Investigation of biochemical and histopathological effects of Sevoflurane and Isoflurane on lung in rat model

Objective:In recent years, the thesis on inhalational anesthetics can be the reason for pulmonary complications during general anesthesia has come into a question. The probable mechanism of lung injury due to these agents has been considered as; endothelial cell injury caused by activated neutrophils, formation of reactive oxygen radicals and/or proteases. In this trial, it has been aimed to investigate the effects of sevoflurane and isoflurane on lung tissue in rat model.Method:After the approval of ethics committee for Research Animals, 21 adult male Wistar Albino rats were randomly allocated into three groups. The subjects were mechanically ventilated for 2 hours in Control group (n=7) with 50 % oxygen + 50 % air mixture; in Isoflurane group (n=7) with % 1.2 ( 1 MAC) isoflurane + 50 % oxygen + 50 % air and in Sevoflurane Group (n=7) with %2.4 ( 1 MAC) sevoflurane + 50 % oxygen + 50 % air mixture. At the end of the study, a median sternotomy was performed, lungs were removed and rats were sacrified. Left lung was used for pulmonary tissue myeloperoxidase activity and thiobarbituric acid reactive substances (MPO and TBARS ) determinations, right lung was used for histopathological determinations. Histopathological determinations were included, light microscope image analysis, alveolar macrophage count and M-30 immune histochemical analysis of apoptosis. Data were analyzed using Kruskal Wallis and Mann - Whitney U tests and p< 0.05 were regarded as statistically significant.Results: There were no statistical significance between groups when hemodynamic (heart rate, systolic blood pressures- diastolic blood pressures) and blood gases parameters (pH, PaO2, PaCO2) were compared. MPO activity in Sevoflurane group compared to isoflurane and control groups (p:0.001, p:0.041, respectively.) were significantly low. Furthermore, TBARS levels in Sevoflurane group compared to the other groups (p:0.035, p:0.041, respectively) were also significantly low. MPO activity in Isoflurane group were significantly high compared to control group.Alveolar macrophage counts (p:0.001, p:0.001, respectively) and M-30 positive cell counts (p:0.001, p:0.001, respectively) in Isoflurane group were significantly high compared to sevoflurane and control groups. On the other hand, the alveolar macrophage counts (p:0.002) and M-30 positive cell counts (p:0.002) in sevoflurane group were significantly high compared to control group. Light microscopic findings observed in sevoflurane group and any more in isoflurane group were; diffuse mononuclear cell infiltration, diffuse alveolar injury, alveolary oedema, thickening of alveolar septums, dense alveolar macrophage and light neutrophil and type II pneumocytes infiltration in alveol lumen. Furthermore, the paranchimal changes were diffuse hemorrhage, mononuclear cell infiltration, oedema and vascular congestion.Conclusion:This study is concluded as, sevoflurane produces pulmonary macrophage activation and apoptosis less than isoflurane does and since sevoflurane group has lower pulmonary tissue MPO activity and TBARS levels than control group, it can be pronounced that sevoflurane has an anti-inflammatory activity. Nevertheless, more studies should be made on injured lung tissue.Keywords: isoflurane, sevoflurane, lung injury, apoptosis, inhalational agent, general anesthesiaObjective:In recent years, the thesis on inhalational anesthetics can be the reason for pulmonary complications during general anesthesia has come into a question. The probable mechanism of lung injury due to these agents has been considered as; endothelial cell injury caused by activated neutrophils, formation of reactive oxygen radicals and/or proteases. In this trial, it has been aimed to investigate the effects of sevoflurane and isoflurane on lung tissue in rat model.Method:After the approval of ethics committee for Research Animals, 21 adult male Wistar Albino rats were randomly allocated into three groups. The subjects were mechanically ventilated for 2 hours in Control group (n=7) with 50 % oxygen + 50 % air mixture; in Isoflurane group (n=7) with % 1.2 ( 1 MAC) isoflurane + 50 % oxygen + 50 % air and in Sevoflurane Group (n=7) with %2.4 ( 1 MAC) sevoflurane + 50 % oxygen + 50 % air mixture. At the end of the study, a median sternotomy was performed, lungs were removed and rats were sacrified. Left lung was used for pulmonary tissue myeloperoxidase activity and thiobarbituric acid reactive substances (MPO and TBARS ) determinations, right lung was used for histopathological determinations. Histopathological determinations were included, light microscope image analysis, alveolar macrophage count and M-30 immune histochemical analysis of apoptosis. Data were analyzed using Kruskal Wallis and Mann - Whitney U tests and p< 0.05 were regarded as statistically significant.Results: There were no statistical significance between groups when hemodynamic (heart rate, systolic blood pressures- diastolic