Mitochondrial function in canine experimental cardiac hypertrophy

Mohammed A. Matlib; Judith C. Rembert; Ronald W. Millard; Muhammad Ashraf; William Rouslin; Goro Asano; Joseph C. Greenfield; Arnold Schwartz

doi:10.1016/0022-2828(83)90277-8

Mitochondrial function in canine experimental cardiac hypertrophy

Mohammed A. Matlib, Judith C. Rembert, Ronald W. Millard, Muhammad Ashraf, William Rouslin, Goro Asano, Joseph C. Greenfield, Arnold Schwartz

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

11 Scopus citations

Abstract

Concentric left ventricular hypertrophy was produced in puppies by coarcation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 ± 16 mmHg in experimental dogs compared with 115 ± 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 ± 4 and 64 ± 7, respectively. The left ventricular end-diastolic pressure was 6.0 ± 0.4 in control and 8.4 ± 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.

Original language	English (US)
Pages (from-to)	221-232
Number of pages	12
Journal	Journal of molecular and cellular cardiology
Volume	15
Issue number	4
DOIs	https://doi.org/10.1016/0022-2828(83)90277-8
State	Published - Apr 1983
Externally published	Yes

Keywords

Aortic constriction
Aortic stenosis
Cardiac hypertrophy
Mitochondria
Oxidative phosphorylation
Ventricular function

ASJC Scopus subject areas

Molecular Biology
Cardiology and Cardiovascular Medicine

Access to Document

10.1016/0022-2828(83)90277-8

Cite this

@article{d377065ff1654100abd8a3f8097bbc0f,

title = "Mitochondrial function in canine experimental cardiac hypertrophy",

abstract = "Concentric left ventricular hypertrophy was produced in puppies by coarcation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 ± 16 mmHg in experimental dogs compared with 115 ± 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 ± 4 and 64 ± 7, respectively. The left ventricular end-diastolic pressure was 6.0 ± 0.4 in control and 8.4 ± 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.",

keywords = "Aortic constriction, Aortic stenosis, Cardiac hypertrophy, Mitochondria, Oxidative phosphorylation, Ventricular function",

author = "Matlib, {Mohammed A.} and Rembert, {Judith C.} and Millard, {Ronald W.} and Muhammad Ashraf and William Rouslin and Goro Asano and Greenfield, {Joseph C.} and Arnold Schwartz",

note = "Funding Information: This work was supported by grants from NIH, POl-HL 22619-02 (IV B, Cores 1 and 5), ROl-HL 18468, ROI HL 23558, ROI-HL 23597. The authors acknowledge the expert technical assistance of Mr Billy Joe Rice, Mr Paul Harper, and MS Diana Rebman. Drs Frederick R. Cobb and Ken Morris, aided by MS Maggie Wilson, carried out the radionuclide ventriculograms.",

year = "1983",

month = apr,

doi = "10.1016/0022-2828(83)90277-8",

language = "English (US)",

volume = "15",

pages = "221--232",

journal = "Journal of molecular and cellular cardiology",

issn = "0022-2828",

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TY - JOUR

T1 - Mitochondrial function in canine experimental cardiac hypertrophy

AU - Matlib, Mohammed A.

AU - Rembert, Judith C.

AU - Millard, Ronald W.

AU - Ashraf, Muhammad

AU - Rouslin, William

AU - Asano, Goro

AU - Greenfield, Joseph C.

AU - Schwartz, Arnold

N1 - Funding Information: This work was supported by grants from NIH, POl-HL 22619-02 (IV B, Cores 1 and 5), ROl-HL 18468, ROI HL 23558, ROI-HL 23597. The authors acknowledge the expert technical assistance of Mr Billy Joe Rice, Mr Paul Harper, and MS Diana Rebman. Drs Frederick R. Cobb and Ken Morris, aided by MS Maggie Wilson, carried out the radionuclide ventriculograms.

PY - 1983/4

Y1 - 1983/4

N2 - Concentric left ventricular hypertrophy was produced in puppies by coarcation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 ± 16 mmHg in experimental dogs compared with 115 ± 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 ± 4 and 64 ± 7, respectively. The left ventricular end-diastolic pressure was 6.0 ± 0.4 in control and 8.4 ± 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.

AB - Concentric left ventricular hypertrophy was produced in puppies by coarcation banding of the aorta at age 7 weeks. Hemodynamic, morphologic and biochemical studies were carried out 18 months after the operation. Systolic blood pressure proximal to the aortic constriction was 216 ± 16 mmHg in experimental dogs compared with 115 ± 5 mmHg in littermate control dogs. Ejection fraction of control and experimental dogs were 59 ± 4 and 64 ± 7, respectively. The left ventricular end-diastolic pressure was 6.0 ± 0.4 in control and 8.4 ± 1.1 in experimental dogs. There was no sign of overt heart failure in the experimental dogs. Anatomical analysis of different regions of the heart indicated that LV mass in the experimental dogs was increased by about 60%. Ultrastructure of mitochondria in situ, as observed under electron microscope, was normal both in control and hypertrophic hearts. Mitochondria isolated from epicardial and endocardial regions of the stable hypertrophic hearts showed normal rates of respiration, phosphorylation, citrate synthase, and cytochrome c oxidase activities compared to those isolated from hearts of littermate control dogs. It was, therefore, concluded that mitochondrial function is adequately preserved to meet the increased demand for energy in this model of stable cardiac hypertrophy of long duration.

KW - Aortic constriction

KW - Aortic stenosis

KW - Cardiac hypertrophy

KW - Mitochondria

KW - Oxidative phosphorylation

KW - Ventricular function

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JO - Journal of molecular and cellular cardiology

JF - Journal of molecular and cellular cardiology

IS - 4

ER -

Mitochondrial function in canine experimental cardiac hypertrophy

Abstract

Keywords

ASJC Scopus subject areas

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