The Resource Endotoxemia-induced myocardial dysfunction : role of myofilament ca2+ responsiveness, by Sherri L. Rigby

Endotoxemia-induced myocardial dysfunction : role of myofilament ca2+ responsiveness, by Sherri L. Rigby

Label
Endotoxemia-induced myocardial dysfunction : role of myofilament ca2+ responsiveness
Title
Endotoxemia-induced myocardial dysfunction
Title remainder
role of myofilament ca2+ responsiveness
Statement of responsibility
by Sherri L. Rigby
Title variation
Myofilament ca2+ responsiveness during endotoxemia
Creator
Subject
Language
eng
Summary
Myocardial contractility is depressed following the onset of endotoxemia and is intrinsic to the ventricular myocyte. The cellular mechanism(s) mediating contractile dysfunction remain(s) unclear; however, defective Ca$\sp{2+}$ handling may play a major role. The primary objective of these studies was to determine whether basal myofilament Ca$\sp{2+}$ responsiveness is reduced during endotoxemia contributing to contractile dysfunction of the ventricular myocyte. A nonhypotensive model of endotoxemia was induced in the guinea pig by intraperitoneal injection of 4mg/kg E. coli lipopolysaccharide (LPS). Ventricular myocytes were isolated 4 hours later (LPS) myocytes). Myofilament Ca$\sp{2+}$ responsiveness was assessed by image analysis of unloaded shortening of enzymatically isolated, saponin skinned myocytes and also by isometric tension measurements of mechanically isolated ventricular which were skinned with Triton X-100. These studies indicate that basal myofilament Ca$\sp{2+}$ responsiveness of LPS myocytes is not depressed. Thus, the contractile dysfunction of the heart during early, nonhypertensive endotoxemia, is not due to decreased myofilament Ca$\sp{2+}$ responsiveness. A second objective of these studies was to examine the cellular mechanism for the positive inotropic effect of endothelin-1 (ET-1) on ventricular myocytes isolated from normal and diseased hearts. The cellular mechanism for the positive inotropic effect of ET-1 is complex and appears to result from increased responsiveness to Ca$\sp{2+}.$ The 4 hour guinea pig model of nonhypotensive endotoxemia was used as the diseased heart model for these studies. We hypothesized that subtle changes in Ca$\sp{2+}$ responsiveness mediated by ET-1 may be more easily detected in a model exhibiting decreased myocardial contractility. Contractile responses of sarcolemmal-intact myocytes to ET-1 were assessed by image analysis of unloaded shortening. ET-1 receptor-signaling effects on myofilament Ca$\sp{2+}$ responsiveness were determined by image analysis of shortening of Staphylococcus aureus $\alpha$-toxin permeabilized myocytes. In myocytes isolated from normal hearts (CTL), the positive inotropic effect of ET-1 was seen only in myocytes contracting at low frequency. ET-1 did not alter the free Ca$\sp{2+}$-shortening relationship of permeabilized myocytes. In contrast, ET-1 enhanced the contractile response of sarcolemmal-intact LPS myocytes and shifted the pCa$\sb{50}$ of the free Ca$\sp{2+}$-shortening relationship of $\alpha$-toxin permeabilized myocytes to the left. These results suggest that ET-1 receptor-mediated signaling events do not directly alter Ca$\sp{2+}$ responsiveness of myofilaments in CTL myocytes. However, ET-1 receptor-mediated signaling events enhanced Ca$\sp{2+}$ responsiveness of permeabilized LPS myocytes. Although basal myofilament Ca$\sp{2+}$ responsiveness of LPS myocytes is not different from CTL myocytes, these results suggest that second messenger pathways or contractile proteins of LPS myocytes respond differently to ET-1 than those of CTL myocytes
Additional physical form
Also available on the Internet.
Cataloging source
MMU
http://library.link/vocab/creatorDate
1956-
http://library.link/vocab/creatorName
Rigby, Sherri L.
Degree
Ph. D.
Dissertation year
1997.
Government publication
government publication of a state province territory dependency etc
Granting institution
University of Missouri--Columbia
Illustrations
illustrations
Index
no index present
Literary form
non fiction
Nature of contents
theses
http://library.link/vocab/subjectName
  • Calcium
  • Endotoxins
  • Heart
  • Cytoplasmic filaments
  • Cytoplasmic filaments
  • Guinea pigs
  • Heart
Label
Endotoxemia-induced myocardial dysfunction : role of myofilament ca2+ responsiveness, by Sherri L. Rigby
Instantiates
Publication
Note
  • "December 1997."
  • Typescript
  • Vita
Bibliography note
Includes bibliographical references (leaves 176-196)
Carrier category
online resource
Carrier category code
  • cr
Carrier MARC source
rdacarrier.
Content category
text
Content type code
  • txt
Content type MARC source
rdacontent.
Control code
41626518
Dimensions
28 cm.
Dimensions
unknown
Extent
xi, 197 leaves
Media category
computer
Media MARC source
rdamedia.
Media type code
  • c
Other physical details
illustrations
Specific material designation
remote
Label
Endotoxemia-induced myocardial dysfunction : role of myofilament ca2+ responsiveness, by Sherri L. Rigby
Publication
Note
  • "December 1997."
  • Typescript
  • Vita
Bibliography note
Includes bibliographical references (leaves 176-196)
Carrier category
online resource
Carrier category code
  • cr
Carrier MARC source
rdacarrier.
Content category
text
Content type code
  • txt
Content type MARC source
rdacontent.
Control code
41626518
Dimensions
28 cm.
Dimensions
unknown
Extent
xi, 197 leaves
Media category
computer
Media MARC source
rdamedia.
Media type code
  • c
Other physical details
illustrations
Specific material designation
remote

Library Locations

    • Zalk Veterinary Medical LibraryBorrow it
      Veterinary Medicine West, Columbia, MO, 65211, US
      38.941099 -92.317911
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