blood pressures) and blood gases parameters (pH, PaO2, PaCO2) were compared. MPO activity in Sevoflurane group compared to isoflurane and control groups (p:0.001, p:0.041, respectively.) were significantly low. Furthermore, TBARS levels in Sevoflurane group compared to the other groups (p:0.035, p:0.041, respectively) were also significantly low. MPO activity in Isoflurane group were significantly high compared to control group.Alveolar macrophage counts (p:0.001, p:0.001, respectively) and M-30 positive cell counts (p:0.001, p:0.001, respectively) in Isoflurane group were significantly high compared to sevoflurane and control groups. On the other hand, the alveolar macrophage counts (p:0.002) and M-30 positive cell counts (p:0.002) in sevoflurane group were significantly high compared to control group. Light microscopic findings observed in sevoflurane group and any more in isoflurane group were; diffuse mononuclear cell infiltration, diffuse alveolar injury, alveolary oedema, thickening of alveolar septums, dense alveolar macrophage and light neutrophil and type II pneumocytes infiltration in alveol lumen. Furthermore, the paranchimal changes were diffuse hemorrhage, mononuclear cell infiltration, oedema and vascular congestion.Conclusion:This study is concluded as, sevoflurane produces pulmonary macrophage activation and apoptosis less than isoflurane does and since sevoflurane group has lower pulmonary tissue MPO activity and TBARS levels than control group, it can be pronounced that sevoflurane has an anti-inflammatory activity. Nevertheless, more studies should be made on injured lung tissue.Keywords: isoflurane, sevoflurane, lung injury, apoptosis, inhalational agent, general anesthesiaObjective:In recent years, the thesis on inhalational anesthetics can be the reason for pulmonary complications during general anesthesia has come into a question. The probable mechanism of lung injury due to these agents has been considered as; endothelial cell injury caused by activated neutrophils, formation of reactive oxygen radicals and/or proteases. In this trial, it has been aimed to investigate the effects of sevoflurane and isoflurane on lung tissue in rat model.Method:After the approval of ethics committee for Research Animals, 21 adult male Wistar Albino rats were randomly allocated into three groups. The subjects were mechanically ventilated for 2 hours in Control group (n=7) with 50 % oxygen + 50 % air mixture; in Isoflurane group (n=7) with % 1.2 ( 1 MAC) isoflurane + 50 % oxygen + 50 % air and in Sevoflurane Group (n=7) with %2.4 ( 1 MAC) sevoflurane + 50 % oxygen + 50 % air mixture. At the end of the study, a median sternotomy was performed, lungs were removed and rats were sacrified. Left lung was used for pulmonary tissue myeloperoxidase activity and thiobarbituric acid reactive substances (MPO and TBARS ) determinations, right lung was used for histopathological determinations. Histopathological determinations were included, light microscope image analysis, alveolar macrophage count and M-30 immune histochemical analysis of apoptosis. Data were analyzed using Kruskal Wallis and Mann - Whitney U tests and p< 0.05 were regarded as statistically significant.Results: There were no statistical significance between groups when hemodynamic (heart rate, systolic blood pressures- diastolic blood pressures) and blood gases parameters (pH, PaO2, PaCO2) were compared. MPO activity in Sevoflurane group compared to isoflurane and control groups (p:0.001, p:0.041, respectively.) were significantly low. Furthermore, TBARS levels in Sevoflurane group compared to the other groups (p:0.035, p:0.041, respectively) were also significantly low. MPO activity in Isoflurane group were significantly high compared to control group.Alveolar macrophage counts (p:0.001, p:0.001, respectively) and M-30 positive cell counts (p:0.001, p:0.001, respectively) in Isoflurane group were significantly high compared to sevoflurane and control groups. On the other hand, the alveolar macrophage counts (p:0.002) and M-30 positive cell counts (p:0.002) in sevoflurane group were significantly high compared to control group. Light microscopic findings observed in sevoflurane group and any more in isoflurane group were; diffuse mononuclear cell infiltration, diffuse alveolar injury, alveolary oedema, thickening of alveolar septums, dense alveolar macrophage and light neutrophil and type II pneumocytes infiltration in alveol lumen. Furthermore, the paranchimal changes were diffuse hemorrhage, mononuclear cell infiltration, oedema and vascular congestion.Conclusion:This study is concluded as, sevoflurane produces pulmonary macrophage activation and apoptosis less than isoflurane does and since sevoflurane group has lower pulmonary tissue MPO activity and TBARS levels than control group, it can be pronounced that sevoflurane has an anti-inflammatory activity. Nevertheless, more studies should be made on injured lung tissue.Keywords: isoflurane, sevoflurane, lung injury, apoptosis, inhalational agent, general anesthesia