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Objetivo:Avaliar a capacidade da clonidina de reduzir a pressão arterial pulmonar de pacientes com hipertensão pulmonar, submetidos a cirurgia cardíaca, seja pela diminuição dos valores pressóricos a partir da aferição direta da pressão de artéria pulmonar, seja pela redução ouabolição da necessidade de dobutamina e nitroprussiato de sódio no intraoperatório.Método:Trata-se de estudo controlado, comparativo, randomizado e duplamente encoberto feito com 30 pacientes portadores de hipertensão arterial pulmonar tipo 2, submetidos a cirurgia cardíaca. Avaliaram-se a pressão média de artéria pulmonar e a posologia de dobutaminae nitroprussiato de sódio em quatro momentos: (M0) antes da administração de 2 µg/kg declonidina intravenosa ou placebo; (M1) decorridos 30 minutos do tratamento testado e antes da circulação extracorpórea; (M2) imediatamente após a circulação extracorpórea; e (M3)10 minutos após a injeção de protamina.Resultados:Não houve diferenças significativas em relação à pressão média de artéria pulmonarem nenhum dos momentos estudados. Entre os grupos não houve também diferença significativa entre as demais variáveis estudadas, como pressão arterial sistêmica média, frequência cardíaca, dosagem total de dobutamina, dosagem total de nitroprussiato de sódio e necessidade do hipnoanalgésico fentanil.Conclusão:A análise dos dados obtidos dos pacientes incluídos neste estudo permite concluir que a clonidina, na dose de 2 µg/kg administrada via intravenosa, não foi capaz de reduzir a pressão média de artéria pulmonar de pacientes com hipertensão pulmonar do grupo 2 (hipertensão venosa pulmonar), submetidos a cirurgia cardíaca, e nem reduzir ou abolir a necessidade da administração de dobutamina e nitroprussiato de sódio no intraoperatório. Objective:Evaluate the ability of clonidine to reduce pulmonary arterial pressure in patients with pulmonary hypertension undergoing heart surgery, either by reducing the pressure values from the direct measurement of pulmonary arterial pressure or by reducing or eliminating the need for intraoperative dobutamine and nitroprusside.Method:Randomized, double-blind, placebo-controlled, comparative study conducted in 30 patients with pulmonary arterial hypertension type 2 undergoing cardiac surgery. Mean pulmonary arterial pressure and dosage of dobutamine and sodium nitroprusside were assessed four times: before intravenous administration of clonidine (2 µg/kg) or placebo (T0), 30 min after tested treatment and before cardiopulmonary bypass (T1), immediately after CPB (T2), 10 min after protamine injection (T3).Results:There were no significant differences regarding mean pulmonary arterial pressure at any time of evaluation. There was no significant difference between groups regarding other variables, such as mean systemic arterial pressure, heart rate, total dose of dobutamine, total dose of sodium nitroprusside, and need for fentanyl.Conclusion:Data analysis from patients included in this study allows us to conclude that intra-venous clonidine (2 µg/kg) was not able to reduce the mean pulmonary arterial pressure inpatients with pulmonary hypertension in group 2 (pulmonary venous hypertension), undergoing heart surgery, or reduce or eliminate the need for intraoperative administration of dobutamineand sodium nitroprusside. Objetivo:Evaluar la capacidad de la clonidina de reducir la presión arterial pulmonar de pacientes con hipertensión pulmonar sometidos a cirugía cardíaca, sea por la disminución de los valores tensionales a partir de la comprobación directa de la presión de la arteria pulmonar, o por la reducción o supresión de la necesidad de dobutamina y nitroprusiato de sodio en el intraoperatorio.Método:Se trata de un estudio controlado, comparativo, aleatorizado y doble ciego hecho con 30 pacientes con hipertensión arterial pulmonar tipo 2, sometidos a cirugía cardíaca. Fueron evaluados la presión promedio de la arteria pulmonar y la posología de dobutamina y nitroprusiato de sodio en 4 momentos: (M0) antes de la administración de 2 µg/kg de clonidina intravenosa o placebo; (M1) transcurridos 30 min del tratamiento testado y antes de la circulación extracorpórea; (M2) inmediatamente después de la circulación extracorpórea; y (M3) 10 min después de la inyección de protamina.Resultados:No fueron verificadas diferencias significativas con relación a la presión promedio de la arteria pulmonar en ninguno de los momentos estudiados. Entre los grupos tampoco hubo diferencia significativa entre las demás variables estudiadas, como presión arterial sistémica promedio, frecuencia cardíaca, dosificación total de dobutamina, dosificación total de nitroprusiato de sodio y la necesidad del hipnoanalgésico fentanilo.Conclusiones:El análisis de los datos obtenidos de los pacientes incluidos en este estudio permite concluir que la clonidina en una dosis de 2 µg/kg administrada por vía intravenosa no fue capaz de reducir la presión promedio de la arteria pulmonar de pacientes con hipertensión pulmonar del grupo 2 (hipertensión venosa pulmonar), sometidos a cirugía cardíaca, ni tampoco reducir o suprimir la necesidad de la administración de dobutamina y nitroprusiato de sodio en el intraoperatorio. Universidade Federal de São Paulo (UNIFESP) Hospital São Paulo Hospital Beneficência Portuguesa Universidade Federal de São Paulo (UNIFESP) UNIFESP, Hospital São Paulo UNIFESP SciELO

