AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats w...AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats were deprived of food for 24 h. Under chloral hydrate （300 mg/kg） anesthesia, bilateral carotid artery ligation was performed. The pylorus and carotid esophagus of the rats were also ligated. The stomachs were then irrigated for 3 h with either normal saline or simulated gastric juice containing 100 mmol/L HCI plus 17.4 mmol/L pepsin and 54 mmol/L NaCI. Rats were killed and stomachs were dissected. Gastric mucosa and gastric contents were harvested. The rat brain was dissected for the examination of ischemia by triphenyltetrazolium chloride staining method. Changes in gastric ulcerogenic parameters, such as decreased mucosal glutathione level as well as enhanced gastric acid back-diffusion, mucosal lipid peroxide generation, histamine concentration, luminal hemoglobin content and mucosal erosion in gastric samples, were measured. RESULTS： Bilateral carotid artery ligation produced severe brain ischemia （BI） in rats. An exacerbation of various ulcerogenic parameters and mucosal hemorrhagic erosions were observed in these rats. The exacerbated ulcerogenic parameters were significantly （P〈 0.05） attenuated by antioxidants, such as exogenous glutathione and allopurinol. These gastric parameters were also improved by intraperitoneal aminoguanidine （100 mg/kg） but were aggravated by N^G-nitro-L-argininemethyl ester （L-NAME： 25 mg/kg）. Intraperitoneal L-arginine （0-500 mg/kg） dose-dependently attenuated BI-induced aggravation of ulcerogenic parameters and hemorrhagic erosions that were reversed by L-NAME. CONCLUSION： BI could produce hemorrhagic erosions through gastric oxidative stress and activation of arginine-nitric oxide pathway.展开更多
Objective: To investigate the early changes and clinical significance of plasma endothelin (ET), nitric oxide (NO) and arginine vasopressin (AVP) in patients with acute moderate or severe cerebral injury. Methods: The...Objective: To investigate the early changes and clinical significance of plasma endothelin (ET), nitric oxide (NO) and arginine vasopressin (AVP) in patients with acute moderate or severe cerebral injury. Methods: The early (at 24 hours after injury) plasma concentrations of ET, NO and AVP were measured with radioimmunoassay and Green technique in 48 cases of acute moderate (GCS≤8 in 27cases ) or severe (GCS>8 in 21 cases) cerebral injury (Group A), in 42 cases of non cerebral injury (Group B) and in 38 normal individuals (Group C), respectively. Results: The early plasma concentrations of ET ( 109.73 ng/L±12.61 ng/L ), NO ( 92.82 μmol/L± 18.21 μmol/L ) and AVP ( 49.78 ng/L±14.29 ng/L ) in Group A were higher than those in Group B ( 67.90 ng/L ±11.33 ng/L , 52.66 μmol/L±12.82 μmol/L and 29.93 ng/L±12.11 ng/L , respectively, P<0.01 ) and Group C ( 50.65 ng/L±17.12 ng/L , 36.12 μmol/L ±12.16 μmol/L and 5.18 ng/L ± 4.18 ng/L , respectively, P<0.001 ). The amounts of ET, NO and AVP in patients with severe cerebral injury were 116.18 ng/L± 18.12 ng/L , 108.19 μmol/L±13.28 μmol/L and 58.13 ng/L±16.78 ng/L , respectively, which were significantly higher than that of the patients with moderate cerebral injury ( 92.33 ng/L±16.32 ng/L , 76.38 μmol/L ±12.71 μmol/L and 36.18 ng/L±12.13 ng/L respectively, P<0.01 ). The early levels of ET, NO and AVP in Group A were negatively related to the GCS scales. The amounts of ET, NO and AVP were 126.23 ng/L± 15.23 ng/L , 118.18 μmol/L±10.12 μmol/L and 63.49 ng/L±14.36 ng/L respectively in patients with subdural hematoma, which were significantly higher than those in patients with epidural hematoma ( 81.13 ng/L ±12.37 ng/L , 68.02 μmol/L±13.18 μmol/L and 45.63 ng/L±12.41 ng/L respectively, P<0.01 ). The plasma concentrations of ET, NO and AVP in stable duration (at 336 hours after injury) in Group A and Group B were similar to those in Group C. Conclusions: ET, NO and AVP were related to the pathophysiological process that occurs in the early stage of acute cerebral injury and the values of ET, NO and AVP correlate positively with the clinical manifestations. The changes of plasma ET, NO and AVP can be regarded as important indices to assess the severity of acute cerebral injury.展开更多
