Treatment of intertrochanteric fractures with minimally invasive dynamic hip screws in the eiderly;Total hip replacement for treament of the subtrochanteric fractures combined with ischemic necrosis of femoral head;Us...Treatment of intertrochanteric fractures with minimally invasive dynamic hip screws in the eiderly;Total hip replacement for treament of the subtrochanteric fractures combined with ischemic necrosis of femoral head;Use of extensively porous-coated femoral stem in revision total hip arthroplasty; Revision of non-infective total hip replacement in 28 cases;Clinical significance of measurement of platelet activation and free fat at early stage after hip prosthesis replacement;展开更多
The study was to explore the protective effect of basic fibroblast growth factor (bFGF) on brain injury following global ischemia reperfusion and its mechanisms. Brain injury following global ischemia was induced by f...The study was to explore the protective effect of basic fibroblast growth factor (bFGF) on brain injury following global ischemia reperfusion and its mechanisms. Brain injury following global ischemia was induced by four vessels occlusion and systemic hypotension. Twenty-four rabbits were randomized into three groups: group A, only dissection of vessels; group B, intravenous infusion of normal saline after reperfusion for 6 h; group C, 30 μg/kg bFGF injected intravenously at the onset of reperfusion, then infused with 10 μg/(kg·h) for 6 h. Serum neuron specific enolase (NSE), S-100B, tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-8 (IL-8) were measured before ischemia, 30 min after ischemia, 0.5, 1, 3, 6 h after reperfusion. Brain water content was determined and cerebral histopathological damages were compared. NSE and S-100B were increased 1 h after reperfusion and reached their peaks 6 h after reperfusion, but were much higher in group B than those in group C 3, 6 h after reperfusion. In groups B and C, TNF-a was increased after ischemia and IL-1 and IL-8 were increased significantly 0.5 h after reperfusion, then reached their peaks 6 h, 3 h, 6 h after reperfusion respectively. TNF-a and IL-8 at the time points of 1 h and 3 h and IL-1 at 3 h and 6 h in group C were correspondingly lower than those in group B. These indices in group A were nearly unchanged. There were less severe cerebral histopathological damages in group C compared with group B, but no difference in brain water content. It could be concluded that bFGF alleviates brain injury following global ischemia and reperfusion by down-regulating expression of inflammatory factors and inhibiting their activities.展开更多
AIM： To investigate the role of Sonic hedgehog （Shh） on the course of liver ischemia and reperfusion （I/R） in rats, and the interaction between treatment with nitric oxide donor L-Arginine-methyl ester （L-Arg） ...AIM： To investigate the role of Sonic hedgehog （Shh） on the course of liver ischemia and reperfusion （I/R） in rats, and the interaction between treatment with nitric oxide donor L-Arginine-methyl ester （L-Arg） and up-regulation of Shh expression.METHODS： A total of 30 male Sprague-Dawley rats weighing 220-240 g were used in this study. Shamcontrol group （G1, n = 10）： a sham operation was performed （except for liver I/R）. I/R-untreated group （G2, n = 10）： rats underwent liver ischemia for 1 h followed by reperfusion for 45 min. I/R-L-Arg group （G3, n = 10）： after performing the same surgical procedure as in group 2, animals were treated with L-Arg. Liver tissues were taken for determination of malondialdehyde （MDA） levels, and biochemical and histological evaluations were made.RESULTS： Plasma alanine aminotransferase （ALT）, aspartate aminotransferase （AS-T）, lactate dehydrogenase （LDH） and T-glutamyltranspeptidase （GGT） activities were higher in group 2 than in group 3. MDA values and the hepatic injury score decreased in the L-Arg treated group compared to the I/R-untreated group. In group 2, the hepatoo/tes were swollen with marked vacuolization. Group 3 rats showed well-preserved liver parenchyma, with hepatocytes extending from the central vein. The morphology of the hepatocytes and the sinusoidal structures was normal, without any signs of congestion. Mild Shh positive immunostaining was detected in group 2 animals. The expression of immunoreactive cells was increased markedly in liver tissue from I/R-L-Arg rats.CONCLUSION： Our findings suggest that Shh molecules are critical factors in the pathophysiology of inflammatory liver injury induced by I/R. In addition, NO plays an important role in the immunohistochemical expression of these molecules.展开更多
