Ischemia and activated neutrophils alter coronary microvascular but not epicardial coronary artery reactivity Margit Kadletz, MDa, Rebecca J. Dignan,

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Presentation transcript:

Ischemia and activated neutrophils alter coronary microvascular but not epicardial coronary artery reactivity Margit Kadletz, MDa, Rebecca J. Dignan, MDa, Kathryn E. Loesser, PhDb, Michael L. Hess, MDb, Andrew S. Wechsler, MDa The Journal of Thoracic and Cardiovascular Surgery Volume 108, Issue 4, Pages 648-657 (October 1994) DOI: 10.5555/uri:pii:S0022522394702896 Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 1 Diagram of the preparation. PMN's, Polymorphonuclear leukocytes. The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 2 Scanning electron micrographs of vascular endothelium from epicardial arteries (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Low-power micrograph of control endothelium shows a normal morphology. B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen. C, Ischemic endothelium without added polymorphonuclear leukocytes exhibited blebbing (open arrow) and small holes (black arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when polymorphonuclear leukocytes were added. Whole areas were denuded of endothelial cells (arrowhead); platelets and fibrin (arrow) were evident. Other areas were undamaged (plus sign) except for that caused by ischemia. (Original magnifications ×1200; bar = 10 μm.) The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 2 Scanning electron micrographs of vascular endothelium from epicardial arteries (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Low-power micrograph of control endothelium shows a normal morphology. B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen. C, Ischemic endothelium without added polymorphonuclear leukocytes exhibited blebbing (open arrow) and small holes (black arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when polymorphonuclear leukocytes were added. Whole areas were denuded of endothelial cells (arrowhead); platelets and fibrin (arrow) were evident. Other areas were undamaged (plus sign) except for that caused by ischemia. (Original magnifications ×1200; bar = 10 μm.) The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 2 Scanning electron micrographs of vascular endothelium from epicardial arteries (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Low-power micrograph of control endothelium shows a normal morphology. B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen. C, Ischemic endothelium without added polymorphonuclear leukocytes exhibited blebbing (open arrow) and small holes (black arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when polymorphonuclear leukocytes were added. Whole areas were denuded of endothelial cells (arrowhead); platelets and fibrin (arrow) were evident. Other areas were undamaged (plus sign) except for that caused by ischemia. (Original magnifications ×1200; bar = 10 μm.) The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 2 Scanning electron micrographs of vascular endothelium from epicardial arteries (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Low-power micrograph of control endothelium shows a normal morphology. B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen. C, Ischemic endothelium without added polymorphonuclear leukocytes exhibited blebbing (open arrow) and small holes (black arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when polymorphonuclear leukocytes were added. Whole areas were denuded of endothelial cells (arrowhead); platelets and fibrin (arrow) were evident. Other areas were undamaged (plus sign) except for that caused by ischemia. (Original magnifications ×1200; bar = 10 μm.) The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 3 Bar graphs comparing intramyocardial arteries: A, Maximum smooth muscle (SM) contraction to a 125 mmol/L concentration of potassium (KCl) is not significantly different in any group. B, Contraction to a 45 mmol/L concentration of KCl after ischemia and incubation with activated neutrophils (PMN's) is slightly increased compared to control (no ischemia, no PMN's, p = 0.06). C, Total SM relaxation after ischemia alone and after ischemia with PMN's, expressed as percent of contraction to a 45 mmol/L concentration of KCl, is significantly decreased compared to control and after PMN's alone (p < 0.05). D, Endothelium-mediated relaxation, expressed as percent of maximum SM relaxation (bradykinin and sodium nitroprusside) is significantly decreased in arteries exposed to combined ischemia and PMN's (p < 0.05). The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 3 Bar graphs comparing intramyocardial arteries: A, Maximum smooth muscle (SM) contraction to a 125 mmol/L concentration of potassium (KCl) is not significantly different in any group. B, Contraction to a 45 mmol/L concentration of KCl after ischemia and incubation with activated neutrophils (PMN's) is slightly increased compared to control (no ischemia, no PMN's, p = 0.06). C, Total SM relaxation after ischemia alone and after ischemia with PMN's, expressed as percent of contraction to a 45 mmol/L concentration of KCl, is significantly decreased compared to control and after PMN's alone (p < 0.05). D, Endothelium-mediated relaxation, expressed as percent of maximum SM relaxation (bradykinin and sodium nitroprusside) is significantly decreased in arteries exposed to combined ischemia and PMN's (p < 0.05). The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 3 Bar graphs comparing intramyocardial arteries: A, Maximum smooth muscle (SM) contraction to a 125 mmol/L concentration of potassium (KCl) is not significantly different in any group. B, Contraction to a 45 mmol/L concentration of KCl after ischemia and incubation with activated neutrophils (PMN's) is slightly increased