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Cited by 80Cardiac Ischemia and ReperfusionCardiac Fibrosis and RemodelingCardiac Imaging and Diagnostics

Reperfusion injury is not affected by blockade of P-selectin in the diabetic mouse heart

Jones, Steven P., Girod, Wesley G., Granger, D. Neil, Palazzo, Anthony J., Lefer, David J.·1999·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.1999.277.2.h763
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Abstract

We examined the mechanisms responsible for myocardial ischemia-reperfusion (MI-R) injury in a well-characterized animal model of type II diabetes mellitus. Diabetic ( db/db) mice and their littermate nondiabetic controls were subjected to 30 min of left anterior descending coronary artery occlusion and 2 h of reperfusion. Diabetic and nondiabetic mice experienced similar-sized areas at risk per left ventricle: 50.4 ± 2.0 and 53.4 ± 4.1%, respectively. However, myocardial necrosis (percentage of area at risk) was significantly greater ( P < 0.001) in diabetic than in nondiabetic animals: 56.3 ± 2.8 and 27.2 ± 3.1%, respectively. Histological examination revealed significantly ( P < 0.05) more neutrophils (PMNs) in the diabetic than in the nondiabetic hearts. Coronary endothelial expression of P-selectin was determined using radiolabeled monoclonal antibodies (MAbs). MI-R elicited a more intense ( P < 0.05) upregulation of P-selectin in the ischemic zone of diabetic than of nondiabetic myocardium: 0.310 ± 0.034 and 0.161 ± 0.042 μg MAb/g tissue. Immunoneutralization of P-selectin (RB40.34) reduced PMN accumulation in the diabetic myocardium but failed to reduce the extent of myocardial necrosis. Conversely, administration of an MAb directed against CD18 (GAME46) reduced PMN infiltration and attenuated the infarct size in the diabetic hearts. These results suggest that the diabetic heart is more susceptible to ischemia-reperfusion injury than normal myocardium. Furthermore, the mechanism of this injury may not be critically dependent on P-selectin in diabetic hearts.

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  • Infarct size is unchanged in high-fat fed models but increased in db/db mice.

    “Infarct size is unchanged in high-fat fed models (347) but increased in db/db mice (160).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [160]

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Authors
Jones, S. P., Girod, W. G., Granger, D. N., Palazzo, A. J., & Lefer, D. J.
Affiliations
Louisiana State University (US)
ORCID
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
1999-08-01
Volume
277
Issue
2
Pages
H763-H769
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.1999.277.2.h763
OpenAlex
W2335895544
Cited by
80
References
40
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2021: 2 · 2020: 1 · 2018: 1 · 2017: 3 · 2016: 1 · 2015: 1 · 2014: 4 · 2013: 2 · 2012: 4
FWCI
3.18
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (P01 DK-43785, P01DK043785)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
Keywords
myocardial ischemia-reperfusion injury, P-selectin, type 2 diabetes, db/db mice, neutrophil infiltration, CD18, myocardial necrosis, infarct size, coronary endothelium, immunoneutralization, leukocyte adhesion
MeSH terms
Animals, Blood Glucose, Cholesterol, Diabetes Mellitus, Hemodynamics, Leukocyte Count, Mice, Inbred C57BL, Mice, Transgenic, Myocardial Infarction, Myocardium, Neutrophils, Platelet Count, Myocardial Reperfusion Injury, Myocardial Ischemia, P-Selectin, Mice

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