Objective: To study the effects of mild hypothermia on cerebral oxygen partial pressure, carbon dioxide partial pressure, pH and body temperature （PbrO2, PbrCO2, pHbr and BT） in patients with acute severe head injur...Objective: To study the effects of mild hypothermia on cerebral oxygen partial pressure, carbon dioxide partial pressure, pH and body temperature （PbrO2, PbrCO2, pHbr and BT） in patients with acute severe head injury. Methods: Thirty-eight patients with acute severe head injury were treated with mild hypothermia, meantime PbrO2, PbrCO2, pHbr and BT were monitored in order to study the changes of PbrO2, PbrCO2, pHbr and BT. Results: In patients with acute head injury, mild hypothermia obviously increased PbrO2, decreased PbrCO2 and CO2 accumulation and acidosis in brain tissue. BT was 1℃-（1.5）℃ higher than rectal temperature（RT） after injury. The BT and RT were decreased when the patients were treated with mild hypothermia, but at the same time the difference between BT and RT was increased. Conclusions: In patients with acute severe head injury the direct monitoring of PbrO2, PbrCO2, pHbr and BT was safe and reliable, and is helpful in estimating prognosis and mild hypothermia therapy.展开更多
Objective:To examine the effects of modified Shenmai Yin on invigorating vital energy, promoting blood flow, and protection against neural impairment in an endotoxin-induced shock rat model. Methods: Ninety-six SD rat...Objective:To examine the effects of modified Shenmai Yin on invigorating vital energy, promoting blood flow, and protection against neural impairment in an endotoxin-induced shock rat model. Methods: Ninety-six SD rats were randomly divided into four groups: sham operation (saline 20 ml/kg), shock model (lipopolysaccharide, LPS, 8 mg/kg), Reformed Shengmai Yin (加味生脉饮 Pulse-activating Decoction) (LPS 8 mg/kg + reformed Shengmai Yin Injection 10 ml/kg), and dexamethasone (LPS 8 mg/kg + dexamethasone 5 mg/kg) groups. Each group was subdivided into 1 h, 2 h, 3 h, and 6 h time points for observation. The carotid artery was separated and connected with a biological functional system to monitor mean arterial pressure (MAP). Brain water levels, malonaldehyde (MDA) content, and superoxide dismutase (SOD) activity were also determined. Results: In the shock model group, MAP was progressively decreased after injection of LPS, brain water and MDA contents were increased, brain SOD activity was decreased, and capillary vessel edema in brain tissue was also observed. All these parameters were improved significantly in both treatment groups, although the effects were more marked with Shengmai Yin than with dexamethasone. Conclusion: Modified Shengmai Yin exhibits strong anti-shock and neuroprotective effects against Endotoxininduced shock.展开更多
Objective： To investigate the effects of sodium ferulate （SF）, an intravenous drug made from traditional Chinese herbs, on activation of postsynaptic density-95 （PSD-95） and neuroprotection after transient cerebr...Objective： To investigate the effects of sodium ferulate （SF）, an intravenous drug made from traditional Chinese herbs, on activation of postsynaptic density-95 （PSD-95） and neuroprotection after transient cerebral artery occlusion in rats. Methods： Forty-six male Sprague-Dawley rats were randomized into 2 groups （ n = 23 in each group） ： the control group and the SF group. After anesthesia, the middle cerebral artery occlusion （MCAO） was conducted with the intraluminal filament technique. The neurological deficit was assessed with the method devised by Bederson et al.^ 8 The 2, 3, 4-triphenyltetrazolium chloride staining was used to assess the infarct volume. We adopted a modified six-point scale to conduct neurobehavioral evaluation. Immediately the activation of postsynaptic density-95 （ PSD- 95 ） was studied with Western blot analysis system in the cortex and striatum of rat brain. Results ： The neurologic deficit score of the SF group decreased substantially compared with that of the control group （ P 〈0.05）. The infarct volume of the control group （168.1 mm^3 ± 42.2 mm^3） was significantly larger than that of the SF group （61.5 mm^3 ± 28.7 mm^3 ） at 24 hours after reperfusion （P 〈 0.01 ）. And the rats showed some neurological deficit. The activity of PSD-95 in the SF group at most timepoints was less than that in the control group. No upregulation of PSD-95 protein could be detected in the contralateral cortex. Conclusions ： Sodium ferulate can induce a neuroproteetive effect against the transient focal cerebral isehemie injury and weaken the activation of PSD-95 in isehemie area after MCAO.展开更多
