Beatriz Mangueira Saraiva

Evaluation of exhaled nitric oxide in patients undergoing myocardial revascularization with cardiopulmonary bypass

BACKGROUND AND OBJECTIVES Cardiopulmonary bypass (CPB) can cause pulmonary dysfunction. Inflammatory changes may affect the release of nitric oxide (NO). The objective of this study was to evaluate exhaled NO in patients undergoing myocardial revascularization (MR) with CPB. METHODS This is a prospective study with nine adult patients undergoing MR with CPB. Initially, air samples were collected to analyze the presence of NO in the system that feeds the anesthesia equipment. Intravenous anesthesia was then initiated with ethomidate (0.3 mg x kg-1), sufentanil (0.3 microg x kg-1), and pancuronium (0.08 mg x kg-1), and maintained with isoflurane (MAC from 0.5 to 1.0) and sufentanil (5 microg x kg-1 x h-1). Tidal volume was fixed at 8 mL.kg-1 and FiO2 0.6, except during CPB. Thirty minutes after induction and 30 minutes after CPB, three sequential samples of exhaled air were collected for NO analysis by chemiluminescence. Data were analyzed by the Student t test. RESULTS The level of NO in room air was 5.05 +/- 3.37 ppb. Levels of exhaled NO decreased after CPB, varying from 11.25 +/- 5.65 ppb to 8.37 +/- 3.71 ppb (p = 0.031). CONCLUSIONS The reduction of exhaled NO after CPB observed in this study does not confirm the role of this molecule as a marker of pulmonary lesion. However, the different degrees of pulmonary parenchymal collapse, the method used to collect the data, and the drugs, among others, could have contributed for this reduction.BACKGROUND AND OBJECTIVES: Cardiopulmonary bypass (CPB) can cause pulmonary dysfunction. Inflammatory changes may affect the release of nitric oxide (NO). The objective of this study was to evaluate exhaled NO in patients undergoing myocardial revascularization (MR) with CPB. METHODS: This is a prospective study with nine adult patients undergoing MR with CPB. Initially, air samples were collected to analyze the presence of NO in the system that feeds the anesthesia equipment. Intravenous anesthesia was then initiated with ethomidate (0.3 mg.kg-1), sufentanil (0.3 µg.kg-1), and pancuronium (0.08 mg.kg-1), and maintained with isoflurane (MAC from 0.5 to 1.0) and sufentanil (5 µg.kg-1.h-1). Tidal volume was fixed at 8 mL.kg-1 and FiO2 0.6, except during CPB. Thirty minutes after induction and 30 minutes after CPB, three sequential samples of exhaled air were collected for NO analysis by chemiluminescence. Data were analyzed by the Student t test. RESULTS: The level of NO in room air was 5.05 ± 3.37 ppb. Levels of exhaled NO decreased after CPB, varying from 11.25 ± 5.65 ppb to 8.37 ± 3.71 ppb (p = 0.031). CONCLUSIONS: The reduction of exhaled NO after CPB observed in this study does not confirm the role of this molecule as a marker of pulmonary lesion. However, the different degrees of pulmonary parenchymal collapse, the method used to collect the data, and the drugs, among others, could have contributed for this reduction.

Avaliação do óxido nítrico exalado em pacientes submetidos à revascularização do miocárdio com circulação extracorpórea