AIM: To investigate if ischemia/reperfusion (I/R) injury in aged liver could be alleviated by heme oxygenase-1 (HO-1).METHODS: Three groups of SD rats (16 mo old) were studied. Group 1: control donors received physiol...AIM: To investigate if ischemia/reperfusion (I/R) injury in aged liver could be alleviated by heme oxygenase-1 (HO-1).METHODS: Three groups of SD rats (16 mo old) were studied. Group 1: control donors received physiological saline 24 h before their livers were harvested; group 2: donors were pretreated with hemih 24 h before their livers were harvested; and group 3: donors received hemin 24 h before their livers were harvested and zinc protoporphyrin (ZnPP,HO-1 inhibitor) was given to recipients at reperfusion. The harvested livers were stored in University of Wisconsin solution (4 ℃) for 6 h, and then transplanted to syngeneic rats. Serum glutamic oxaloacetic transaminase (SGOT),apoptotic cells, and apoptotic gene were measured 3, 6,12, 24, 48 h after reperfusion. We measured the apoptotic index by TUNEL, determined the expression of antiapoptotic Bcl-2 and proapoptotic (caspase-3) gene products by Western blot.RESULTS: After 3, 6, 12, 24, and 48 h of reperfusion, the SGOT levels (584.4±85.8 u/L, 999.2±125.2 u/L, 423.4±161.3u/L, 257.8±95.8 u/L, and 122.4±26.4 u/L) in hemin group were significantly (all P＜0.05) lower than those in saline group (1082.2±101.2 u/L, 1775.2±328.3 u/L, 840.4±137.8 u/L,448.6±74.3 u/L, and 306.2±49.3 u/L). Liver HO-1 enzymatic activity correlated with beneficial effects of hemin and deleterious effects of adjunctive ZnPP treatment. Markedly less apoptotic (TUNEL+) liver cells 3, 6, 12, 24, and 48 h after reperfusion (5.16±0.73, 10.2±0.67, 9.28±0.78, 7.14±1.12,and 4.78±0.65) (P＜0.05) could be detected in hemin liver grafts, as compared to controls (7.82±1.05, 15.94±1.82,11.67±1.59, 8.28±1.09, and 6.36±0.67). We detected the increased levels of Bcl-2 (1.5-fold) expression and compared with saline controls. These differences were most pronounced at 12 h after transplantation. In contrast, an active form of proapoptotic caspase-3 (p20) protein was found to be 2.9-fold lower at 24 h in hemin-pretreated group, as compared to saline liver transplant controls.CONCLUSION: HO-1 overexpression can provide potent protection against cold I/R injury. This effect depends, at least in part, on HO-1-mediated inhibition of antiapoptotic mechanism.展开更多
Objectives: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomi...Objectives: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin,intestinal bacterial counts, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. Results: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in the I/R group campared to those in the sham group. Intestinal Bifidobacteria and Lactobacilli decreased and intestinal Enterobacterium and Enterococcus, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group.Conclusion: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function,which contributes to endotoxemia and bacterial translocation to kidney.展开更多
AIM:To determine whether Saiko-keishi-to(TJ-10),a Japanese herbal medicine,could protect liver injury induced by gut ischemia/reperfusion(I/R),and to investigate the role of NO. METHODS:Male Wistar rats were exposed t...AIM:To determine whether Saiko-keishi-to(TJ-10),a Japanese herbal medicine,could protect liver injury induced by gut ischemia/reperfusion(I/R),and to investigate the role of NO. METHODS:Male Wistar rats were exposed to 30-min gut isohemia followed by 60 min of reperfusion.Intravital microscopy was used to monitor leukocyte recruitment.Plasma tumor necrosis factor(TNF)levels and alanine aminotransferase (ALT)activities were measured.TJ-10 1 g/(kg.d)was intragastrically administered to rats for 7 d.A NO synthase inhibitor was administered. RESULTS:In control rats,gut I/R elicited increases in the number of stationary leukocytes,and plasma TNF levels and ALT activities were mitigated by pretreatment with TJ-10.Pretreatment with the NO synthase inhibitor diminished the protective effects of TJ-10 on leukostasis in the liver,and the increase of plasma TNF levels and ALT activities.Pretreatment with TJ-10 increased plasma nitrite/nitrate levels. CONCLUSION:TJ-10 attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential hepatocellular injury via enhancement of NO production.展开更多
