RESUMEN
OBJECTIVE: To investigate the protective effect and mechanism of dexmedetomidine (Dex) on perioperative myocardial injury in patients with Stanford type-A aortic dissection (AD). METHODS: Eighty-six patients with Stanford type-A AD were randomly divided into Dex and control groups, with 43 cases in each group. During the surgery, the control group received the routine anesthesia, and the Dex group received Dex treatment based on routine anesthesia. The heart rate (HR) and mean arterial pressure (MAP) were recorded before Dex loading (t0), 10 min after Dex loading (t1), at the skin incision (t2), sternum sawing (t3), before cardiopulmonary bypass (t4), at the extubation (t5), and at end of surgery (t6). The blood indexes were determined before anesthesia induction (T0) and postoperatively after 12h (T1), 24h (T2), 48h (T3), and 72h (T4). RESULTS: At t2 and t3, the HR and MAP in the Dex group were lower than in the control group (P < 0.05). Compared with the control group, in the Dex group at T1, T2, and T3, the serum creatine kinase-MB, cardiac troponin-I, C-reactive protein, and tumor necrosis factor-α levels were decreased, and the interleukin-10 level, the serum total superoxide dismutase, and total anti-oxidant capability increased, while the myeloperoxidase and malondialdehyde levels decreased (all P < 0.05). CONCLUSIONS: Dex treatment may alleviate perioperative myocardial injury in patients with Stanford type-A AD by resisting inflammatory response and oxidative stress.
Asunto(s)
Disección Aórtica , Dexmedetomidina , Disección Aórtica/prevención & control , Disección Aórtica/cirugía , Frecuencia Cardíaca , Humanos , Peroxidasa , Factor de Necrosis Tumoral alfaRESUMEN
SUMMARY OBJECTIVE: To investigate the protective effect and mechanism of dexmedetomidine (Dex) on perioperative myocardial injury in patients with Stanford type-A aortic dissection (AD). METHODS: Eighty-six patients with Stanford type-A AD were randomly divided into Dex and control groups, with 43 cases in each group. During the surgery, the control group received the routine anesthesia, and the Dex group received Dex treatment based on routine anesthesia. The heart rate (HR) and mean arterial pressure (MAP) were recorded before Dex loading (t0), 10 min after Dex loading (t1), at the skin incision (t2), sternum sawing (t3), before cardiopulmonary bypass (t4), at the extubation (t5), and at end of surgery (t6). The blood indexes were determined before anesthesia induction (T0) and postoperatively after 12h (T1), 24h (T2), 48h (T3), and 72h (T4). RESULTS: At t2 and t3, the HR and MAP in the Dex group were lower than in the control group (P < 0.05). Compared with the control group, in the Dex group at T1, T2, and T3, the serum creatine kinase-MB, cardiac troponin-I, C-reactive protein, and tumor necrosis factor-α levels were decreased, and the interleukin-10 level, the serum total superoxide dismutase, and total anti-oxidant capability increased, while the myeloperoxidase and malondialdehyde levels decreased (all P < 0.05). CONCLUSIONS: Dex treatment may alleviate perioperative myocardial injury in patients with Stanford type-A AD by resisting inflammatory response and oxidative stress.
RESUMO OBJETIVO: Investigar o efeito protetor e o mecanismo da dexmedetomidina (Dex) na lesão perioperativa do miocárdio em doentes com dissecação aórtica Tipo A de Stanford (AD). MÉTODOS: Oitenta e seis pacientes com o Tipo A de Stanford foram aleatoriamente divididos em Dex e grupos de controle, 43 casos em cada grupo. Durante a cirurgia, o grupo de controle recebeu a anestesia de rotina, e o grupo Dex recebeu tratamento Dex baseado na anestesia de rotina. A frequência cardíaca (AR) e a pressão arterial média (MAP) foram registradas no momento anterior ao Dex carregar (t0), 10 minutos após o Dex carregar (t1), incisão cutânea (t2), serragem de esterno (t3), antes do bypass cardiopulmonar (t4), extubação (t5) e fim da cirurgia (t6). Os índices de sangue foram determinados no momento antes da indução da anestesia (T0) e no pós-operatório 12 horas (T1), 24 horas (T2), 48 horas (T3) e 72 horas (T4). RESULTADOS: Em T2 e t3, o RH e o MAP do grupo Dex foram inferiores ao grupo de controle (p<0,05). Em comparação com o grupo de controle, no grupo Dex em T1, T2 e T3, os níveis séricos de creatina quinase-MB, troponina-I, proteína C-reativa e necrose do fator-α do tumor diminuíram, o nível interleucina-10 aumentou, o desalinhamento total do superóxido sérico e a capacidade antioxidante total aumentaram e os níveis de mielopeperóxido e malondialdeído diminuíram (todos p<0,05). CONCLUSÃO: O tratamento com Dex pode aliviar a lesão do miocárdio perioperativo em doentes com o Tipo A de Stanford por resistência à resposta inflamatória e ao estresse oxidativo.