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dc.contributor.authorHeard, Stephen O.
dc.contributor.authorToth, Ildiko E.
dc.contributor.authorPerkins, Michael W.
dc.contributor.authorLeonard, Jack L.
dc.date2022-08-11T08:07:58.000
dc.date.accessioned2022-08-23T15:37:47Z
dc.date.available2022-08-23T15:37:47Z
dc.date.issued1994-06-01
dc.date.submitted2012-08-01
dc.identifier.citation<p>Shock. 1994 Jun;1(6):419-24.</p>
dc.identifier.issn1073-2322 (Linking)
dc.identifier.doi10.1097/00024382-199406000-00005
dc.identifier.pmid7735971
dc.identifier.urihttp://hdl.handle.net/20.500.14038/25797
dc.description.abstractThe effect of lipopolysaccharide (LPS) on cardiac protein kinase C (PKC) activation and cardiac depression was evaluated. Guinea pigs (n = 44) received intraperitoneal injections of saline or Escherichia coli LPS (2 mg/kg). Left atria were harvested 16 h later and suspended in oxygenated low calcium (1 mM) (n = 24) or high calcium (5 mM) (n = 20) 30 degrees C Krebs-Henseleit buffer. Atria were treated with H-7 (n = 23), a PKC inhibitor, or vehicle (n = 21). Contractile responses to changes in preload and stimulating frequency, in the resting and potentiated states, and to escalating doses of phenylephrine were measured. PKC activation in ventricular muscle was also determined. LPS activated ventricular PKC (p < .05) but treatment with H-7 failed to reverse LPS-induced atrial dysfunction in the low calcium buffer. Contractile function in the potentiated state indicated that LPS appears to interfere with calcium release from the sarcoplasmic reticulum (SR). The contractile response to phenylephrine was markedly attenuated in atria harvested from endotoxic animals. These data indicate that LPS-induced cardiac depression is mediated, in part, by alterations in SR calcium release. LPS activates cardiac PKC but a causal relationship among LPS, PKC, and cardiac dysfunction remains to be established.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=7735971&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1097/00024382-199406000-00005
dc.subjectAnimals
dc.subjectEnzyme Activation
dc.subjectFemale
dc.subjectGuinea Pigs
dc.subjectHeart
dc.subjectInjections, Intraperitoneal
dc.subjectLipopolysaccharides
dc.subjectMale
dc.subjectMyocardial Contraction
dc.subjectProtein Kinase C
dc.subjectSepsis
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectAnesthesiology
dc.subjectBiological Factors
dc.subjectCarbohydrates
dc.subjectEnzymes and Coenzymes
dc.subjectLipids
dc.subjectPhysiology
dc.titleThe role of protein kinase C in lipopolysaccharide-induced myocardial depression in guinea pigs
dc.typeJournal Article
dc.source.journaltitleShock (Augusta, Ga.)
dc.source.volume1
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/anesthesiology_pubs/39
dc.identifier.contextkey3168573
html.description.abstract<p>The effect of lipopolysaccharide (LPS) on cardiac protein kinase C (PKC) activation and cardiac depression was evaluated. Guinea pigs (n = 44) received intraperitoneal injections of saline or Escherichia coli LPS (2 mg/kg). Left atria were harvested 16 h later and suspended in oxygenated low calcium (1 mM) (n = 24) or high calcium (5 mM) (n = 20) 30 degrees C Krebs-Henseleit buffer. Atria were treated with H-7 (n = 23), a PKC inhibitor, or vehicle (n = 21). Contractile responses to changes in preload and stimulating frequency, in the resting and potentiated states, and to escalating doses of phenylephrine were measured. PKC activation in ventricular muscle was also determined. LPS activated ventricular PKC (p < .05) but treatment with H-7 failed to reverse LPS-induced atrial dysfunction in the low calcium buffer. Contractile function in the potentiated state indicated that LPS appears to interfere with calcium release from the sarcoplasmic reticulum (SR). The contractile response to phenylephrine was markedly attenuated in atria harvested from endotoxic animals. These data indicate that LPS-induced cardiac depression is mediated, in part, by alterations in SR calcium release. LPS activates cardiac PKC but a causal relationship among LPS, PKC, and cardiac dysfunction remains to be established.</p>
dc.identifier.submissionpathanesthesiology_pubs/39
dc.contributor.departmentDepartment of Surgery
dc.contributor.departmentDepartment of Physiology
dc.contributor.departmentDepartment of Anesthesiology
dc.source.pages419-24


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