BACKGROUND AND OBJECTIVES Cardiopulmonary bypass (CPB) can cause pulmonary dysfunction. Inflammatory changes may affect the release of nitric oxide (NO). The objective of this study was to evaluate exhaled NO in patients undergoing myocardial revascularization (MR) with CPB. METHODS This is a prospective study with nine adult patients undergoing MR with CPB. Initially, air samples were collected to analyze the presence of NO in the system that feeds the anesthesia equipment. Intravenous anesthesia was then initiated with ethomidate (0.3 mg x kg-1), sufentanil (0.3 microg x kg-1), and pancuronium (0.08 mg x kg-1), and maintained with isoflurane (MAC from 0.5 to 1.0) and sufentanil (5 microg x kg-1 x h-1). Tidal volume was fixed at 8 mL.kg-1 and FiO2 0.6, except during CPB. Thirty minutes after induction and 30 minutes after CPB, three sequential samples of exhaled air were collected for NO analysis by chemiluminescence. Data were analyzed by the Student t test. RESULTS The level of NO in room air was 5.05 +/- 3.37 ppb. Levels of exhaled NO decreased after CPB, varying from 11.25 +/- 5.65 ppb to 8.37 +/- 3.71 ppb (p = 0.031). CONCLUSIONS The reduction of exhaled NO after CPB observed in this study does not confirm the role of this molecule as a marker of pulmonary lesion. However, the different degrees of pulmonary parenchymal collapse, the method used to collect the data, and the drugs, among others, could have contributed for this reduction.BACKGROUND AND OBJECTIVES: Cardiopulmonary bypass (CPB) can cause pulmonary dysfunction. Inflammatory changes may affect the release of nitric oxide (NO). The objective of this study was to evaluate exhaled NO in patients undergoing myocardial revascularization (MR) with CPB. METHODS: This is a prospective study with nine adult patients undergoing MR with CPB. Initially, air samples were collected to analyze the presence of NO in the system that feeds the anesthesia equipment. Intravenous anesthesia was then initiated with ethomidate (0.3 mg.kg-1), sufentanil (0.3 µg.kg-1), and pancuronium (0.08 mg.kg-1), and maintained with isoflurane (MAC from 0.5 to 1.0) and sufentanil (5 µg.kg-1.h-1). Tidal volume was fixed at 8 mL.kg-1 and FiO2 0.6, except during CPB. Thirty minutes after induction and 30 minutes after CPB, three sequential samples of exhaled air were collected for NO analysis by chemiluminescence. Data were analyzed by the Student t test. RESULTS: The level of NO in room air was 5.05 ± 3.37 ppb. Levels of exhaled NO decreased after CPB, varying from 11.25 ± 5.65 ppb to 8.37 ± 3.71 ppb (p = 0.031). CONCLUSIONS: The reduction of exhaled NO after CPB observed in this study does not confirm the role of this molecule as a marker of pulmonary lesion. However, the different degrees of pulmonary parenchymal collapse, the method used to collect the data, and the drugs, among others, could have contributed for this reduction.

Evaluación del óxido nítrico exhalado en pacientes sometidos a la revascularización del miocardio con circulación extracorpórea

BACKGROUND AND OBJECTIVES Cardiopulmonary bypass (CPB) can cause pulmonary dysfunction. Inflammatory changes may affect the release of nitric oxide (NO). The objective of this study was to evaluate exhaled NO in patients undergoing myocardial revascularization (MR) with CPB. METHODS This is a prospective study with nine adult patients undergoing MR with CPB. Initially, air samples were collected to analyze the presence of NO in the system that feeds the anesthesia equipment. Intravenous anesthesia was then initiated with ethomidate (0.3 mg x kg-1), sufentanil (0.3 microg x kg-1), and pancuronium (0.08 mg x kg-1), and maintained with isoflurane (MAC from 0.5 to 1.0) and sufentanil (5 microg x kg-1 x h-1). Tidal volume was fixed at 8 mL.kg-1 and FiO2 0.6, except during CPB. Thirty minutes after induction and 30 minutes after CPB, three sequential samples of exhaled air were collected for NO analysis by chemiluminescence. Data were analyzed by the Student t test. RESULTS The level of NO in room air was 5.05 +/- 3.37 ppb. Levels of exhaled NO decreased after CPB, varying from 11.25 +/- 5.65 ppb to 8.37 +/- 3.71 ppb (p = 0.031). CONCLUSIONS The reduction of exhaled NO after CPB observed in this study does not confirm the role of this molecule as a marker of pulmonary lesion. However, the different degrees of pulmonary parenchymal collapse, the method used to collect the data, and the drugs, among others, could have contributed for this reduction.BACKGROUND AND OBJECTIVES: Cardiopulmonary bypass (CPB) can cause pulmonary dysfunction. Inflammatory changes may affect the release of nitric oxide (NO). The objective of this study was to evaluate exhaled NO in patients undergoing myocardial revascularization (MR) with CPB. METHODS: This is a prospective study with nine adult patients undergoing MR with CPB. Initially, air samples were collected to analyze the presence of NO in the system that feeds the anesthesia equipment. Intravenous anesthesia was then initiated with ethomidate (0.3 mg.kg-1), sufentanil (0.3 µg.kg-1), and pancuronium (0.08 mg.kg-1), and maintained with isoflurane (MAC from 0.5 to 1.0) and sufentanil (5 µg.kg-1.h-1). Tidal volume was fixed at 8 mL.kg-1 and FiO2 0.6, except during CPB. Thirty minutes after induction and 30 minutes after CPB, three sequential samples of exhaled air were collected for NO analysis by chemiluminescence. Data were analyzed by the Student t test. RESULTS: The level of NO in room air was 5.05 ± 3.37 ppb. Levels of exhaled NO decreased after CPB, varying from 11.25 ± 5.65 ppb to 8.37 ± 3.71 ppb (p = 0.031). CONCLUSIONS: The reduction of exhaled NO after CPB observed in this study does not confirm the role of this molecule as a marker of pulmonary lesion. However, the different degrees of pulmonary parenchymal collapse, the method used to collect the data, and the drugs, among others, could have contributed for this reduction.