Influence of chlorpromazine on lysosomal alterations during myocardial ischaemia

Kenneth R. Chien; J. Stanley Crie; Robert S. Decker; Kern Wildenthal

doi:10.1093/cvrese/17.7.407

Influence of chlorpromazine on lysosomal alterations during myocardial ischaemia

Kenneth R. Chien, J. Stanley Crie, Robert S. Decker, Kern Wildenthal

Internal Medicine

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

4 Scopus citations

Abstract

Summary: Ligation of the circumflex artery of anaesthetised, open-chest rabbits caused a progressive increase in nonsedimentable cathepsin D activity in severely ischaemic myocardium and an anatomical redistribution of the enzyme from lysosomes into the cytosol, along with progressive ultrastructural signs of cellular damage and necrosis. Chlorpromazine pretreatment (15 mg·kg^-1 intravenously) reduced the increase in nonsedimentable cathepsin D activity slightly, but no appreciable protective effect on the anatomical redistribution of the enzyme or the development of ultrastructural signs of necrosis could be detected. It is concluded that in this experimental model of myocardial infarction, high concentrations of chlorpromazine have a mild stabilising action on lysosomes, but the drug has minimal if any effect in protecting the heart from ischaemic damage.

Original language	English (US)
Pages (from-to)	407-414
Number of pages	8
Journal	Cardiovascular Research
Volume	17
Issue number	7
DOIs	https://doi.org/10.1093/cvrese/17.7.407
State	Published - Jul 1983

ASJC Scopus subject areas

Statistics, Probability and Uncertainty
Applied Mathematics
Physiology (medical)
Physiology
Cardiology and Cardiovascular Medicine

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title = "Influence of chlorpromazine on lysosomal alterations during myocardial ischaemia",

abstract = "Summary: Ligation of the circumflex artery of anaesthetised, open-chest rabbits caused a progressive increase in nonsedimentable cathepsin D activity in severely ischaemic myocardium and an anatomical redistribution of the enzyme from lysosomes into the cytosol, along with progressive ultrastructural signs of cellular damage and necrosis. Chlorpromazine pretreatment (15 mg·kg-1 intravenously) reduced the increase in nonsedimentable cathepsin D activity slightly, but no appreciable protective effect on the anatomical redistribution of the enzyme or the development of ultrastructural signs of necrosis could be detected. It is concluded that in this experimental model of myocardial infarction, high concentrations of chlorpromazine have a mild stabilising action on lysosomes, but the drug has minimal if any effect in protecting the heart from ischaemic damage.",

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T1 - Influence of chlorpromazine on lysosomal alterations during myocardial ischaemia

AU - Chien, Kenneth R.

AU - Crie, J. Stanley

AU - Decker, Robert S.

AU - Wildenthal, Kern

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N2 - Summary: Ligation of the circumflex artery of anaesthetised, open-chest rabbits caused a progressive increase in nonsedimentable cathepsin D activity in severely ischaemic myocardium and an anatomical redistribution of the enzyme from lysosomes into the cytosol, along with progressive ultrastructural signs of cellular damage and necrosis. Chlorpromazine pretreatment (15 mg·kg-1 intravenously) reduced the increase in nonsedimentable cathepsin D activity slightly, but no appreciable protective effect on the anatomical redistribution of the enzyme or the development of ultrastructural signs of necrosis could be detected. It is concluded that in this experimental model of myocardial infarction, high concentrations of chlorpromazine have a mild stabilising action on lysosomes, but the drug has minimal if any effect in protecting the heart from ischaemic damage.

AB - Summary: Ligation of the circumflex artery of anaesthetised, open-chest rabbits caused a progressive increase in nonsedimentable cathepsin D activity in severely ischaemic myocardium and an anatomical redistribution of the enzyme from lysosomes into the cytosol, along with progressive ultrastructural signs of cellular damage and necrosis. Chlorpromazine pretreatment (15 mg·kg-1 intravenously) reduced the increase in nonsedimentable cathepsin D activity slightly, but no appreciable protective effect on the anatomical redistribution of the enzyme or the development of ultrastructural signs of necrosis could be detected. It is concluded that in this experimental model of myocardial infarction, high concentrations of chlorpromazine have a mild stabilising action on lysosomes, but the drug has minimal if any effect in protecting the heart from ischaemic damage.

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Influence of chlorpromazine on lysosomal alterations during myocardial ischaemia

Abstract

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