Diabetes enhances leukocyte accumulation in the coronary microcirculation early in reperfusion following ischemia

Jason Y. Hokama, Leslie S Ritter, Grace Davis-Gorman, Adriana D. Cimetta, Jack G. Copeland, Paul F. McDonagh

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Background: Diabetic hearts are particularly vulnerable to ischemia- reperfusion injury. For leukocytes to participate in ischemia-reperfusion injury, they must first sequester in the microcirculation. The aim of this study was to determine, by direct observation, if early leukocyte deposition was increased in the diabetic coronary microcirculation early in reperfusion following myocardial ischemia. Methods: Non-diabetic and streptozotocin (STZ)-induced diabetic rat hearts, subjected to 30 min of 37°C, no-flow ischemia, were initially reperfused with blood containing labeled leukocytes. The deposition of fluorescent leukocytes in coronary capillaries and venules was directly visualized and recorded using intravital fluorescence microscopy. In addition, flow cytometry was used to measure CD11b adhesion molecule expression on polymorphonuclear (PMN) leukocytes from non-diabetic and STZ-diabetic rats. Results: In the non-diabetic, control hearts, early in reperfusion, leukocytes trapped in coronary capillaries and adhered to the walls of post-capillary venules. In the diabetic hearts, leukocyte trapping in capillaries and adhesion to venules were both significantly increased (P < 0.05). PMN CD11b expression was also significantly increased in the diabetic blood compared to the non-diabetic blood (P < 0.05). Conclusions: Early in reperfusion following myocardial ischemia, leukocytes rapidly accumulate in greater numbers in the coronary microcirculation of the diabetic heart by both trapping in coronary capillaries and by adhering to venules. The enhanced retention of leukocytes in the diabetic coronary microcirculation increases the likelihood of inflammation-mediated reperfusion injury and may explain, in part, the poor recovery of diabetic hearts from an ischemic event. (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)96-107
Number of pages12
JournalJournal of Diabetes and its Complications
Volume14
Issue number2
DOIs
StatePublished - Mar 2000

Fingerprint

Microcirculation
Reperfusion
Leukocytes
Ischemia
Venules
Reperfusion Injury
Streptozocin
Myocardial Ischemia
Fluorescence Microscopy
Flow Cytometry
Neutrophils
Observation
Inflammation

Keywords

  • Coronary microcirculation
  • Diabetes
  • Ischemia-reperfusion
  • Leukocytes
  • Rats

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Diabetes enhances leukocyte accumulation in the coronary microcirculation early in reperfusion following ischemia. / Hokama, Jason Y.; Ritter, Leslie S; Davis-Gorman, Grace; Cimetta, Adriana D.; Copeland, Jack G.; McDonagh, Paul F.

In: Journal of Diabetes and its Complications, Vol. 14, No. 2, 03.2000, p. 96-107.

Research output: Contribution to journalArticle

Hokama, Jason Y. ; Ritter, Leslie S ; Davis-Gorman, Grace ; Cimetta, Adriana D. ; Copeland, Jack G. ; McDonagh, Paul F. / Diabetes enhances leukocyte accumulation in the coronary microcirculation early in reperfusion following ischemia. In: Journal of Diabetes and its Complications. 2000 ; Vol. 14, No. 2. pp. 96-107.
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abstract = "Background: Diabetic hearts are particularly vulnerable to ischemia- reperfusion injury. For leukocytes to participate in ischemia-reperfusion injury, they must first sequester in the microcirculation. The aim of this study was to determine, by direct observation, if early leukocyte deposition was increased in the diabetic coronary microcirculation early in reperfusion following myocardial ischemia. Methods: Non-diabetic and streptozotocin (STZ)-induced diabetic rat hearts, subjected to 30 min of 37°C, no-flow ischemia, were initially reperfused with blood containing labeled leukocytes. The deposition of fluorescent leukocytes in coronary capillaries and venules was directly visualized and recorded using intravital fluorescence microscopy. In addition, flow cytometry was used to measure CD11b adhesion molecule expression on polymorphonuclear (PMN) leukocytes from non-diabetic and STZ-diabetic rats. Results: In the non-diabetic, control hearts, early in reperfusion, leukocytes trapped in coronary capillaries and adhered to the walls of post-capillary venules. In the diabetic hearts, leukocyte trapping in capillaries and adhesion to venules were both significantly increased (P < 0.05). PMN CD11b expression was also significantly increased in the diabetic blood compared to the non-diabetic blood (P < 0.05). Conclusions: Early in reperfusion following myocardial ischemia, leukocytes rapidly accumulate in greater numbers in the coronary microcirculation of the diabetic heart by both trapping in coronary capillaries and by adhering to venules. The enhanced retention of leukocytes in the diabetic coronary microcirculation increases the likelihood of inflammation-mediated reperfusion injury and may explain, in part, the poor recovery of diabetic hearts from an ischemic event. (C) 2000 Elsevier Science Inc.",
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T1 - Diabetes enhances leukocyte accumulation in the coronary microcirculation early in reperfusion following ischemia

