Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock.
Identifieur interne : 000491 ( PubMed/Corpus ); précédent : 000490; suivant : 000492Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock.
Auteurs : S M Song ; S M Lu ; Z G Wang ; J C Liu ; S Q Guo ; Z. LiSource :
- Injury [ 0020-1383 ] ; 1999.
English descriptors
- KwdEn :
- Animals, Chloroquine (therapeutic use), Chlorpromazine (therapeutic use), Enzyme Inhibitors (therapeutic use), Intracellular Membranes (drug effects), Intracellular Membranes (physiology), Membrane Fluidity (drug effects), Membrane Fluidity (physiology), Mitochondria (drug effects), Mitochondria (physiology), Phospholipases A (antagonists & inhibitors), Phospholipases A (physiology), Phospholipases A2, Rabbits, Shock, Septic (enzymology), Shock, Septic (pathology), Shock, Septic (prevention & control).
- MESH :
- chemical , antagonists & inhibitors : Phospholipases A.
- chemical , physiology : Phospholipases A.
- chemical , therapeutic use : Chloroquine, Chlorpromazine, Enzyme Inhibitors.
- drug effects : Intracellular Membranes, Membrane Fluidity, Mitochondria.
- enzymology : Shock, Septic.
- pathology : Shock, Septic.
- physiology : Intracellular Membranes, Membrane Fluidity, Mitochondria.
- prevention & control : Shock, Septic.
- Animals, Phospholipases A2, Rabbits.
Abstract
The study aims at elucidating the mechanism involved in the cell dysfunction or impairment and the protective effects of phospholipase A2 (PLA2) inhibitors in endotoxin shock. Thirty-four rabbits were divided randomly into four groups: (1) normal control group (NC, n = 6), receiving saline intravenously; (2) endotoxin shock group (ES, n = 12), receiving 3 mg/kg of E. coli endotoxin; (3) chloroquine pretreated group (CQ, n = 8), receiving 3 mg/kg of chloroquine 3 min before endotoxin injection and (4) chlorpromazine pretreated group (CPZ, n = 8), receiving 0.3 mg/kg of chlorpromazine 30 min before endotoxin injection. Hepatic mitochondria were extracted either 8 h after commencement of the experiment or when the animals died for detecting PLA2 activity, membrane fluidity, membrane bound succinate dehydrogenate (SDH) and malondialdehyde (MDA). Mitochondria of the lung, heart and kidney were also used for detection of the membrane fluidity. It was revealed that the survival rate of 8 h was 100% (NC), 58% (ES), 87.5% (CQ) and 75% (CPZ), respectively. Mean arterial pressure (MAP) dropped soon after endotoxin injection and descended continuously afterwards in the ES group (P < 0.01). Fluorescence polarization, microviscosity and anisotrophy with a DPH probe were elevated above control levels (P < 0.01). SDH was decreased obviously following endotoxin infusion (P < 0.01). Chloroquine and chlorpromazine, serving as PLA2 inhibitors, could abate cellular dysfunction and increase survival rate. It is proposed that PLA2 plays a pivotal role in cellular injury in endotoxin shock. PLA2 inhibitor might serve as a useful adjunct in combating sepsis and shock.