Objective: To observe the change of nitric oxide (NO) levels in the blood and the morphological change of the muscles in the limbs of rats during the (IR) injury and after being intervened by L-arginine (L-Arg) and L-...Objective: To observe the change of nitric oxide (NO) levels in the blood and the morphological change of the muscles in the limbs of rats during the (IR) injury and after being intervened by L-arginine (L-Arg) and L-nitroarginine (L-NNA). Methods: Sixty-six male Sprague-Dawley (SD) rats were used and grouped into the normal controls, the sham injury controls, the IR injury group and the intervention groups (L-Arg group and L-NNA group). After 6 hours of ischemia, followed by reperfusion for 3, 12 or 24 hours, the samples in the IR injury group were obtained. The rats in the intervention groups were given L-Arg (100 mmol/L) and L-NNA (10 mmol/L), respectively, through the abdominal cavity. Then the anterior tibial muscle in the right limb was obtained for histological examination, the anterior tibial muscle in the left limb for ultrastructure observation and the blood for assay of NO in all the rats. NO was assayed by indirect measurement of NO 2 -/NO 3 - with Griess method. Results: There was no significant difference of NO between the normal controls and the sham injury controls (P> 0.05). But NO significantly decreased in the IR injury group (P< 0.01), and further decreased with reperfusion (P< 0.01) and reached the lowest point at 12 hours after reperfusion. The level of NO in the L-Arg group was significantly higher than that in the IR injury group (P< 0.01), but was not significantly different from that in the controls (P> 0.05). In the L-NNA group, NO decreased to the undetectable level (P< 0.01). Histological examination and ultrastructure observation showed the muscles were normal in the control groups. After 6 hours of ischemia, the skeletal muscles displayed injuries, and they were most severely injured after 12 hours of reperfusion. In the L-Arg group, the skeletal muscles were less injured, while in the L-NNA group, the injury was similar to that in the IR injury group. Conclusions: When the limbs of the rats sustain IR, NO in the blood decreases. Meanwhile, the muscles in the limbs are injured. When L-Arg is given, NO in the blood is restored and the muscles are protected. When L-NNA completely inhibits NO, no protection of the muscles is shown.展开更多
文摘Treatment of intertrochanteric fractures with minimally invasive dynamic hip screws in the eiderly;Total hip replacement for treament of the subtrochanteric fractures combined with ischemic necrosis of femoral head;Use of extensively porous-coated femoral stem in revision total hip arthroplasty; Revision of non-infective total hip replacement in 28 cases;Clinical significance of measurement of platelet activation and free fat at early stage after hip prosthesis replacement;
文摘The study was to explore the protective effect of basic fibroblast growth factor (bFGF) on brain injury following global ischemia reperfusion and its mechanisms. Brain injury following global ischemia was induced by four vessels occlusion and systemic hypotension. Twenty-four rabbits were randomized into three groups: group A, only dissection of vessels; group B, intravenous infusion of normal saline after reperfusion for 6 h; group C, 30 μg/kg bFGF injected intravenously at the onset of reperfusion, then infused with 10 μg/(kg·h) for 6 h. Serum neuron specific enolase (NSE), S-100B, tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-8 (IL-8) were measured before ischemia, 30 min after ischemia, 0.5, 1, 3, 6 h after reperfusion. Brain water content was determined and cerebral histopathological damages were compared. NSE and S-100B were increased 1 h after reperfusion and reached their peaks 6 h after reperfusion, but were much higher in group B than those in group C 3, 6 h after reperfusion. In groups B and C, TNF-a was increased after ischemia and IL-1 and IL-8 were increased significantly 0.5 h after reperfusion, then reached their peaks 6 h, 3 h, 6 h after reperfusion respectively. TNF-a and IL-8 at the time points of 1 h and 3 h and IL-1 at 3 h and 6 h in group C were correspondingly lower than those in group B. These indices in group A were nearly unchanged. There were less severe cerebral histopathological damages in group C compared with group B, but no difference in brain water content. It could be concluded that bFGF alleviates brain injury following global ischemia and reperfusion by down-regulating expression of inflammatory factors and inhibiting their activities.