AU - Hokama, Jason Y.

AU - Ritter, Leslie S

AU - Davis-Gorman, Grace

AU - Cimetta, Adriana D.

AU - Copeland, Jack G.

AU - McDonagh, Paul F.

PY - 2000/3

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N2 - Background: Diabetic hearts are particularly vulnerable to ischemia- reperfusion injury. For leukocytes to participate in ischemia-reperfusion injury, they must first sequester in the microcirculation. The aim of this study was to determine, by direct observation, if early leukocyte deposition was increased in the diabetic coronary microcirculation early in reperfusion following myocardial ischemia. Methods: Non-diabetic and streptozotocin (STZ)-induced diabetic rat hearts, subjected to 30 min of 37°C, no-flow ischemia, were initially reperfused with blood containing labeled leukocytes. The deposition of fluorescent leukocytes in coronary capillaries and venules was directly visualized and recorded using intravital fluorescence microscopy. In addition, flow cytometry was used to measure CD11b adhesion molecule expression on polymorphonuclear (PMN) leukocytes from non-diabetic and STZ-diabetic rats. Results: In the non-diabetic, control hearts, early in reperfusion, leukocytes trapped in coronary capillaries and adhered to the walls of post-capillary venules. In the diabetic hearts, leukocyte trapping in capillaries and adhesion to venules were both significantly increased (P < 0.05). PMN CD11b expression was also significantly increased in the diabetic blood compared to the non-diabetic blood (P < 0.05). Conclusions: Early in reperfusion following myocardial ischemia, leukocytes rapidly accumulate in greater numbers in the coronary microcirculation of the diabetic heart by both trapping in coronary capillaries and by adhering to venules. The enhanced retention of leukocytes in the diabetic coronary microcirculation increases the likelihood of inflammation-mediated reperfusion injury and may explain, in part, the poor recovery of diabetic hearts from an ischemic event. (C) 2000 Elsevier Science Inc.

AB - Background: Diabetic hearts are particularly vulnerable to ischemia- reperfusion injury. For leukocytes to participate in ischemia-reperfusion injury, they must first sequester in the microcirculation. The aim of this study was to determine, by direct observation, if early leukocyte deposition was increased in the diabetic coronary microcirculation early in reperfusion following myocardial ischemia. Methods: Non-diabetic and streptozotocin (STZ)-induced diabetic rat hearts, subjected to 30 min of 37°C, no-flow ischemia, were initially reperfused with blood containing labeled leukocytes. The deposition of fluorescent leukocytes in coronary capillaries and venules was directly visualized and recorded using intravital fluorescence microscopy. In addition, flow cytometry was used to measure CD11b adhesion molecule expression on polymorphonuclear (PMN) leukocytes from non-diabetic and STZ-diabetic rats. Results: In the non-diabetic, control hearts, early in reperfusion, leukocytes trapped in coronary capillaries and adhered to the walls of post-capillary venules. In the diabetic hearts, leukocyte trapping in capillaries and adhesion to venules were both significantly increased (P < 0.05). PMN CD11b expression was also significantly increased in the diabetic blood compared to the non-diabetic blood (P < 0.05). Conclusions: Early in reperfusion following myocardial ischemia, leukocytes rapidly accumulate in greater numbers in the coronary microcirculation of the diabetic heart by both trapping in coronary capillaries and by adhering to venules. The enhanced retention of leukocytes in the diabetic coronary microcirculation increases the likelihood of inflammation-mediated reperfusion injury and may explain, in part, the poor recovery of diabetic hearts from an ischemic event. (C) 2000 Elsevier Science Inc.

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KW - Ischemia-reperfusion

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