The antioxidant effect of preischemic dexmedetomidine in a rat model: increased expression of Nrf2/HO-1 via the PKC pathway

Abstract Background The precise underlying mechanism of antioxidant effects of dexmedetomidine-induced neuroprotection against cerebral ischemia has not yet been fully elucidated. Activation of Nuclear factor erythroid 2-related factor (Nrf2) and Heme Oxygenase-1 (HO-1) represents a major antioxidant-defense mechanism. Therefore, we determined whether dexmedetomidine increases Nrf2/HO-1 expression after global transient cerebral ischemia and assessed the involvement of Protein Kinase C (PKC) in the dexmedetomidine-related antioxidant mechanism. Methods Thirty-eight rats were randomly assigned to five groups: sham (n = 6), ischemic (n = 8), chelerythrine (a PKC inhibitor; 5 mg.kg-1 IV administered 30 min before cerebral ischemia) (n = 8), dexmedetomidine (100 µg.kg-1 IP administered 30 min before cerebral ischemia (n = 8), and dexmedetomidine + chelerythrine (n = 8). Global transient cerebral ischemia (10 min) was applied in all groups, except the sham group; histopathologic changes and levels of nuclear Nrf2 and cytoplasmic HO-1 were examined 24 hours after ischemia insult. Results We found fewer necrotic and apoptotic cells in the dexmedetomidine group relative to the ischemic group (p< 0.01) and significantly higher Nrf2 and HO-1 levels in the dexmedetomidine group than in the ischemic group (p< 0.01). Additionally, chelerythrine co-administration with dexmedetomidine attenuated the dexmedetomidine-induced increases in Nrf2 and HO-1 levels (p< 0.05 and p< 0.01, respectively) and diminished its beneficial neuroprotective effects. Conclusion Preischemic dexmedetomidine administration elicited neuroprotection against global transient cerebral ischemia in rats by increasing Nrf2/HO-1 expression partly via PKC signaling, suggesting that this is the antioxidant mechanism underlying dexmedetomidine-mediated neuroprotection.

The antioxidant effect of preischemic dexmedetomidine in a rat model: increased expression of Nrf2/HO-1 via the PKC pathway.

BACKGROUND: The precise underlying mechanism of antioxidant effects of dexmedetomidine-induced neuroprotection against cerebral ischemia has not yet been fully elucidated. Activation of Nuclear factor erythroid 2-related factor (Nrf2) and Heme Oxygenase-1 (HO-1) represents a major antioxidant-defense mechanism. Therefore, we determined whether dexmedetomidine increases Nrf2/HO-1 expression after global transient cerebral ischemia and assessed the involvement of Protein Kinase C (PKC) in the dexmedetomidine-related antioxidant mechanism. METHODS: Thirty-eight rats were randomly assigned to five groups: sham (n...=...6), ischemic (n...=...8), chelerythrine (a PKC inhibitor; 5...mg.kg-1 IV administered 30...min before cerebral ischemia) (n...=...8), dexmedetomidine (100.....g.kg-1 IP administered 30...min before cerebral ischemia (n...=...8), and dexmedetomidine...+...chelerythrine (n...=...8). Global transient cerebral ischemia (10...min) was applied in all groups, except the sham group; histopathologic changes and levels of nuclear Nrf2 and cytoplasmic HO-1 were examined 24...hours after ischemia insult. RESULTS: We found fewer necrotic and apoptotic cells in the dexmedetomidine group relative to the ischemic group (p...<...0.01) and significantly higher Nrf2 and HO-1 levels in the dexmedetomidine group than in the ischemic group (p...<...0.01). Additionally, chelerythrine co-administration with dexmedetomidine attenuated the dexmedetomidine-induced increases in Nrf2 and HO-1 levels (p...<...0.05 and p...<...0.01, respectively) and diminished its beneficial neuroprotective effects. CONCLUSION: Preischemic dexmedetomidine administration elicited neuroprotection against global transient cerebral ischemia in rats by increasing Nrf2/HO-1 expression partly via PKC signaling, suggesting that this is the antioxidant mechanism underlying dexmedetomidine-mediated neuroprotection.

