Experimental Studies of Brain-Gaster Syndrome Induced by Intracerebral Hemorrhage

Part I: Experimental study of intracerebral hemorrhage and brain tissue of MMP-9 expression and brain damage relations Citation: intracerebral hemorrhage (ICH) perihematoma brain tissue presence of an inflammatory reaction and edema. Inflammatory reaction can lead to brain cell damage, apoptosis or necrosis. The inflammatory reaction Similarly cause cell swelling and extracellular edema. Brain cell damage and edema affecting the change of the patient's condition and prognosis. Hematoma surrounding brain tissue inflammatory response after cerebral hemorrhage prerequisite basement membrane into the brain tissue is the inflammatory cell breakthrough BBB (blood-brain barrier, Blood-brain barrier). MMP-9 (matrix metalloproteinase-9, matrix metalloproteinases-9) in inflammatory cells play an important role in the breakthrough BBB basement membrane. Objective: To study in rat brain hemorrhage perihematoma expression of MMP-9 in the law, and to explore the relationship of the expression of MMP-9 and brain damage, which set forth the expression of MMP-9 in the cerebral hemorrhage perihematoma the role of the brain tissue, for cerebral hemorrhage treatment to find new ways and means. Methods: The clinical cerebral hemorrhage condensate fresh from the body and tail of arterial blood was injected into the right caudate nucleus of established animal models of cerebral hemorrhage, analog. Selection of 64 Sprague-Dawley (SD) rats were randomly divided into normal group, sham group and cerebral hemorrhage group. The ICH group is divided into 12 hours after ICH, 24h, 48h, 72h, 96h, l2Oh group, n = 8. Observed in each group the expression of MMP-9 by RT-PCR and immunohistochemistry, TUNEL assay apoptosis of brain cells, with a wet weight - dry weight (wet-dry weight) Determination of brain water content changes, behavioral ratings evaluate the neurological function of the extent of damage, the electron microscope perihematoma morphology of brain cells change. Results: 1. Observed the the model group perihematoma brain tissue water content at 12h after ICH increased (P lt; 0.O1) 72h reached a peak (P lt; 0.01), decreased slowly thereafter has not yet fully recovered, and 120h to normal levels. 12h after ICH 2.MMP -9 expression started 48h reached peak (P lt; 0.01), still higher expression until 120h. . Perihematoma brain cell apoptosis began to appear in the 12h, 48h continue to increase, 72h to reach the peak, followed by a gradual decline. ICH perihematoma weeks brain tissue MMP-9 expression levels and brain water content was positively correlated (r = 0.914, P lt; 0.05). ICH perihematoma brain tissue expression of MMP-9 and the expression of brain cell apoptosis was positively correlated (r = 0.829, P lt; 0.05). In the control group, MMP-9 and apoptosis in brain cells had no significant expression. Electron microscopy to nerve cells, edema, microvascular surrounding edema and cerebral apoptosis is most obvious in the 72h. Conclusions: ICH 12h ~ 120h perihematoma brain tissue after the first increase in the expression of MMP-9 decreased and was positively correlated with the the hematoma surrounding brain tissue water content and brain cells, the number of apoptotic, MMP-9 involved in acute cerebral hemorrhage cerebral edema and the occurrence and development of brain cells apoptosis, antagonize the expression of MMP-9 may play the role of prevention and treatment of brain edema and reduce brain cell apoptosis. Part II: Experimental study of acute gastric mucosal injury after cerebral hemorrhage Introduction: cerebral hemorrhage is common and frequently occurring clinical high morbidity and mortality. Acute gastric mucosal lesions are a common complication of cerebral hemorrhage, and performance for the congestion, erosion and ulceration of the gastric mucosa to form, its occurrence is the result of multiple factors. Related to neuroendocrine disorders, gastric mucosal barrier weakened relative enhancement and injury factors other. The prostaglandin E2 the basic coordination mucosal injury stimulus important mediators of the protective response, one component of each of the mucosal defense: inhibition of gastric acid secretion, the promotion of secretion of mucus and bicarbonate, increased gastric mucosal blood flow (GMBF was) promote ulcer healing. Multiple drugs or physical and chemical factors affecting the repair of gastric mucosal injury by regulating PGE2 synthesis. Objective: To study the cerebral hemorrhage (ICH) PH value of gastric juice, gastric mucosal blood flow (GMBF) and prostaglandin E2 (PGE2) content to change, and to explore the relationship between the degree of gastric mucosal injury and PGE2 in cerebral hemorrhage causes acute gastric mucosal injury in rats. Methods: 64 Sprague-Dawley (SD) rats were randomly divided into normal group, sham group and model group, which, in turn, is divided into 12h, 24h, 48h, 72h, 96h, 120h group, n = 8. Brain stereotactic autologous fresh not condensate the tail arterial injection the caudate nucleus Prepared rat cerebral hemorrhage model, rats were sacrificed at the corresponding point in time. Radioimmunoassay detection of gastric mucosal PGE2 content and to detect gastric juice PH value of gastric mucosal blood flow (GMBF) and ulcer index (UI) changes. Results: 1. Gastric PH value of the model group after cerebral hemorrhage 12h decreased (P lt; 0.05), 24h reached the lowest value, then rise slowly, but in 120h is still lower than the normal group and sham group (P lt; 0.05 ). 2. Gastric mucosal blood flow (GMBF) 12h significantly reduced (P lt; 0.01), with the passage of time, and value continue to decline, 96h reached its lowest point, after the rapid recovery did not recover to the level of the normal group at 120h. Cerebral hemorrhage 12h gastric mucosal PGE2 content decreased significantly (P lt; 0.01), with the passage of time, of PGE2 content continues to decline, 96h down to a minimum, after a rapid recovery, 120h gastric mucosal PGE2 content recovery to 45.72 ± 5.35. 4. 12h gastric UI cerebral hemorrhage was significantly higher (P lt; 0.01), with the passage of time, UI continues to rise and reaches a maximum in the 120h. The 5.PGE2 the UI was a negative correlation (r = -9.63, P = 0.008), PH and UI within 24h was negatively correlated (r = -9.28, P = 0.023), after 24h no correlation, GMBF the UI was significant negative correlation (r = -0.966, P = 0.007), and GMBF and PGE2 was positively correlated (r = 0.977, P = 0.004). Conclusion: cerebral hemorrhage gastric mucosa obvious damage, decreased gastric PH value decline in gastric mucosal blood flow (GMBF), reduce prostaglandin E2 (PGE2) is closely related to.