Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress

Thomas A. Fischer, Paul L McNeil, Robert Khakee, Peter Finn, Ralph A. Kelly, Marc A. Pfeffer, Janice M. Pfeffer

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase-labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.

Original languageEnglish (US)
Pages (from-to)1041-1046
Number of pages6
JournalHypertension
Volume30
Issue number5
DOIs
StatePublished - Jan 1 1997

Fingerprint

Cardiac Myocytes
Hemodynamics
Pressure
Membranes
Frozen Sections
Horseradish Peroxidase
Hypertrophy
Aorta
Anti-Idiotypic Antibodies
Albumins
Permeability
Signal Transduction
Staining and Labeling

Keywords

  • Cardiomyocyte wounding
  • Pressure overload
  • Stress, left ventricular wall

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Fischer, T. A., McNeil, P. L., Khakee, R., Finn, P., Kelly, R. A., Pfeffer, M. A., & Pfeffer, J. M. (1997). Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress. Hypertension, 30(5), 1041-1046. https://doi.org/10.1161/01.HYP.30.5.1041

Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress. / Fischer, Thomas A.; McNeil, Paul L; Khakee, Robert; Finn, Peter; Kelly, Ralph A.; Pfeffer, Marc A.; Pfeffer, Janice M.

In: Hypertension, Vol. 30, No. 5, 01.01.1997, p. 1041-1046.

Research output: Contribution to journalArticle

Fischer, TA, McNeil, PL, Khakee, R, Finn, P, Kelly, RA, Pfeffer, MA & Pfeffer, JM 1997, 'Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress', Hypertension, vol. 30, no. 5, pp. 1041-1046. https://doi.org/10.1161/01.HYP.30.5.1041
Fischer, Thomas A. ; McNeil, Paul L ; Khakee, Robert ; Finn, Peter ; Kelly, Ralph A. ; Pfeffer, Marc A. ; Pfeffer, Janice M. / Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress. In: Hypertension. 1997 ; Vol. 30, No. 5. pp. 1041-1046.
@article{5f1cc5af323544c391dddcaae4e74c5e,
title = "Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress",
abstract = "The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase-labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.",
keywords = "Cardiomyocyte wounding, Pressure overload, Stress, left ventricular wall",
author = "Fischer, {Thomas A.} and McNeil, {Paul L} and Robert Khakee and Peter Finn and Kelly, {Ralph A.} and Pfeffer, {Marc A.} and Pfeffer, {Janice M.}",
year = "1997",
month = "1",
day = "1",
doi = "10.1161/01.HYP.30.5.1041",
language = "English (US)",
volume = "30",
pages = "1041--1046",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress

AU - Fischer, Thomas A.

AU - McNeil, Paul L

AU - Khakee, Robert

AU - Finn, Peter

AU - Kelly, Ralph A.

AU - Pfeffer, Marc A.

AU - Pfeffer, Janice M.

PY - 1997/1/1

Y1 - 1997/1/1

N2 - The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase-labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.

AB - The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase-labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.

KW - Cardiomyocyte wounding

KW - Pressure overload

KW - Stress, left ventricular wall

UR - http://www.scopus.com/inward/record.url?scp=0030723311&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030723311&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.30.5.1041

DO - 10.1161/01.HYP.30.5.1041

M3 - Article

C2 - 9369253

AN - SCOPUS:0030723311

VL - 30

SP - 1041

EP - 1046

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 5

ER -