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Related Experiment Video

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Author Spotlight: Neuromotor Control and Recovery of Diaphragm Function Following Cervical Spinal Hemisection in Rats
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Challenging cardiac function post-spinal cord injury with dobutamine.

Kathryn M DeVeau1, Emily K Martin2, Nicholas T King2

  • 1Anatomical Sciences & Neurobiology, University of Louisville, Louisville, KY, United States; Department of Neurological Surgery, University of Louisville, Louisville, KY, United States.

Autonomic Neuroscience : Basic & Clinical
|January 10, 2017
PubMed
Summary

Spinal cord injuries (SCI) disrupt heart function, reducing cardiac output and stroke volume. Dobutamine stress testing revealed that SCI impairs the heart's ability to increase stroke volume, even with enhanced sympathetic activity.

Keywords:
CardiacEchocardiographySpinal cord injury

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Area of Science:

  • Cardiovascular Physiology
  • Neurotrauma Research
  • Cardiac Function Assessment

Background:

  • Spinal cord injuries (SCI) above T6 alter cardiac sympathetic control, negatively impacting heart structure and function.
  • Investigating cardiac responses under enhanced sympathetic activity is crucial for understanding SCI-related cardiac dysfunction.

Purpose of the Study:

  • To investigate cardiac responses to dobutamine (DOB) stress echocardiography in a contusive SCI model.
  • To assess the impact of SCI on systolic function and cardiac responses to DOB over time.

Main Methods:

  • Utilized dobutamine (DOB) stress echocardiography in T2 contusive SCI and control groups.
  • Echocardiography performed pre-SCI and at 1, 2, and 6 weeks post-SCI with increasing DOB doses.
  • Parasternal-short axis imaging analyzed systolic function and changes in response to SCI and DOB.

Main Results:

  • SCI reduced stroke volume (SV), end diastolic volume (EDV), cardiac output (CO), and ejection fraction (EF) compared to controls, persisting to 6 weeks.
  • SCI led to increased collagen deposition at 6 weeks.
  • Pre-SCI, DOB increased CO, EF, and heart rate (HR) but decreased EDV and did not change SV. Post-SCI, DOB increased CO, EF, HR, and notably, SV.

Conclusions:

  • Impaired descending cardiac control directly contributes to reduced resting SV after SCI.
  • The ability of DOB to increase SV post-SCI suggests that disrupted sympathetic pathways limit cardiac output.
  • This study provides novel insights into DOB responses in a contusive SCI model with persistent cardiac impairments.