基金Supported by a grant from National Sciences Council of Taiwan,NSC 88-2314-B006-028
文摘AIM： To investigate the role of gastric oxidative stress and nitric oxide （NO） in the formation of gastric hemorrhagic erosion and their protection by drugs in rats with ischemic brain. METHODS： Male Wistar rats were deprived of food for 24 h. Under chloral hydrate （300 mg/kg） anesthesia, bilateral carotid artery ligation was performed. The pylorus and carotid esophagus of the rats were also ligated. The stomachs were then irrigated for 3 h with either normal saline or simulated gastric juice containing 100 mmol/L HCI plus 17.4 mmol/L pepsin and 54 mmol/L NaCI. Rats were killed and stomachs were dissected. Gastric mucosa and gastric contents were harvested. The rat brain was dissected for the examination of ischemia by triphenyltetrazolium chloride staining method. Changes in gastric ulcerogenic parameters, such as decreased mucosal glutathione level as well as enhanced gastric acid back-diffusion, mucosal lipid peroxide generation, histamine concentration, luminal hemoglobin content and mucosal erosion in gastric samples, were measured. RESULTS： Bilateral carotid artery ligation produced severe brain ischemia （BI） in rats. An exacerbation of various ulcerogenic parameters and mucosal hemorrhagic erosions were observed in these rats. The exacerbated ulcerogenic parameters were significantly （P〈 0.05） attenuated by antioxidants, such as exogenous glutathione and allopurinol. These gastric parameters were also improved by intraperitoneal aminoguanidine （100 mg/kg） but were aggravated by N^G-nitro-L-argininemethyl ester （L-NAME： 25 mg/kg）. Intraperitoneal L-arginine （0-500 mg/kg） dose-dependently attenuated BI-induced aggravation of ulcerogenic parameters and hemorrhagic erosions that were reversed by L-NAME. CONCLUSION： BI could produce hemorrhagic erosions through gastric oxidative stress and activation of arginine-nitric oxide pathway.
基金ThisstudywassupportedbytheFundFoundationofHealthDepartmentofZhejiangProvince (No .96 174 )
文摘Objective: To investigate the early changes and clinical significance of plasma endothelin (ET), nitric oxide (NO) and arginine vasopressin (AVP) in patients with acute moderate or severe cerebral injury. Methods: The early (at 24 hours after injury) plasma concentrations of ET, NO and AVP were measured with radioimmunoassay and Green technique in 48 cases of acute moderate (GCS≤8 in 27cases ) or severe (GCS>8 in 21 cases) cerebral injury (Group A), in 42 cases of non cerebral injury (Group B) and in 38 normal individuals (Group C), respectively. Results: The early plasma concentrations of ET ( 109.73 ng/L±12.61 ng/L ), NO ( 92.82 μmol/L± 18.21 μmol/L ) and AVP ( 49.78 ng/L±14.29 ng/L ) in Group A were higher than those in Group B ( 67.90 ng/L ±11.33 ng/L , 52.66 μmol/L±12.82 μmol/L and 29.93 ng/L±12.11 ng/L , respectively, P<0.01 ) and Group C ( 50.65 ng/L±17.12 ng/L , 36.12 μmol/L ±12.16 μmol/L and 5.18 ng/L ± 4.18 ng/L , respectively, P<0.001 ). The amounts of ET, NO and AVP in patients with severe cerebral injury were 116.18 ng/L± 18.12 ng/L , 108.19 μmol/L±13.28 μmol/L and 58.13 ng/L±16.78 ng/L , respectively, which were significantly higher than that of the patients with moderate cerebral injury ( 92.33 ng/L±16.32 ng/L , 76.38 μmol/L ±12.71 μmol/L and 36.18 ng/L±12.13 ng/L respectively, P<0.01 ). The early levels of ET, NO and AVP in Group A were negatively related to the GCS scales. The amounts of ET, NO and AVP were 126.23 ng/L± 15.23 ng/L , 118.18 μmol/L±10.12 μmol/L and 63.49 ng/L±14.36 ng/L respectively in patients with subdural hematoma, which were significantly higher than those in patients with epidural hematoma ( 81.13 ng/L ±12.37 ng/L , 68.02 μmol/L±13.18 μmol/L and 45.63 ng/L±12.41 ng/L respectively, P<0.01 ). The plasma concentrations of ET, NO and AVP in stable duration (at 336 hours after injury) in Group A and Group B were similar to those in Group C. Conclusions: ET, NO and AVP were related to the pathophysiological process that occurs in the early stage of acute cerebral injury and the values of ET, NO and AVP correlate positively with the clinical manifestations. The changes of plasma ET, NO and AVP can be regarded as important indices to assess the severity of acute cerebral injury.