Fatal cardiac tamponade that developed in the post-anesthesia care unit: a rare complication after lung lobectomy / Tamponamento cardíaco fatal desencadeado na sala de recuperação pós-anestésica: uma complicação rara após lobectomia pulmonar

Abstract Background and objectives: Cardiac tamponade is potentially fatal medical condition, which rarely occurs as a complication of lung lobectomy. We present the first case of cardiac tamponade to develop in a Post-Anesthesia Care Unit following a lung lobectomy. Case report: A 54-year-old man with pulmonary squamous cell carcinoma underwent an apparently uncomplicated lung lobectomy. His hemodynamics was unremarkable throughout the surgery and initially in the Post-Anesthesia Care Unit. However, after 5 min in the Post-Anesthesia Care Unit, he suddenly became hypotensive and dyspneic. He responded poorly to inotropics and fluid resuscitation. Transesophageal echocardiography conducted by an anesthesiologist who suspected a cardiac etiology revealed a pericardial effusion compressing the heart. After a failed attempt of pericardiocentesis, an emergency pericardial window operation was performed. The patient improved dramatically once the heart was decompressed. Conclusion: Since cardiac tamponade is generally not suspected as a cause of hemodynamic instability after a lung lobectomy, as it was in this case, a misdiagnosis of the patient's condition may have led to improper management resulting in death. As anesthesiologists are often involved in the initial resuscitation of morbid patients in Post-Anesthesia Care Units, their acquaintance with various postoperative complications and competence in echocardiography for assessing cardiac problems may contribute to patient survival.

Resumo Justificativa e objetivos: O tamponamento cardíaco é uma condição médica potencialmente fatal, cuja ocorrência como uma complicação da lobectomia pulmonar é muito rara. Apresentamos o primeiro caso de tamponamento cardíaco desencadeado na sala de recuperação pós-anestésica (SRPA) após uma lobectomia pulmonar. Relato de caso: Paciente do sexo masculino, 54 anos, com carcinoma de células escamosas pulmonares, submetido à lobectomia pulmonar aparentemente sem complicações. Sua hemodinâmica não apresentou alteração durante toda a cirurgia e também inicialmente na sala de recuperação pós-anestésica. Porém, após cinco minutos na SRPA, o paciente apresentou hipotensão e dispneia de forma repentina e respondeu mal ao inotrópico e à reanimação hídrica. Uma ecocardiografia transesofágica feita por um anestesiologista que suspeitou de etiologia cardíaca revelou um derrame pericárdico que comprimia o coração. Após tentativa malsucedida de pericardiocentese, foi feita uma janela pericárdica de emergência. O paciente apresentou melhoria dramática com a descompressão do coração. Conclusão: Como o tamponamento cardíaco geralmente não é suspeito como causa de instabilidade hemodinâmica após lobectomia pulmonar, como ocorreu neste caso, um diagnóstico errado da condição do paciente poderia ter levado a um manejo inadequado, que resultaria em morte. Como os anestesiologistas estão frequentemente envolvidos na reanimação inicial de pacientes debilitados em salas de recuperação pós-anestésica, seu conhecimento de várias complicações pós-operatórias e competência na ecocardiografia para avaliar problemas cardíacos podem contribuir para a sobrevivência do paciente.

[Fatal cardiac tamponade that developed in the post-anesthesia care unit: a rare complication after lung lobectomy]. / Tamponamento cardíaco fatal desencadeado na sala de recuperação pós-anestésica: uma complicação rara após lobectomia pulmonar.

