Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization 

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Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization  Hiroki Sato, MDa, Zhi-Qing Zhao, MD, PhDa, James E. Jordan, BSb, James C. Todd, MDa, Robert D. Riley, MDa, C.Spencer Taft, BSa, John W. Hammon Jr, MDa, Ping Li, MD, PhDc, Xin-liang Ma, MD, PhDd, J. Vinten-Johansen, PhDa,b  The Journal of Thoracic and Cardiovascular Surgery  Volume 113, Issue 2, Pages 399-409 (February 1997) DOI: 10.1016/S0022-5223(97)70338-6 Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 1 Segmental shortening (top panel) and segmental work (bottom panel) in ischemic-reperfused zone at baseline (CTRL, control), at the end of coronary occlusion (ISCH, ischemia), and after 60 minutes of reperfusion (REP) in the working heart. Bar heights represent mean plus or minus the standard error of the mean. There were no significant differences among the three groups. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 2 Segmental stiffness, indexed as β-coefficient or modulus of stiffness derived from the exponential end-diastolic pressure-segment length relationship. Value of β in SBCP group was significantly less than that in the other two groups at reperfusion. Symbol heights represent mean plus or minus the standard error of the mean. CTRL, Control; ISCH, ischemia; REP, reperfusion. *p < 0.05 versus other two groups; †p < 0.05 versus previous value. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 3 Mass of the area at risk versus mass of left ventricle as percentage (Ar/LV, top panel), mass of the area of necrosis versus mass of left ventricle as percentage (An/LV, middle panel), and area of necrosis as percent of area at risk (An/Ar, bottom panel). Although the area placed at risk was comparable among groups, the areas of necrosis as percent of area at risk was significantly increased in LNA-BR and LNA-R groups relative to that in SBCP group. Bars represent mean plus or minus the standard error of the mean; circles represent individual values for each group. *p < 0.05 versus SBCP group. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 4 Myeloperoxidase (MPO) activity in nonischemic zone (NIZ), ischemic but nonnecrotic zone (IZ), and ischemic-necrotic zone (NEC). Myeloperoxidase activity was significantly less in SBCP group in ischemic but nonnecrotic zone. Bar heights represent mean plus or minus the standard error of the mean. *p < 0.05 versus SBCP group; †p = 0.06 versus SBCP group. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 5 Dialysate interstitial l-[14C]citrulline concentration in area at risk (percent change of control value). Citrulline level was significantly higher in SBCP group at the end of reperfusion. Symbol heights represent mean plus or minus the standard error of the mean. PRE, Preischemia; ISCH1, first 30 minutes of occlusion; ISCH2, 30 to 60 minutes of occlusion; ISCH3, 60 to 90 minutes of occlusion; BCP1, first 30 minutes of blood cardioplegic arrest; BCP2, 30 to 60 minutes of blood cardioplegic arrest; BE, 30 minutes of beating empty period; BW, 30 minutes of beating working period. *p < 0.05 versus other two groups; †p < 0.05 versus previous period. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 6 Adherence of unactivated polymorphonuclear leukocytes (PMNs) to the endothelium of normal coronary arterial ring segments (CTRL), ischemic-reperfused LAD ring segments from each group (SBCP L, LNA-BR L, LNA-R L, where L indicates LAD), and LCx ring segments from each group (SBCP C, LNA-BR C, LNA-R C, where C indicates LCx). Polymorphonuclear leukocyte adherence to LAD segments was significantly increased in all three groups. However, adherence in l-NA–treated groups was significantly higher than that in the SBCP group. There was no increase in adherence and no group differences in LCx ring segments. Bar heights represent mean plus or minus the standard error of the mean; numbers in bars represent numbers of coronary arterial ring segments studied. *p < 0.05 versus other groups. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions

Fig. 7 Vasodilator responses in LAD and LCx vascular rings to acetylcholine, the receptor-dependent, endothelium-dependent stimulator of NO (upper panel); receptor-independent, endothelium-dependent NO-stimulator calcium ionophore A23187 (middle panel); and smooth-muscle relaxing NO donor agent acidified NaNO2 (bottom panel). Relaxation responses were expressed as percentage of U46619-induced precontraction. Symbol heights represent mean plus or minus the standard error of the estimate. *p < 0.05 versus other three groups; **p < 0.05 LNA-BR group versus control (CTRL) group; †p < 0.05 control and SBCP groups versus LNA-BR and LNA-R groups. The Journal of Thoracic and Cardiovascular Surgery 1997 113, 399-409DOI: (10.1016/S0022-5223(97)70338-6) Copyright © 1997 Mosby, Inc. Terms and Conditions