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Diastolic function during hemorrhagic shock in rabbits.

Verónica D'Annunzio1, Martín Donato, Andrea Fellet

  • 1School of Medicine, Institute of Cardiovascular Physiopathology and Department of Pathology, University of Buenos Aires, and Laboratory of Oxygen Metabolism, University Hospital, JE Uriburu 950-2nd floor, 1114, Buenos Aires, Argentina.

Molecular and Cellular Biochemistry
|August 16, 2011
PubMed
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Acute hemorrhage impairs left ventricular diastolic function temporarily, increasing myocardial stiffness. This dysfunction is mediated by nitric oxide synthase (NOS) isoforms, as L-NAME administration reversed the effects.

Area of Science:

  • Cardiovascular Physiology
  • Hemorrhage Pathophysiology
  • Nitric Oxide Signaling

Background:

  • Hemorrhage (H) is known to cause left ventricular (LV) dysfunction.
  • Diastolic dysfunction following hemorrhage has not been extensively studied.
  • Nitric oxide synthase (NOS) isoforms play a role in cardiovascular regulation.

Purpose of the Study:

  • To assess LV diastolic function during and after hemorrhage.
  • To investigate the role of nitric oxide (NO) in hemorrhage-induced diastolic dysfunction.
  • To determine changes in NOS isoform expression post-hemorrhage.

Main Methods:

  • Animal model: New Zealand rabbits subjected to sham procedure, hemorrhage (20% blood volume), or hemorrhage with L-NAME treatment.
  • In vivo and in vitro assessments of LV systolic and diastolic function, including isovolumetric relaxation time (t½) and myocardial stiffness.

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  • Analysis of inducible (iNOS) and neuronal (nNOS) nitric oxide synthase mRNA and protein expression.

    • Main Results:

    • Hemorrhage increased isovolumetric relaxation time (t½) during bleeding, returning to baseline 120 minutes post-hemorrhage.
    • L-NAME administration attenuated the increase in t½ and prevented a leftward shift in the LV end-diastolic pressure-volume curve.
    • Hemorrhage led to increased iNOS and nNOS mRNA and protein expression 120 minutes post-bleeding.

    Conclusions:

    • Acute hemorrhage causes early, transient impairment of isovolumetric relaxation and increased myocardial stiffness.
    • Nitric oxide, via iNOS and nNOS, plays a significant role in modulating ventricular dysfunction following hemorrhage.
    • L-NAME effectively blunted the observed left ventricular dysfunction, highlighting NO's modulatory role.