compared to control (no ischemia, no PMN's, p = 0.06). C, Total SM relaxation after ischemia alone and after ischemia with PMN's, expressed as percent of contraction to a 45 mmol/L concentration of KCl, is significantly decreased compared to control and after PMN's alone (p < 0.05). D, Endothelium-mediated relaxation, expressed as percent of maximum SM relaxation (bradykinin and sodium nitroprusside) is significantly decreased in arteries exposed to combined ischemia and PMN's (p < 0.05). The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 3 Bar graphs comparing intramyocardial arteries: A, Maximum smooth muscle (SM) contraction to a 125 mmol/L concentration of potassium (KCl) is not significantly different in any group. B, Contraction to a 45 mmol/L concentration of KCl after ischemia and incubation with activated neutrophils (PMN's) is slightly increased compared to control (no ischemia, no PMN's, p = 0.06). C, Total SM relaxation after ischemia alone and after ischemia with PMN's, expressed as percent of contraction to a 45 mmol/L concentration of KCl, is significantly decreased compared to control and after PMN's alone (p < 0.05). D, Endothelium-mediated relaxation, expressed as percent of maximum SM relaxation (bradykinin and sodium nitroprusside) is significantly decreased in arteries exposed to combined ischemia and PMN's (p < 0.05). The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 4 Cumulative concentration response curves to bradykinin in control ring segments (no ischemia, no activated neutrophils [PMN's]) (square), ring segments after incubation with PMN's (diamond), and ring segments after 30 minutes of ischemia and without PMN's (circle). Values are shown as mean bradykinin relaxation ± standard error of the mean. Concentration response curves and EC50 (concentration of bradykinin producing 50% of maximum endothelium-mediated relaxation) after ischemia and after ischemia followed by incubation with PMN's is shifted to the right (p < 0.05). EC50 for intramyocardial arteries incubated with PMN's after 30 minutes of ischemia could not be calculated because most ring segments did not respond to bradykinin. This demonstrates maximum injury in intramyocardial artery endothelium after combined ischemia and incubation with neutrophils. The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 5 Scanning electron micrographs of intramyocardial arterial endothelium (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Control endothelium exhibited normal morphology, with an occasional PMN (P), associated with some endothelial damage (arrow). B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen (arrow). C, Ischemic endothelium without added PMNs exhibited blebbing (open arrow)and small holes (small arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when PMNs were added. Damage appears "lacy" in the first stages; eventually nothing recognizable is left of the endothelial cell (long arrow). Other areas appear undamaged (plus sign) and platelets (short arrow) and fibrin are evident in abundance. All micrographs are of the same magnification; bar = 10 μm. The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 5 Scanning electron micrographs of intramyocardial arterial endothelium (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Control endothelium exhibited normal morphology, with an occasional PMN (P), associated with some endothelial damage (arrow). B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen (arrow). C, Ischemic endothelium without added PMNs exhibited blebbing (open arrow)and small holes (small arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when PMNs were added. Damage appears "lacy" in the first stages; eventually nothing recognizable is left of the endothelial cell (long arrow). Other areas appear undamaged (plus sign) and platelets (short arrow) and fibrin are evident in abundance. All micrographs are of the same magnification; bar = 10 μm. The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 5 Scanning electron micrographs of intramyocardial arterial endothelium (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Control endothelium exhibited normal morphology, with an occasional PMN (P), associated with some endothelial damage (arrow). B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen (arrow). C, Ischemic endothelium without added PMNs exhibited blebbing (open arrow)and small holes (small arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when PMNs were added. Damage appears "lacy" in the first stages; eventually nothing recognizable is left of the endothelial cell (long arrow). Other areas appear undamaged (plus sign) and platelets (short arrow) and fibrin are evident in abundance. All micrographs are of the same magnification; bar = 10 μm. The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 5 Scanning electron micrographs of intramyocardial arterial endothelium (with and without ischemia) incubated with and without activated neutrophils (PMNs). A, Control endothelium exhibited normal morphology, with an occasional PMN (P), associated with some endothelial damage (arrow). B, Activated neutrophils (P) did little damage to the normal endothelium; only occasional holes were seen (arrow). C, Ischemic endothelium without added PMNs exhibited blebbing (open arrow)and small holes (small arrow), but was fairly intact. D, Ischemic endothelium exhibited extensive damage when PMNs were added. Damage appears "lacy" in the first stages; eventually nothing recognizable is left of the endothelial cell (long arrow). Other areas appear undamaged (plus sign) and platelets (short arrow) and fibrin are evident in abundance. All micrographs are of the same magnification; bar = 10 μm. The Journal of Thoracic and Cardiovascular Surgery 1994 108, 648-657DOI: (10.5555/uri:pii:S0022522394702896) Copyright © 1994 Mosby, Inc. Terms and Conditions