BACKGROUND AND OBJECTIVES: Cardiac tamponade is potentially fatal medical condition, which rarely occurs as a complication of lung lobectomy. We present the first case of cardiac tamponade to develop in a Post-Anesthesia Care Unit following a lung lobectomy. CASE REPORT: A 54-year-old man with pulmonary squamous cell carcinoma underwent an apparently uncomplicated lung lobectomy. His hemodynamics was unremarkable throughout the surgery and initially in the Post-Anesthesia Care Unit. However, after 5min in the Post-Anesthesia Care Unit, he suddenly became hypotensive and dyspneic. He responded poorly to inotropics and fluid resuscitation. Transesophageal echocardiography conducted by an anesthesiologist who suspected a cardiac etiology revealed a pericardial effusion compressing the heart. After a failed attempt of pericardiocentesis, an emergency pericardial window operation was performed. The patient improved dramatically once the heart was decompressed. CONCLUSION: Since cardiac tamponade is generally not suspected as a cause of hemodynamic instability after a lung lobectomy, as it was in this case, a misdiagnosis of the patient's condition may have led to improper management resulting in death. As anesthesiologists are often involved in the initial resuscitation of morbid patients in Post-Anesthesia Care Units, their acquaintance with various postoperative complications and competence in echocardiography for assessing cardiac problems may contribute to patient survival.

High-efficiency tooth bleaching using non-thermal atmospheric pressure plasma with low concentration of hydrogen peroxide.

UNLABELLED: Light-activated tooth bleaching with a high hydrogen peroxide (HP; H2O2) concentration has risks and the actual role of the light source is doubtful. The use of conventional light might result in an increase in the temperature and cause thermal damage to the health of the tooth tissue. OBJECTIVE: This study investigated the efficacy of tooth bleaching using non-thermal atmospheric pressure plasma (NAPP) with 15% carbamide peroxide (CP; CH6N2O3) including 5.4% HP, as compared with conventional light sources. MATERIAL AND METHODS: Forty human teeth were randomly divided into four groups: Group I (CP+NAPP), Group II (CP+plasma arc lamp; PAC), Group III (CP+diode laser), and Group IV (CP alone). Color changes (∆E) of the tooth and tooth surface temperatures were measured. Data were evaluated by one-way analysis of variance (ANOVA) and post-hoc Tukey's tests. RESULTS: Group I showed the highest bleaching efficacy, with a ∆E value of 1.92-, 2.61 and 2.97-fold greater than those of Groups II, III and IV, respectively (P<0.05). The tooth surface temperature was maintained around 37°C in Group I, but it reached 43°C in Groups II and III. CONCLUSIONS: The NAPP has a greater capability for effective tooth bleaching than conventional light sources with a low concentration of HP without causing thermal damage. Tooth bleaching using NAPP can become a major technique for in-office bleaching in the near future.

High-efficiency tooth bleaching using non-thermal atmospheric pressure plasma with low concentration of hydrogen peroxide

Light-activated tooth bleaching with a high hydrogen peroxide (HP; H2O2) concentration has risks and the actual role of the light source is doubtful. The use of conventional light might result in an increase in the temperature and cause thermal damage to the health of the tooth tissue. Objective This study investigated the efficacy of tooth bleaching using non-thermal atmospheric pressure plasma (NAPP) with 15% carbamide peroxide (CP; CH6N2O3) including 5.4% HP, as compared with conventional light sources. Material and Methods Forty human teeth were randomly divided into four groups: Group I (CP+NAPP), Group II (CP+plasma arc lamp; PAC), Group III (CP+diode laser), and Group IV (CP alone). Color changes (∆E) of the tooth and tooth surface temperatures were measured. Data were evaluated by one-way analysis of variance (ANOVA) and post-hoc Tukey's tests. Results Group I showed the highest bleaching efficacy, with a ∆E value of 1.92-, 2.61 and 2.97-fold greater than those of Groups II, III and IV, respectively (P<0.05). The tooth surface temperature was maintained around 37°C in Group I, but it reached 43°C in Groups II and III. Conclusions The NAPP has a greater capability for effective tooth bleaching than conventional light sources with a low concentration of HP without causing thermal damage. Tooth bleaching using NAPP can become a major technique for in-office bleaching in the near future. .