The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium

Kenneth McDonald; Cuixia Chu; Gary Francis; Dianne Judd; Wenda Carlyle; Cynthia Toher; Katherine Hauer; Malinda Hartman

doi:10.1016/S0008-6363(97)00201-0

The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium

Kenneth McDonald, Cuixia Chu, Gary Francis, Dianne Judd, Wenda Carlyle, Cynthia Toher, Katherine Hauer, Malinda Hartman

Medicine - Cardiology Division

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Objective: Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood. Methods: Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham- operated group (n = 10). Results: Analysis of infarct size (planimetry) in a separate group of rots demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 ± 8 vs. RP: 35 ± 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 ± 3 vs. 167 ± 4 μm, p = 0.02), in the right ventricle (154 ± 4 vs. 167 ± 3 μm, p = 0.02) and in the septum (158 ± 4 vs. 169 ± 4 μm, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 ± 1.7 X 10³ vs. 44.1 ± 1.6 x 10³ μm³, p = 0.06; right ventricle 36.7 ± 1.6 x 10³ vs. 42.7 ± 2.0 x 10³ μm³, p = 0.02; septum 41.0 ± 1.6 x 10³ vs. 44.2 ± 1.8 x 10³ μm³, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups. Conclusion: Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti- remodeling effect remote from the area perfused by this artery.

Original language	English (US)
Pages (from-to)	347-353
Number of pages	7
Journal	Cardiovascular Research
Volume	36
Issue number	3
DOIs	https://doi.org/10.1016/S0008-6363(97)00201-0
State	Published - Dec 1997

Bibliographical note

Funding Information:
The authors acknowledge Dr. Jay N. Cohn for his critical review of the data and Susan Quirt for her expert assistance in the preparation of this manuscript. This work was supported in part by Program Project Grant PO-132427 from the National Heart, Lung and Blood Institute.

Keywords

Collagen
Myocyte hypertrophy
Rat myocardial infarction
Reperfusion
Ventricular remodeling

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10.1016/S0008-6363(97)00201-0

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@article{0ba53d0ebb30411892cfd56be0b9de1c,

title = "The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium",

abstract = "Objective: Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood. Methods: Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham- operated group (n = 10). Results: Analysis of infarct size (planimetry) in a separate group of rots demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 ± 8 vs. RP: 35 ± 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 ± 3 vs. 167 ± 4 μm, p = 0.02), in the right ventricle (154 ± 4 vs. 167 ± 3 μm, p = 0.02) and in the septum (158 ± 4 vs. 169 ± 4 μm, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 ± 1.7 X 103 vs. 44.1 ± 1.6 x 103 μm3, p = 0.06; right ventricle 36.7 ± 1.6 x 103 vs. 42.7 ± 2.0 x 103 μm3, p = 0.02; septum 41.0 ± 1.6 x 103 vs. 44.2 ± 1.8 x 103 μm3, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups. Conclusion: Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti- remodeling effect remote from the area perfused by this artery.",

keywords = "Collagen, Myocyte hypertrophy, Rat myocardial infarction, Reperfusion, Ventricular remodeling",

author = "Kenneth McDonald and Cuixia Chu and Gary Francis and Dianne Judd and Wenda Carlyle and Cynthia Toher and Katherine Hauer and Malinda Hartman",

note = "Funding Information: The authors acknowledge Dr. Jay N. Cohn for his critical review of the data and Susan Quirt for her expert assistance in the preparation of this manuscript. This work was supported in part by Program Project Grant PO-132427 from the National Heart, Lung and Blood Institute.",

year = "1997",

month = dec,

doi = "10.1016/S0008-6363(97)00201-0",

language = "English (US)",

volume = "36",

pages = "347--353",

journal = "Cardiovascular Research",

issn = "0008-6363",

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T1 - The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium

AU - McDonald, Kenneth

AU - Chu, Cuixia

AU - Francis, Gary

AU - Judd, Dianne

AU - Carlyle, Wenda

AU - Toher, Cynthia

AU - Hauer, Katherine

AU - Hartman, Malinda

N1 - Funding Information: The authors acknowledge Dr. Jay N. Cohn for his critical review of the data and Susan Quirt for her expert assistance in the preparation of this manuscript. This work was supported in part by Program Project Grant PO-132427 from the National Heart, Lung and Blood Institute.

PY - 1997/12

Y1 - 1997/12

N2 - Objective: Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood. Methods: Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham- operated group (n = 10). Results: Analysis of infarct size (planimetry) in a separate group of rots demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 ± 8 vs. RP: 35 ± 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 ± 3 vs. 167 ± 4 μm, p = 0.02), in the right ventricle (154 ± 4 vs. 167 ± 3 μm, p = 0.02) and in the septum (158 ± 4 vs. 169 ± 4 μm, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 ± 1.7 X 103 vs. 44.1 ± 1.6 x 103 μm3, p = 0.06; right ventricle 36.7 ± 1.6 x 103 vs. 42.7 ± 2.0 x 103 μm3, p = 0.02; septum 41.0 ± 1.6 x 103 vs. 44.2 ± 1.8 x 103 μm3, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups. Conclusion: Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti- remodeling effect remote from the area perfused by this artery.

AB - Objective: Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood. Methods: Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham- operated group (n = 10). Results: Analysis of infarct size (planimetry) in a separate group of rots demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 ± 8 vs. RP: 35 ± 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 ± 3 vs. 167 ± 4 μm, p = 0.02), in the right ventricle (154 ± 4 vs. 167 ± 3 μm, p = 0.02) and in the septum (158 ± 4 vs. 169 ± 4 μm, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 ± 1.7 X 103 vs. 44.1 ± 1.6 x 103 μm3, p = 0.06; right ventricle 36.7 ± 1.6 x 103 vs. 42.7 ± 2.0 x 103 μm3, p = 0.02; septum 41.0 ± 1.6 x 103 vs. 44.2 ± 1.8 x 103 μm3, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups. Conclusion: Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti- remodeling effect remote from the area perfused by this artery.

KW - Collagen

KW - Myocyte hypertrophy

KW - Rat myocardial infarction

KW - Reperfusion

KW - Ventricular remodeling

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JO - Cardiovascular Research

JF - Cardiovascular Research

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The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium

Abstract

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Keywords

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