文摘Objective: To study the effects of mild hypothermia on cerebral oxygen partial pressure, carbon dioxide partial pressure, pH and body temperature （PbrO2, PbrCO2, pHbr and BT） in patients with acute severe head injury. Methods: Thirty-eight patients with acute severe head injury were treated with mild hypothermia, meantime PbrO2, PbrCO2, pHbr and BT were monitored in order to study the changes of PbrO2, PbrCO2, pHbr and BT. Results: In patients with acute head injury, mild hypothermia obviously increased PbrO2, decreased PbrCO2 and CO2 accumulation and acidosis in brain tissue. BT was 1℃-（1.5）℃ higher than rectal temperature（RT） after injury. The BT and RT were decreased when the patients were treated with mild hypothermia, but at the same time the difference between BT and RT was increased. Conclusions: In patients with acute severe head injury the direct monitoring of PbrO2, PbrCO2, pHbr and BT was safe and reliable, and is helpful in estimating prognosis and mild hypothermia therapy.
基金supported by a grant from National Natural Science Foundation of China (No.30672737)
文摘Objective:To examine the effects of modified Shenmai Yin on invigorating vital energy, promoting blood flow, and protection against neural impairment in an endotoxin-induced shock rat model. Methods: Ninety-six SD rats were randomly divided into four groups: sham operation (saline 20 ml/kg), shock model (lipopolysaccharide, LPS, 8 mg/kg), Reformed Shengmai Yin (加味生脉饮 Pulse-activating Decoction) (LPS 8 mg/kg + reformed Shengmai Yin Injection 10 ml/kg), and dexamethasone (LPS 8 mg/kg + dexamethasone 5 mg/kg) groups. Each group was subdivided into 1 h, 2 h, 3 h, and 6 h time points for observation. The carotid artery was separated and connected with a biological functional system to monitor mean arterial pressure (MAP). Brain water levels, malonaldehyde (MDA) content, and superoxide dismutase (SOD) activity were also determined. Results: In the shock model group, MAP was progressively decreased after injection of LPS, brain water and MDA contents were increased, brain SOD activity was decreased, and capillary vessel edema in brain tissue was also observed. All these parameters were improved significantly in both treatment groups, although the effects were more marked with Shengmai Yin than with dexamethasone. Conclusion: Modified Shengmai Yin exhibits strong anti-shock and neuroprotective effects against Endotoxininduced shock.
文摘Objective： To investigate the effects of sodium ferulate （SF）, an intravenous drug made from traditional Chinese herbs, on activation of postsynaptic density-95 （PSD-95） and neuroprotection after transient cerebral artery occlusion in rats. Methods： Forty-six male Sprague-Dawley rats were randomized into 2 groups （ n = 23 in each group） ： the control group and the SF group. After anesthesia, the middle cerebral artery occlusion （MCAO） was conducted with the intraluminal filament technique. The neurological deficit was assessed with the method devised by Bederson et al.^ 8 The 2, 3, 4-triphenyltetrazolium chloride staining was used to assess the infarct volume. We adopted a modified six-point scale to conduct neurobehavioral evaluation. Immediately the activation of postsynaptic density-95 （ PSD- 95 ） was studied with Western blot analysis system in the cortex and striatum of rat brain. Results ： The neurologic deficit score of the SF group decreased substantially compared with that of the control group （ P 〈0.05）. The infarct volume of the control group （168.1 mm^3 ± 42.2 mm^3） was significantly larger than that of the SF group （61.5 mm^3 ± 28.7 mm^3 ） at 24 hours after reperfusion （P 〈 0.01 ）. And the rats showed some neurological deficit. The activity of PSD-95 in the SF group at most timepoints was less than that in the control group. No upregulation of PSD-95 protein could be detected in the contralateral cortex. Conclusions ： Sodium ferulate can induce a neuroproteetive effect against the transient focal cerebral isehemie injury and weaken the activation of PSD-95 in isehemie area after MCAO.
