Journal of Chest Surgery

The Korean Society for Thoracic and Cardiovascular Surgery (대한심장혈관흉부외과학회)
권호 표지

Comparison of Inflammatory Response and Myocardial injury Between Normoxic and Hyperoxic Condition during Cardiopulmonary Bypass

체외순환 시 정상 산소분압과 고 산소분압의 염증반응 및 심근손상에 관한 비교연구

  • 김기봉 (인제대학교 의과대학 일산 백병원 흉부외과학 교실) ;
  • 최석철 (인제대학교 의과대학 부산 백병원 흉부외과 체외순환 연구실) ;
  • 최국렬 (인제대학교 데이터 정보학과) ;
  • 정석목 (인제대학교 의과대학 부산 백병원 흉부외과 체외순환 연구실) ;
  • 최강주 (인제대학교 의과대학 일산 백병원 흉부외과학 교실) ;
  • 김양원 (인제대학교 의과대학 부산 백병원 응급의학과) ;
  • 김병훈 (인제대학교 의과대학 일산 백병원 흉부외과학 교실) ;
  • 이양행 (인제대학교 의과대학 일산 백병원 흉부외과학 교실) ;
  • 조광현 (인제대학교 의과대학 일산 백병원 흉부외과학 교실)
  • Published : 2001.07.01
Download PDF
⟨ Previous Next ⟩

Abstract

Background: Hyperoxemic cardiopulmonary bypass (CPB) has been recognized as a safe technique and is widely used in cardiac surgery. However, hyperoxemic CPB may produce higher toxic oxygen species and cause more severe oxidative stress and ischemia/reperfusion injury than normoxemic CPB. This study was undertaken to compare inflammatory responses and myocardial injury between normoxemic and hyperoxemic CPB and to examine the beneficial effect of normoxemic CPB. Material and method: Thirty adult patients scheduled for elective cardiac surgery were randomly divided into normoxic group (n=15), who received normoxemic CPB (about Pa $O_{2}$ 120 mmHg), and hyperoxic group (n=15), who received hyperoxemic CPB (about Pa $O_{2}$ 400 mmHg). Myeloperoxidase (MPO), malondialdehyde (MDA), adenosine monophosphate (AMP), and troponin-T (TnT) concentrations in coronary sinus blood were determined at pre- and post-CPB. Total leukocyte and neutrophil counts in arterial blood were measured at the before, during, and after CPB. Lactate concentration in mixed venous blood was analyzed during CPB, and cardiac index (Cl) and pulmonary vascular

배경: 체외순환 시 동맥혈액의 고 산소분압 유지는 오랫동안 안전한 기법으로 인식되어 임상에 이용하여 왔으나 고 산소분압은 정상 산소분압 보다 상대적으로 더 많은 독성 산소성분을 생성시켜 산화성 장기손상 및 재관류 손상의 원인이 된다. 저자들은 체외순환 시 동맥혈액을 고 산소분압 혹은 정상 산소분압 상태로 순환시켰을 때의 염증반응과 심근손상에 관해 비교검토하고, 정상 산소분압 체외순환의 임상적 유용성을 조사하기 위해 본 연구를 시행하게 되었다. 대상 및 방법: 성인 심장병 환자 30명을 고산소분압군(PaO2 400mmHg, 고산소군, n=15)과 정상산소분압군(Pa $O_{2}$ 120 mmHg, 정상산소군, n=15)으로 나눈 뒤 다음과 같은 변수들을 측정하여 두 그룹간에 비교하였다. 체외순환 전후의 관상정맥동 혈액을 채취하여 myeloperoxidase (MPO), malondialdehyde(MDA), troponin-T(TnT), adenosine monophosphate(AMP)를 분석하였고, 동맥혈액 내 총 백혈구 수 및 호중구 수를 측정하였다. 혼합 정맥혈액의 lactate 농도, 심장지수, 폐혈관저항도 체외순환 전, 중, 후 시기별로 함께 측정하여 두 그룹간에 비교하였다 결과: 체외순환 후 정상산소군이 고산소군에 비해 더 낮은 MDA농도 (4.79$\pm$0.7 vs 5.86$\pm$0.65 $\mu$mo1/L, p=0.04)와 보다 높은 AMP농도 (1.23$\pm$0.07 vs 1.00$\pm$0.04 nmol/L, p=0.05)를 보였으나 TnT농도 (0.50$\pm$0.08 vs 0.60$\pm$0.08 ng/mL, p>0.05)는 유의한 차가 없었다. 체외순환 후 MPO농도(5.38$\pm$1.01 vs 8.73$\pm$0.90 ng/mL, p=0.02)와 총 백혈구 수(10,484$\pm$836 vs 13,572$\pm$1,1671/㎥, p=0.04)는 정상산소군이 고산소군 보다 낮았다. 체외순환 후 lactate농도 (27.90$\pm$3.41 vs 31.49$\pm$4.87 mg/dL, p=0.55)와 심장지수(2.99$\pm$0.21 vs 2.75$\pm$0.18 L/$m^2$/min, p=0.39)는 양 군 간에 차이가 없었으나 폐혈관 저항(90.37$\pm$16.36 vs 118.12$\pm$12.21 dyne/sec/$cm^{5}$, p=0.04)은 정상산소군이 더 낮았다. 결론: 정상 산소분압 체외순환은 고 산소분압 체외순환에 비해 심근손상과 염증반응을 적게 유발하여 체외순환 후 심장 및 폐기능의 손상정도를 감소시킬 것으로 생각되며 이러한 결과는 정상 산소분압 체외순환이 심장수술에 유용하게 적용될 수 있음을 시사하고 있다.