To examine whether treatment with L-arginine (ARG), a substrate of nitric oxide biosynthesis, attenuated intestinal dysfunction caused by ischemia (I) and reperfusion (R), we treated rats with ARG (100 mg/kg intravenously) or saline solution (SS) before 60 minutes of I produced by occlusion of the superior mesenteric artery and/or during 120 minutes of R. After I or I/R, we isolated 2-cm jejunal segments for mounting in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl with the use of a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Jejunal contractions were similar in the sham and I+ARG, but reduced in I+SS, I/R+SS, and I/R+ARG groups. Jejunal enteric nerves were damaged in I+SS, IR+SS, and IR+ARG, but not in the I+ARG group, suggesting that ARG attenuate intestinal dysfunctions due to I but not to R.

To study whether ischemic preconditioning (IPC) attenuated intestinal dysfunction caused by ischemia (I) and reperfusion (R), rats were underwent 60 minutes of I which was produced by occlusion of the superior mesenteric artery, and/or 120 minutes R. The IPC group had the I procedure previously stimulated for 5 minutes and the R for 10 minutes. IPC and sham groups were injected with saline solution (SS) via the femoral vein 5 minutes before the I and R, and for R. After I or I/R, 2-cm jejunal segments were mounted in an organ bath to study neurogenic contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained with hematoxylin and eosin for optical microscopy. Compared with the sham group, jejunal contractions were similar in the IPC + I and the IPC + I/R groups, but reduced in the I + SS and the I/R + SS groups. The jejunal enteric nerves were damaged in the I + SS and the I/R + SS groups, but not in the IPC groups. These results suggested that ischemic preconditioning attenuated intestinal dysfunction caused by I and I/R.

To study if the treatment with adenosine (ADO), an agonist of adenosine receptors, attenuates intestinal dysfunction caused by ischemia (I) and reperfusion (R), we treated rabbits with ADO (15 mg · kg −1 , intravenously) or saline solution (SS) to I (60 minutes) before occlusion of superior mesenteric artery and/or R (120 min). After I or I/R, isolated jejunal segments (2 cm) were mounted in an organ bath to study nerve-mediated contractions stimulated by electrical pulses or KCl using a digital recording system. Thin jejunal slices were stained (hematoxylin and eosin) for analysis by optical microscopy. Compared to the sham group, the jejunal contractions were similar in I + ADO, but reduced in I + SS, I/R + SS, and I/R + ADO groups. We concluded that the jejunal enteric nerves were damaged in I + SS, I/R + SS, and I/R + ADO, but not in I + ADO group. These results suggested that ADO attenuated intestinal dysfunction due to I, but not to R.

Acute respiratory distress syndrome secondary to sepsis is associated with high morbidity and mortality. The purpose of this study was to characterize the effects of ventilatory strategy and the modulating activity of pentoxifylline in a sepsis-induced lung dysfunction model. Male Wistar rats were randomly divided into six groups, undergoing two different ventilatory strategies. Rats received live Escherichia coli or saline intraperitoneally. After 6 hours, the septic animals were treated with either pentoxifylline (25 mg/kg for 20 minutes) or normal saline infusion and ventilated with low tidal volume (6 mL/kg; septic animals with E. coli intraperitoneal [IP] infusion, PTX-treated and ventilated with low tidal volume and septic animals with E. coli IP infusion and ventilated with low tidal volume, respectively) or high tidal volume (12 mL/kg; septic animals with E. coli IP infusion, PTX-treated and ventilated with high tidal volume and septic animals with E. coli IP infusion and ventilated with high tidal volume, respectively) for 3 hours. The control animals received normal saline infusion and, after 6 hours, were ventilated with low or high tidal volume (control animals with saline infusion and ventilated with low tidal volume and control animals with saline infusion and ventilated with high tidal volume, respectively). Lung dysfunctions were assessed by wet-to-dry lung ratios, total cell count, total protein, malondialdehyde, and tumor necrosis factor-alpha concentrations in bronchoalveolar lavage (BAL). Septic animals with E. coli IP infusion and ventilated with high tidal volume presented increased wet-to-dry lung ratios, total cell count, total protein, and malondialdehyde in BAL compared with the septic animals ventilated with low tidal volume. Septic animals treated with pentoxifylline presented higher arterial oxygenation and lower cellular influx, protein leakage, malondialdehyde concentration, and tumor necrosis factor-alpha levels in BAL compared with septic animals undergoing the same ventilatory support strategies (septic animals with E. coli IP infusion and ventilated with low tidal volume and septic animals with E. coli IP infusion and ventilated with high tidal volume). Ventilatory strategy modulated the inflammatory response and pulmonary alterations in a sepsis-induced acute lung injury model, and these effects are improved by pentoxifylline.