文摘AIM： To investigate the role of Sonic hedgehog （Shh） on the course of liver ischemia and reperfusion （I/R） in rats, and the interaction between treatment with nitric oxide donor L-Arginine-methyl ester （L-Arg） and up-regulation of Shh expression.METHODS： A total of 30 male Sprague-Dawley rats weighing 220-240 g were used in this study. Shamcontrol group （G1, n = 10）： a sham operation was performed （except for liver I/R）. I/R-untreated group （G2, n = 10）： rats underwent liver ischemia for 1 h followed by reperfusion for 45 min. I/R-L-Arg group （G3, n = 10）： after performing the same surgical procedure as in group 2, animals were treated with L-Arg. Liver tissues were taken for determination of malondialdehyde （MDA） levels, and biochemical and histological evaluations were made.RESULTS： Plasma alanine aminotransferase （ALT）, aspartate aminotransferase （AS-T）, lactate dehydrogenase （LDH） and T-glutamyltranspeptidase （GGT） activities were higher in group 2 than in group 3. MDA values and the hepatic injury score decreased in the L-Arg treated group compared to the I/R-untreated group. In group 2, the hepatoo/tes were swollen with marked vacuolization. Group 3 rats showed well-preserved liver parenchyma, with hepatocytes extending from the central vein. The morphology of the hepatocytes and the sinusoidal structures was normal, without any signs of congestion. Mild Shh positive immunostaining was detected in group 2 animals. The expression of immunoreactive cells was increased markedly in liver tissue from I/R-L-Arg rats.CONCLUSION： Our findings suggest that Shh molecules are critical factors in the pathophysiology of inflammatory liver injury induced by I/R. In addition, NO plays an important role in the immunohistochemical expression of these molecules.
基金Supported by the "135" Medical Project of Jiangsu, No. 135-10
文摘AIM: To investigate if ischemia/reperfusion (I/R) injury in aged liver could be alleviated by heme oxygenase-1 (HO-1).METHODS: Three groups of SD rats (16 mo old) were studied. Group 1: control donors received physiological saline 24 h before their livers were harvested; group 2: donors were pretreated with hemih 24 h before their livers were harvested; and group 3: donors received hemin 24 h before their livers were harvested and zinc protoporphyrin (ZnPP,HO-1 inhibitor) was given to recipients at reperfusion. The harvested livers were stored in University of Wisconsin solution (4 ℃) for 6 h, and then transplanted to syngeneic rats. Serum glutamic oxaloacetic transaminase (SGOT),apoptotic cells, and apoptotic gene were measured 3, 6,12, 24, 48 h after reperfusion. We measured the apoptotic index by TUNEL, determined the expression of antiapoptotic Bcl-2 and proapoptotic (caspase-3) gene products by Western blot.RESULTS: After 3, 6, 12, 24, and 48 h of reperfusion, the SGOT levels (584.4±85.8 u/L, 999.2±125.2 u/L, 423.4±161.3u/L, 257.8±95.8 u/L, and 122.4±26.4 u/L) in hemin group were significantly (all P＜0.05) lower than those in saline group (1082.2±101.2 u/L, 1775.2±328.3 u/L, 840.4±137.8 u/L,448.6±74.3 u/L, and 306.2±49.3 u/L). Liver HO-1 enzymatic activity correlated with beneficial effects of hemin and deleterious effects of adjunctive ZnPP treatment. Markedly less apoptotic (TUNEL+) liver cells 3, 6, 12, 24, and 48 h after reperfusion (5.16±0.73, 10.2±0.67, 9.28±0.78, 7.14±1.12,and 4.78±0.65) (P＜0.05) could be detected in hemin liver grafts, as compared to controls (7.82±1.05, 15.94±1.82,11.67±1.59, 8.28±1.09, and 6.36±0.67). We detected the increased levels of Bcl-2 (1.5-fold) expression and compared with saline controls. These differences were most pronounced at 12 h after transplantation. In contrast, an active form of proapoptotic caspase-3 (p20) protein was found to be 2.9-fold lower at 24 h in hemin-pretreated group, as compared to saline liver transplant controls.CONCLUSION: HO-1 overexpression can provide potent protection against cold I/R injury. This effect depends, at least in part, on HO-1-mediated inhibition of antiapoptotic mechanism.