DOI: 10.1016/s0020-1383(98)00178-8
PubMed: 10396448
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pubmed:10396448Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock.</title><author><name sortKey="Song, S M" sort="Song, S M" uniqKey="Song S" first="S M" last="Song">S M Song</name><affiliation><nlm:affiliation>Research Institute of Surgery, Chongqing, People's Republic of China.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, S M" sort="Lu, S M" uniqKey="Lu S" first="S M" last="Lu">S M Lu</name></author><author><name sortKey="Wang, Z G" sort="Wang, Z G" uniqKey="Wang Z" first="Z G" last="Wang">Z G Wang</name></author><author><name sortKey="Liu, J C" sort="Liu, J C" uniqKey="Liu J" first="J C" last="Liu">J C Liu</name></author><author><name sortKey="Guo, S Q" sort="Guo, S Q" uniqKey="Guo S" first="S Q" last="Guo">S Q Guo</name></author><author><name sortKey="Li, Z" sort="Li, Z" uniqKey="Li Z" first="Z" last="Li">Z. Li</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:10396448</idno><idno type="pmid">10396448</idno><idno type="doi">10.1016/s0020-1383(98)00178-8</idno><idno type="wicri:Area/PubMed/Corpus">000491</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000491</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock.</title><author><name sortKey="Song, S M" sort="Song, S M" uniqKey="Song S" first="S M" last="Song">S M Song</name><affiliation><nlm:affiliation>Research Institute of Surgery, Chongqing, People's Republic of China.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, S M" sort="Lu, S M" uniqKey="Lu S" first="S M" last="Lu">S M Lu</name></author><author><name sortKey="Wang, Z G" sort="Wang, Z G" uniqKey="Wang Z" first="Z G" last="Wang">Z G Wang</name></author><author><name sortKey="Liu, J C" sort="Liu, J C" uniqKey="Liu J" first="J C" last="Liu">J C Liu</name></author><author><name sortKey="Guo, S Q" sort="Guo, S Q" uniqKey="Guo S" first="S Q" last="Guo">S Q Guo</name></author><author><name sortKey="Li, Z" sort="Li, Z" uniqKey="Li Z" first="Z" last="Li">Z. Li</name></author></analytic><series><title level="j">Injury</title><idno type="ISSN">0020-1383</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Chloroquine (therapeutic use)</term><term>Chlorpromazine (therapeutic use)</term><term>Enzyme Inhibitors (therapeutic use)</term><term>Intracellular Membranes (drug effects)</term><term>Intracellular Membranes (physiology)</term><term>Membrane Fluidity (drug effects)</term><term>Membrane Fluidity (physiology)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (physiology)</term><term>Phospholipases A (antagonists & inhibitors)</term><term>Phospholipases A (physiology)</term><term>Phospholipases A2</term><term>Rabbits</term><term>Shock, Septic (enzymology)</term><term>Shock, Septic (pathology)</term><term>Shock, Septic (prevention & control)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Phospholipases A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Phospholipases A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Chloroquine</term><term>Chlorpromazine</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Intracellular Membranes</term><term>Membrane Fluidity</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Shock, Septic</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Shock, Septic</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Intracellular Membranes</term><term>Membrane Fluidity</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Shock, Septic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Phospholipases A2</term><term>Rabbits</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The study aims at elucidating the mechanism involved in the cell dysfunction or impairment and the protective effects of phospholipase A2 (PLA2) inhibitors in endotoxin shock. Thirty-four rabbits were divided randomly into four groups: (1) normal control group (NC, n = 6), receiving saline intravenously; (2) endotoxin shock group (ES, n = 12), receiving 3 mg/kg of E. coli endotoxin; (3) chloroquine pretreated group (CQ, n = 8), receiving 3 mg/kg of chloroquine 3 min before endotoxin injection and (4) chlorpromazine pretreated group (CPZ, n = 8), receiving 0.3 mg/kg of chlorpromazine 30 min before endotoxin injection. Hepatic mitochondria were extracted either 8 h after commencement of the experiment or when the animals died for detecting PLA2 activity, membrane fluidity, membrane bound succinate dehydrogenate (SDH) and malondialdehyde (MDA). Mitochondria of the lung, heart and kidney were also used for detection of the membrane fluidity. It was revealed that the survival rate of 8 h was 100% (NC), 58% (ES), 87.5% (CQ) and 75% (CPZ), respectively. Mean arterial pressure (MAP) dropped soon after endotoxin injection and descended continuously afterwards in the ES group (P < 0.01). Fluorescence polarization, microviscosity and anisotrophy with a DPH probe were elevated above control levels (P < 0.01). SDH was decreased obviously following endotoxin infusion (P < 0.01). Chloroquine and chlorpromazine, serving as PLA2 inhibitors, could abate cellular dysfunction and increase survival rate. It is proposed that PLA2 plays a pivotal role in cellular injury in endotoxin shock. PLA2 inhibitor might serve as a useful adjunct in combating sepsis and shock.