Document Detail


Depletion of membrane phospholipid and mitochondrial dysfunction associated with coronary reperfusion.
MedLine Citation:
PMID:  4026784     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The role of phospholipase (PLase) in the development of heart mitochondrial dysfunction following reperfusion was studied together with the effects of dilazep on the action of PLases and reperfusion injury. In vivo experiment: Seventy six adult mongrel dogs were divided into 3 groups; the control group (n = 36), the dilazep 0.5 mg group (n = 17) and the dilazep 1 mg group (n = 23). Fifteen min after premedication with physiological saline or dilazep (0.5 mg/kg or 1 mg/kg), the left anterior descending coronary artery was occluded for 15 min and then reperfused for 5 min. Each group was further divided into two subgroups depending on the presence or absence of reperfusion arrhythmia. Immediately after 5 min of reperfusion, myocardial mitochondria were prepared from the normal and the reperfused areas. Pretreatment with dilazep induced a dose-dependent decrease in the incidence of reperfusion arrhythmia from 31% of the control to 24% (0.5 mg/kg) and 9% (1 mg/kg). In the arrhythmia cases in each group, functional deterioration of mitochondria from the reperfused area was observed with the increase in free fatty acids and the decrease in phospholipids in the reperfused mitochondria. In vitro experiment: Using L-alpha-dimyristoyl phosphatidylcholine as a substrate, myristic acid released by PLase A2 or by PLase C with or without pretreatment by dilazep was quantitatively determined. Dilazep inhibited the release of myristic acid by PLase A2 or by PLase C in a concentration-dependent manner. These results suggest that decomposition of mitochondrial membrane phospholipids caused by PLase activation following reperfusion was primarily responsible for the development of mitochondrial dysfunction, and that dilazep showed beneficial effects against reperfusion injury by inhibiting the action of PLases.
Authors:
M Hattori; K Ogawa; T Satake; S Sugiyama; T Ozawa
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Basic research in cardiology     Volume:  80     ISSN:  0300-8428     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:    1985 May-Jun
Date Detail:
Created Date:  1985-09-16     Completed Date:  1985-09-16     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  GERMANY, WEST    
Other Details:
Languages:  eng     Pagination:  241-50     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Coronary Circulation* / drug effects
Coronary Disease / physiopathology*
Dilazep / pharmacology
Dogs
Dose-Response Relationship, Drug
Fatty Acids, Nonesterified / metabolism
Female
Heart Rate / drug effects
Male
Membrane Lipids / metabolism*
Mitochondria, Heart / physiology*
Myocardium / enzymology
Oxygen Consumption / drug effects
Phospholipases / antagonists & inhibitors,  physiology*
Phospholipases A / physiology
Phospholipids / metabolism*
Type C Phospholipases / physiology
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Membrane Lipids; 0/Phospholipids; 35898-87-4/Dilazep; EC 3.1.-/Phospholipases; EC 3.1.1.-/Phospholipases A; EC 3.1.4.-/Type C Phospholipases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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