文摘Objectives: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin,intestinal bacterial counts, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. Results: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in the I/R group campared to those in the sham group. Intestinal Bifidobacteria and Lactobacilli decreased and intestinal Enterobacterium and Enterococcus, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group.Conclusion: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function,which contributes to endotoxemia and bacterial translocation to kidney.
文摘AIM:To determine whether Saiko-keishi-to(TJ-10),a Japanese herbal medicine,could protect liver injury induced by gut ischemia/reperfusion(I/R),and to investigate the role of NO. METHODS:Male Wistar rats were exposed to 30-min gut isohemia followed by 60 min of reperfusion.Intravital microscopy was used to monitor leukocyte recruitment.Plasma tumor necrosis factor(TNF)levels and alanine aminotransferase (ALT)activities were measured.TJ-10 1 g/(kg.d)was intragastrically administered to rats for 7 d.A NO synthase inhibitor was administered. RESULTS:In control rats,gut I/R elicited increases in the number of stationary leukocytes,and plasma TNF levels and ALT activities were mitigated by pretreatment with TJ-10.Pretreatment with the NO synthase inhibitor diminished the protective effects of TJ-10 on leukostasis in the liver,and the increase of plasma TNF levels and ALT activities.Pretreatment with TJ-10 increased plasma nitrite/nitrate levels. CONCLUSION:TJ-10 attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential hepatocellular injury via enhancement of NO production.
文摘Objective: To observe the change of nitric oxide (NO) levels in the blood and the morphological change of the muscles in the limbs of rats during the (IR) injury and after being intervened by L-arginine (L-Arg) and L-nitroarginine (L-NNA). Methods: Sixty-six male Sprague-Dawley (SD) rats were used and grouped into the normal controls, the sham injury controls, the IR injury group and the intervention groups (L-Arg group and L-NNA group). After 6 hours of ischemia, followed by reperfusion for 3, 12 or 24 hours, the samples in the IR injury group were obtained. The rats in the intervention groups were given L-Arg (100 mmol/L) and L-NNA (10 mmol/L), respectively, through the abdominal cavity. Then the anterior tibial muscle in the right limb was obtained for histological examination, the anterior tibial muscle in the left limb for ultrastructure observation and the blood for assay of NO in all the rats. NO was assayed by indirect measurement of NO 2 -/NO 3 - with Griess method. Results: There was no significant difference of NO between the normal controls and the sham injury controls (P> 0.05). But NO significantly decreased in the IR injury group (P< 0.01), and further decreased with reperfusion (P< 0.01) and reached the lowest point at 12 hours after reperfusion. The level of NO in the L-Arg group was significantly higher than that in the IR injury group (P< 0.01), but was not significantly different from that in the controls (P> 0.05). In the L-NNA group, NO decreased to the undetectable level (P< 0.01). Histological examination and ultrastructure observation showed the muscles were normal in the control groups. After 6 hours of ischemia, the skeletal muscles displayed injuries, and they were most severely injured after 12 hours of reperfusion. In the L-Arg group, the skeletal muscles were less injured, while in the L-NNA group, the injury was similar to that in the IR injury group. Conclusions: When the limbs of the rats sustain IR, NO in the blood decreases. Meanwhile, the muscles in the limbs are injured. When L-Arg is given, NO in the blood is restored and the muscles are protected. When L-NNA completely inhibits NO, no protection of the muscles is shown.
