Brazilian Journal of Anesthesiology
https://app.periodikos.com.br/journal/rba/article/doi/10.1590/S0034-70942009000300003
Brazilian Journal of Anesthesiology
Scientific Article

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

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

Célio Gomes de Amorim; Luiz Marcelo Sá Malbouisson; Beatriz Mangueira Saraiva; Fernanda Maria da Silva Pedro; Milton Arruda Martins; Maria José Carvalho Carmona

http://dx.doi.org/10.1590/S0034-70942009000300003 Braz J Anesthesiol, vol.59, n3, p.286-296, 2009
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Resumo

JUSTIFICATIVA E OBJETIVOS: A circulação extracorpórea (CEC) pode causar disfunção pulmonar. As alterações inflamatórias podem afetar a liberação de óxido nítrico (NO). Objetivou-se avaliar o NO exalado em pacientes submetidos à revascularização do miocárdio (RM) com CEC. MÉTODO:Foram estudados prospectivamente nove pacientes adultos submetidos à RM com CEC. Inicialmente, foi coletada amostra de ar para análise de NO no sistema que alimenta o aparelho de anestesia. A seguir, anestesia iniciada por via venosa com etomidato (0,3 mg.kg-1), sufentanil (0,3 µg.kg-1), pancurônio (0,08 mg.kg-1) e mantida com isoflurano (0,5 a 1,0 CAM) e sufentanil (0,5 µg.kg-1.h-1). O volume corrente fixado a 8 mL.kg-1, com FIO2 de 0,6, exceto durante a CEC. Trinta minutos depois da indução, e trinta após a CEC, três amostras sequenciais de ar exalado foram colhidas para análise de NO, por quimioluminescência. Os dados foram analisados por meio do teste t de Student. RESULTADOS: O valor do NO do ar ambiente foi de 5,05 ± 3,37 ppb. O NO exalado decresceu após a CEC, variando de 11,25 ± 5,65 ppb para 8,37 ± 3,17 ppb (p = 0,031). CONCLUSÕES: A redução do NO exalado pós-CEC observada nesse estudo não permite confirmar o papel dessa molécula como marcador de lesão pulmonar. Entretanto, os variados graus de colapso do parênquima pulmonar, o método de obtenção dos dados, os fármacos utilizados, dentre outros, podem ter contribuído para a redução.

Palavras-chave

CIRURGIA CARDÍACA, CIRURGIA CARDÍACA, COMPLICAÇÕES, COMPLICAÇÕES, COMPLICAÇÕES, VENTILAÇÃO, VENTILAÇÃO

Abstract

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.

Keywords

COMPLICATIONS, COMPLICATIONS, COMPLICATIONS, SURGERY, SURGERY, SURGERY, VENTILATION, VENTILATION

Referências

Laffey JG, Boylan JF, Cheng DC. The systemic inflammatory response to cardiac surgery: implications for the anesthesiologist. Anesthesiology. 2002;97:215-252.

Barnes PJ, Liew FY. Nitric oxide and asthmatic inflammation. Immunol Today. 1995;16:128-130.

Engelman DT, Watanabe M, Maulik N. L-arginine reduces endothelial inflammation and myocardial stunning during ischemia/reperfusion. Ann Thorac Surg. 1995;60:1275-1281.

Tsao PS, Lewis NP, Alpert S. Exposure to shear stress alters endothelial adhesiveness: Role of nitric oxide. Circulation. 1995;92:3513-3519.

Moncada S, Higgs A. The L-arginine-nitric oxide pathway. N Engl J Med. 1993;329:2002-2012.

Negri MLS, Camargo EA. Óxido nítrico: uma alternativa no tratamento da hipertensão pulmonar. J Bras Med. 2003;85:15-23.

Rubanyi GM, Ho EH, Cantor EH. Cytoprotective function of nitric oxide: inactivation of superoxide radicals produced by human leukocytes. Biochem Biophys Res Commun. 1991;181:1392-1397.

Sartori C, Lepori M, Busch T. Exhaled nitric oxide does not provide a marker of vascular endothelial function in healthy humans. Am J Respir Crit Care Med. 1999;160:879-882.

Gustafsson LE, Leone AM, Persson MG. Endogenous nitric oxide is present in the exhaled air of rabbits, guinea pigs and humans. Biochem Biophys Res Commun. 1991;181:852-857.

