七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟醚对感染性休克大鼠全身炎性反应及心肺功能的影响

Objective To investigate the effects of sevoflurane on the systemic inflammatory response and cardiopulmonary function in septic shock rats. Methods Thirty-two SD rats, 8-10 months old, weighing 250-300 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S), cecal ligation and puncture (CLP) induced septic shock group (group CLP) , sevoflurane I group (group SEV, ) and sevoflurane II group (group SEV,). The abdomen was opened but CLP was not performed in group S. The septic shock was induced by CLP as described by Baker et al. Group SEV, and SEV, inhaled 2.4% sevoflurane for 30 min at 1 h and 3 h after the successful establishment of the model respectively. At 1, 3 and 5 h after septic shock, MAP and HR were recorded and arterial blood samples were taken for blood gas analysis and determination of plasma concentrations of TNF-α, IL-1, MDA and NO. The left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular fractional shortening (LVFS) and cardiac output (CO) were also detected 5 h after septic shock. The animals were killed after the detection of cardiac function. The lungs were removed for determination of W/D lung weight ratio and Evans blue (EB) content. The tissues from the heart, lung, liver and kidney were taken for detection of NF-kB activity by electrophoretic mobility shift assay (EMSA) ResultsMAP was significantly lower, HR higher, LVEDD, LVESD, LVFS, CO, pH value, PaO2 and PaCO2 lower, and W/D lung weight ratio, EB content, plasma concentrations of TNF-α, IL-1, MDA and NO, and NF-kB activity in the heart, lung, liver and kidney tissues higher in group CLP, SEV, and SEV2 than in group S (P < 0.05). NF-kB activity in the heart, lung, liver and kidney tissues and plasma concentrations of TNF-α, IL-1, MDA and NO were significantly lower in group SEV, than in group CLP and SEV2 ( P < 0.05 ), but no significant differences were found in the other indices between group SEV, and CLP and between group SEV1 and SEV2 ( P > 0.05). Conclusion Inhalation of 2.4% sevoflurane for 30 min 1 h after septic shock can inhibit the systemic inflammatory response slightly, but can not improve the cardiopulmonary function in rats with CLP-induced septic shock.     

七氟烷后处理对大鼠肺缺血再灌注损伤的影响

Objective To investigate the effects of aevoflurane postconditioning on lung iscbemia-reperfusion (IR) injury in rats and the mechanism involved. Methods Ninety-six male SD rots weighing 270-330 g were randomly divided into 4 groups (n = 24 each): sham operation group (group S), group IR, sevoflurane preconditioning group (group SPr), and sevoflurane postconditioning group (group SPo). The animals were anesthetized with intraperitoneal 10% chloral hydrate 400 mg/kg, tracheostomized and mechanically ventilated. Lung IR was produced by occlusion of the hilum of the left lung for 45 min and then it was unclamped for reperfusion, in group SPr, sevoflurane was inhaled at the end-tidal concentration of 2.1% 30 min before lung ischemia. In group SPo, sevoflurane was inhaled at the end-tidal concentration of 2.1% immediately before reperfusiun. Six rats from each group were sacrificed at 30 min, 1 h, 2 h, and 4 h of reperfnsion respectively. The TNF-α, IL-1 and IL-6 concentrations, and WBC count in broncho-alveolar lavage fluid (BALF) were determined.The percentage of PMN in WBC was calculated. The lungs were removed for determination of the cdntent of TNF-α, IL-1 and IL-6 in the lung tissues and microscopic examination. The apoptosis index (AI) was calculated by TUNEL assay. Lung injury was scored. Results The levels of TNF-α, IL-1 and IL-6 in lung tissues and BALF, AI, WBC count, percentage of PMN, and lung injury scores were significantly higher in group IR than in group S (P < 0.01). The content of TNF-α, IL-1 and IL-6 in lung tissues was significantly higher in group SPr and SPo than in group S (P < 0.01). The indices mentioned above were all significantly lower in group SPr and SPo than in group IR (P < 0.05 or 0.01). No significant differences were found in the indices mentioned above between group SPr and SPo (P > 0.05). Conclusion Sevoflurane postconditioning can protect the lungs from IR injury by decreasing the inflammatory reaction and inhibiting the apoptosis in pulmonary vascular endothelial and alveolar epithelial cells, and the effect is similar to that of sevoflurane preconditioning.     

Beat-to-beat change in "myocardial performance index" related to load

BACKGROUND: This study was designed to assess the relationship of the "myocardial performance index" (MPI) to the beat-by-beat change in pre-load with static or unchanged contractile status. METHODS: Eight anesthetized juvenile pigs were studied using direct measurement of the left ventricular pressure and volume. Transient inflation of a vena cava balloon catheter produced controlled pre-load alterations. Consecutive beats were analyzed, grouped for first, second, third, etc. during the pre-load alteration, and evaluated for the change in MPI during the same contractile status with a controlled pre-load alteration. Two pharmacologic inotropic interventions were also included to generate several myocardial conditions in each animal. RESULTS: MPI demonstrated a strong linear relationship to the pre-load and after-load. MPI increased progressively during decreasing end-diastolic volume, mostly related to changes in ejection time. MPI was observed at the same level for three different myocardial function conditions (all eight animals), with a different relationship between MPI and pre-load noted for each observation. CONCLUSIONS: MPI is strongly load dependent, and can vary widely in value for the same contractile status if the load is varied. The use of this index in critically ill patients should be limited in this respect. Further work is needed to establish the relationship of MPI to load and contractile status.