Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was esta...Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was established in 32 SD (Sprague-Dawley) rats. The rats were randomly divided into control group, no fluid resuscitation group (NF group), controlled fluid resuscitation group (NS40 group) and rapid large scale fluid resuscitation group (NS80 group). Each group contained 8 rats. The curative effects were compared. At the same time, the apoptosis in liver, kidney, lung and small intestinal mucosa of survivors after hemorrhage and resuscitation was detected by light microscopy in HE (hematoxylin and eosin) stained tissue sections, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Results: The survival rate of early fluid resuscitation (14/16) was markedly higher than that of NF group (3/8). There was some apoptosis in liver, kidney, lung and small intestinal mucosa of all survivors. Compared with NF and NS40 groups, the apoptosis of liver, kidney and small intestinal mucosa of NS80 group was obviously increased. Conclusions: Among three fluid resuscitation methods, controlled fluid resuscitation can obviously improve the early survival rate and the apoptosis of liver, kidney and small intestinal mucosa in rats with severe and uncontrolled hemorrhagic shock, and may benefit improvement of prognosis.展开更多
The present study was designed to investigate the production of tumor necrosis factor a (TNFα) in-duced by low-dose (1μg/kg) lipopolysaccharide (LPS) and its cellular source after hemorrhagic shock(HS) in rats, and ...The present study was designed to investigate the production of tumor necrosis factor a (TNFα) in-duced by low-dose (1μg/kg) lipopolysaccharide (LPS) and its cellular source after hemorrhagic shock(HS) in rats, and to further analyze the mechanism for increased sensitivity to LPS through looking at ex-pression of lipopolysaccharide -binding protein (LBP ) mRN A in t he liver, lungs and kidneys. lt wa s foundin uiuo that plasma TNFa levels in the HS+LPS group were 20-fold higher than that in the HS group (P<0. 01 ), and 2. 7-fold higher than that in the LPS group (P<0. 05). lt was shown in ndro that the ca-pacity of peripheral white blood cells to produce TNFa in response to LPS stimulation was significantly de-creased by 126 % (P<0. 01 ) and 57% (P<0. 05) compared with pre-shock levels and the sham group re-spectively at the end of resuscitation following shock, and was still markedly decreased 3 hours after resus-citation, while the capacity of Kupffer Cells was significantly increased by 110% compared with the shamgroup (P<0. 01) after shock and resuscitation. Results from RT-PCR showed that expression of LBPmRNA in the liver, lungs and kidneys was increased after shock and resuscitation. It is suggested thathemorrhagic shock could significantly enhance endotoxin-induced TNFa production, which might be due toup-regulation of LBP expression in tissues after shock, and tissue macrophages might be the main source ofcytokine production.展开更多
文摘Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was established in 32 SD (Sprague-Dawley) rats. The rats were randomly divided into control group, no fluid resuscitation group (NF group), controlled fluid resuscitation group (NS40 group) and rapid large scale fluid resuscitation group (NS80 group). Each group contained 8 rats. The curative effects were compared. At the same time, the apoptosis in liver, kidney, lung and small intestinal mucosa of survivors after hemorrhage and resuscitation was detected by light microscopy in HE (hematoxylin and eosin) stained tissue sections, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Results: The survival rate of early fluid resuscitation (14/16) was markedly higher than that of NF group (3/8). There was some apoptosis in liver, kidney, lung and small intestinal mucosa of all survivors. Compared with NF and NS40 groups, the apoptosis of liver, kidney and small intestinal mucosa of NS80 group was obviously increased. Conclusions: Among three fluid resuscitation methods, controlled fluid resuscitation can obviously improve the early survival rate and the apoptosis of liver, kidney and small intestinal mucosa in rats with severe and uncontrolled hemorrhagic shock, and may benefit improvement of prognosis.
文摘The present study was designed to investigate the production of tumor necrosis factor a (TNFα) in-duced by low-dose (1μg/kg) lipopolysaccharide (LPS) and its cellular source after hemorrhagic shock(HS) in rats, and to further analyze the mechanism for increased sensitivity to LPS through looking at ex-pression of lipopolysaccharide -binding protein (LBP ) mRN A in t he liver, lungs and kidneys. lt wa s foundin uiuo that plasma TNFa levels in the HS+LPS group were 20-fold higher than that in the HS group (P<0. 01 ), and 2. 7-fold higher than that in the LPS group (P<0. 05). lt was shown in ndro that the ca-pacity of peripheral white blood cells to produce TNFa in response to LPS stimulation was significantly de-creased by 126 % (P<0. 01 ) and 57% (P<0. 05) compared with pre-shock levels and the sham group re-spectively at the end of resuscitation following shock, and was still markedly decreased 3 hours after resus-citation, while the capacity of Kupffer Cells was significantly increased by 110% compared with the shamgroup (P<0. 01) after shock and resuscitation. Results from RT-PCR showed that expression of LBPmRNA in the liver, lungs and kidneys was increased after shock and resuscitation. It is suggested thathemorrhagic shock could significantly enhance endotoxin-induced TNFa production, which might be due toup-regulation of LBP expression in tissues after shock, and tissue macrophages might be the main source ofcytokine production.