Tornberg DC, Angdin M, Settergen G. Exhaled nitric oxide before and after cardiac surgery with cardiopulmonary bypass: response to acetylcholine and nitroglycerin. Br J Anaesth. 2005;94:174-180.

Ishibe Y, Liu R, Hirosawa J. Exhaled nitric oxide level decreases after cardiopulmonary bypass in adult patients. Crit Care Med. 2000;28:3823-3827.

Sheppard SV, Gibbs RV, Smith DC. Does the use of leucocyte depletion during cardiopulmonary bypass affect exhaled nitric oxide production?. Perfusion. 2004;19:7-10.

Beghetti M, Black SM, Fineman JR. Endothelin-1 in congenital heart disease. Pediatr Res. 2005;57:16R-20R.

Higgins TL, Estafanous FG, Loop FD. Stratification of morbidity and mortality outcome by preoperative risk factors in coronary artery bypass patients: A clinical severity score. JAMA. 1992;267:2344-2348.

Beghetti M, Silkoff PE, Caramori M. Decreased exhaled nitric oxide may be a marker of cardiopulmonary bypass-induced injury. Ann Thorac Surg. 1998;66:532-534.

Marczin N, Kovesi T, Royston D. Exhaled nitric oxide as a marker of lung injury in coronary artery bypass surgery. Br J Anaesth. 2003;90:101-105.

Wilkins MR, Zhao L, al-Tubuly R. The regulation of pulmonary vascular tone. Br J Clin Pharmacol. 1996;42:127-131.

Kharitonov SA, Barnes PJ. Effects of corticosteroids on noninvasive biomarkers of inflammation in asthma and chronic obstructive pulmonary disease. Proc Am Thoracic Soc. 2004;1:191-199.

Kharitonov SA, Barnes PJ. Clinical aspects of exhaled nitric oxide. Eur Respir J. 2000;16:781-792.

Barnes PJ, Chowdhury B, Kharitonov SA. Pulmonary biomarkers in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2006;174:6-14.

Horvath I, Donnelly LE, Kiss A. Exhaled nitric oxide and hydrogen peroxide concentrations in asthmatic smokers. Respiration. 2004;71:463-468.

Brindicci C, Ito K, Resta O. Exhaled nitric oxide from lung periphery is increased in COPD. Eur Respir J. 2005;26:52-59.

Zegdi R, Fabre O, Cambillau M. Exhaled nitric oxide and acute lung injury in a rat model of extracorporeal circulation. Shock. 2003;20:569-574.

Zegdi R, Fabre O, Cambillau M. Exhaled nitric oxide does not reflect the severity of acute lung injury: an experimental study in a rat model of extracorporeal circulation. Crit Care Med. 2002;30:2096-2102.

Beghetti M, Adatia I. Inhaled nitric oxide and congenital cardiac disease. Cardiol Young. 2001;11:142-152.

ATS/ERS recommendations for standardized procedures for the online and offline measurement of exhaled lower respiratory nitric oxide and nasal nitric oxide, 2005. Am J Respir Crit Care Med. 2005;171:912-930.

Matata BM, Galinanes M. Effect of diabetes on nitric oxide metabolism during cardiac surgery. Diabetes. 2001;50:2603-2610.

Matata BM, Galinanes M. Cardiopulmonary bypass exacerbates oxidative stress but does not increase proinflammatory cytokine release in patients with diabetes compared with patients without diabetes: regulatory effects of exogenous nitric oxide. J Thorac Cardiovasc Surg. 2000;120:1-11.

Hutcheson IR, Griffith TM. Release of endothelium-derived relaxing factor is modulated both by frequency and amplitude of pulsatile flow. Am J Physiol. 1991;261:H257-262.

Macha M, Yamazaki K, Gordon LM. The vasoregulatory role of endothelium derived nitric oxide during pulsatile cardiopulmonary bypass. Asaio J. 1996;42:M800-804.

Hachenberg T, Tenling A, Nystrom SO. Ventilation-perfusion inequality in patients undergoing cardiac surgery. Anesthesiology. 1994;80:509-519.

Magnusson L, Zemgulis V, Wicky S. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology. 1997;87:1153-1163.

Tenling A, Hachenberg T, Tyden H. Atelectasis and gas exchange after cardiac surgery. Anesthesiology. 1998;89:371-378.

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