brain injury groups than that in control (P