Keywords

References

  1. J. Thorac Cardiovasc Surg v.110 Studies of hypoxemic/reoxygenation injury : Without aortic clamping. Ⅱ. Evidence for reoxygenation damage Ihnken K;Morita K;Buckberg GD(et al.)
  2. J Clin Invest v.93 Role of controlled cardiac reoxygenation in reducing nitric oxide production and cardiac oxidant damage in cyanotic infantile hearts Morita K;Ihnken K;Buckberg GD;Sherman MP;Young HH;Ignarro LJ
  3. J Thorac Cardiovasc Surg v.116 Njormoxic cardiopulmonary bypass reduces oxidative myocardial damage and nitric oxide during cardiac operations in the adult Ihnken K;Winkler A;Schlenak C(et al.)
  4. Biochem J v.134 The mitochondrial generation of hydrogen peroxide : general properties and effect of hyperbaric oxygen Boveris A;Chance B
  5. Am J Physiol(Heart Circ. Physio. 2.0) v.251 Role of leukocyte in response to acute myocardial ischemia and reflow in dogs Engler RL;Dahlgren MD;Morris MA(et al.)
  6. Circulation v.74 no.SUP. Oxygen free radical geneation during cardiopulmonary bypass : correlation with complement activation Cavarocchi NC;England MD;Schaff HV(et al.)
  7. J Thorac Cardiovasc Surg v.95 Effect of cardiopulmonary bypass on eicosanoid metabolism during pediatric cardiovascular surgery Greeley WJ;Bushman GA;Kong DL;Oldham HN;Perterson MB
  8. J Extra-Corp Technol v.23 The effects of hyperoxia during cardiopulmonary bypass on blood cell rheology and postoperative morbidity associated with cardiac surgery Belboul A;AI-Khaja N;Ericson C(et al.)
  9. Adv Exp Med Biol v.78 Mitochondrial production of superoxide radical and hydrogen peroxide Boveris A
  10. J Mol Cell Cardiol v.10 The oxygen paradox and the calcium paradox: Two facets of the same problem? Hearse DJ;Humphrey SM;Bullock GR
  11. J Extra-Corp Technol v.31 Avoiding hyperoxemia at the start of cardiopulmonary bypass while optimizing gas flow and temperature Myers GJ;Legare JF
  12. Blood v.65 Leukocyte-endothelial interactions Harlan J
  13. Circ Res v.53 Hydrogen peroxide and hydroxyl radical mediation of activated leukocyte depression of cardiac sarco;lasmic reticulum : participation of the cyclooxygenase pathway Rowe G;Manson N;Caplan M;Hess M
  14. J Thorac Cardiovasc Surg v.91 Increased production of peroxidation products associated with cardiac operation : evidence for free radical generation Royston D;Fleming JS;Desai JB;Westaby S;Tayler KM
  15. Am J Pathol v.111 Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog Engler RL;Schmid-Schonbein GW;Pavalei RS
  16. Am J Pathol v.150 Mediators of ischemia-reperfusion injury of rat lung Eppinger MJ;Deeb GM;Bolling SF;Ward PA
  17. J Thorac Cardiovasc Surg v.102 Myeloperoxidase and elastase as marks of leukocyte activation during cardiopulmonary bypass in humans Faymonville ME;Pincemail J;Duchateau J(et al.)
  18. J Am Coll Cardiol v.6 The oxygen free radical system : potential mediator myocardial injury Hammond B;Hess ML
  19. J Mol Cell Cardiol v.15 Production of free radicals and lipid peroxides in early experimental myocardial ischemia Rao PS;Cohen MV;Mueller HS
  20. Basic Res Cardiol v.77 The role of lipid peroxidation in pathogenesis of ischemic damage and the antioxidant protection of the heart Meerson FZ;Kagan VE;Kozlov YP(et al.)
  21. J Clin Invest v.73 Glutathione redox cycle protects cultured endothelial cells against lysis by extracellularly generated hydrogen peroxid Harlan JM;Levine JD;Callahan KS(et al.)
  22. Life Sci v.35 Decreased defence against free radicals in rat heart during normal reperfusion after hypoxic, ischemic and calcium- free perfusion Julicher RHM;Tijburg LBM;Sterrenberg L(et al.)
  23. J Mol Cell Cardiol v.16 Role of oxygen radicals in cardiac injury due to reoxygenation Gauduel Y;Duvelleoy M
  24. Therapeutic approaches to myocardial infarct size limitation Do leukocytes infuence infarct size? Lucchesi BR;Romson JL;Jolly SR;Hearse DJ(ed.);Yellon DM(ed.)
  25. Biochem J v.191 Generation of superoxide anion by NADH dehydrogenase of bovine heart mitochondria Turner JF;Boveris A
  26. Coronary arterial spasm Effect of molecular oxygen and calcium on heart metabolism during reperfusion Ferrari R;Bongrani S;Cucchini F;Di Lisa F;Guarnieri C;Visioli O;Bertrand ME(ed.)
  27. J Mol Cell Cardiol v.16 Molecular oxygen : friend and foe. The role of oxygen free radical system in the calcium paradox, the oxygen paradox and schemia/reperfusion injury Hess ML;Manson MH
  28. J Clin Invest v.79 Reperfusion after acute coronary occlusion in dogs impairs endothelium-dependent relaxation to acetylcholine and augments contractile reactivity in vitro VanBenthuysen KM;McMurtry IF;Horwitz LD
  29. Surg Forum v.42 Hypoxic pulmonary hypertension in the neonatal piglet is related to decreased intravascular endothelium-derived nitric oxide Haybron DM;Matheis GF;Buckberg GD;Sherman MP;Byrns R;Ignarro LJ