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10396448</PMID><DateCompleted><Year>1999</Year><Month>07</Month><Day>22</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0020-1383</ISSN><JournalIssue CitedMedium="Print"><Volume>30</Volume><Issue>1</Issue><PubDate><Year>1999</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Injury</Title><ISOAbbreviation>Injury</ISOAbbreviation></Journal><ArticleTitle>Subcellular membrane impairment and application of phospholipase A2 inhibitors in endotoxic shock.</ArticleTitle><Pagination><MedlinePgn>9-14</MedlinePgn></Pagination><Abstract><AbstractText>The study aims at elucidating the mechanism involved in the cell dysfunction or impairment and the protective effects of phospholipase A2 (PLA2) inhibitors in endotoxin shock. Thirty-four rabbits were divided randomly into four groups: (1) normal control group (NC, n = 6), receiving saline intravenously; (2) endotoxin shock group (ES, n = 12), receiving 3 mg/kg of E. coli endotoxin; (3) chloroquine pretreated group (CQ, n = 8), receiving 3 mg/kg of chloroquine 3 min before endotoxin injection and (4) chlorpromazine pretreated group (CPZ, n = 8), receiving 0.3 mg/kg of chlorpromazine 30 min before endotoxin injection. Hepatic mitochondria were extracted either 8 h after commencement of the experiment or when the animals died for detecting PLA2 activity, membrane fluidity, membrane bound succinate dehydrogenate (SDH) and malondialdehyde (MDA). Mitochondria of the lung, heart and kidney were also used for detection of the membrane fluidity. It was revealed that the survival rate of 8 h was 100% (NC), 58% (ES), 87.5% (CQ) and 75% (CPZ), respectively. Mean arterial pressure (MAP) dropped soon after endotoxin injection and descended continuously afterwards in the ES group (P < 0.01). Fluorescence polarization, microviscosity and anisotrophy with a DPH probe were elevated above control levels (P < 0.01). SDH was decreased obviously following endotoxin infusion (P < 0.01). Chloroquine and chlorpromazine, serving as PLA2 inhibitors, could abate cellular dysfunction and increase survival rate. It is proposed that PLA2 plays a pivotal role in cellular injury in endotoxin shock. PLA2 inhibitor might serve as a useful adjunct in combating sepsis and shock.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Song</LastName><ForeName>S M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Research Institute of Surgery, Chongqing, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>S M</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Z G</ForeName><Initials>ZG</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>J C</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>S Q</ForeName><Initials>SQ</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Z</ForeName><Initials>Z</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Injury</MedlineTA><NlmUniqueID>0226040</NlmUniqueID><ISSNLinking>0020-1383</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.32</RegistryNumber><NameOfSubstance UI="D010741">Phospholipases A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.4</RegistryNumber><NameOfSubstance UI="D054467">Phospholipases A2</NameOfSubstance></Chemical><Chemical><RegistryNumber>U42B7VYA4P</RegistryNumber><NameOfSubstance UI="D002746">Chlorpromazine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002746" MajorTopicYN="N">Chlorpromazine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007425" MajorTopicYN="N">Intracellular Membranes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008560" MajorTopicYN="N">Membrane Fluidity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010741" MajorTopicYN="N">Phospholipases A</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054467" MajorTopicYN="N">Phospholipases A2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012772" MajorTopicYN="N">Shock, Septic</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>7</Month><Day>9</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>7</Month><Day>9</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>7</Month><Day>9</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10396448</ArticleId><ArticleId IdType="pii">S0020138398001788</ArticleId><ArticleId IdType="doi">10.1016/s0020-1383(98)00178-8</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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