Revisiting the surgical creation of volume load by aorto-caval shunt in rats

Catherina Ocampo1, Paul Ingram, Michel Ilbawi

  • 1The Heart Institute for Children, Advocate Hope Children's Hospital, Oak Lawn, IL 60453, USA.

Insights

Researchers improved a surgical method for creating volume load-induced cardiac hypertrophy in rats. This new technique offers a more reliable experimental model for studying heart conditions like heart failure.

Area of Science:

  • Cardiovascular Physiology
  • Experimental Surgery
  • Heart Failure Research

Background:

  • Cardiac hypertrophy is a key indicator in heart failure progression, increasing morbidity and mortality.
  • While pressure overload hypertrophy is well-studied, volume overload hypertrophy models require further refinement.
  • Existing surgical aorto-caval shunt (ACS) methods for volume overload (VO) in rats have technical limitations.

Purpose of the Study:

  • To enhance the experimental method for inducing cardiac volume overload hypertrophy (VO) in rats.
  • To address limitations of previous surgical aorto-caval shunt (ACS) procedures, specifically those involving glue.

Main Methods:

  • Modified the surgical aorto-caval shunt (ACS) procedure by replacing glue with aortic adventitial suture.
  • Utilized an 18G angiocatheter instead of a 16G needle for improved precision.
  • Validated the model through visual confirmation, heart/body weight ratios, liver/body weight ratios, and atrial natriuretic peptide (ANF) mRNA expression.

Main Results:

  • The modified ACS technique eliminated technical difficulties associated with glue.
  • Demonstrated significant time-related increases in heart weight/body weight ratio (78% at 4 weeks to 87% at 10 weeks) and liver/body weight ratio (+22% at 10 weeks).
  • Observed significant time-related increases in ANF mRNA expression (+275% at 4 weeks, +370% at 10 weeks).

Conclusions:

  • The modified ACS technique provides a simpler, reproducible, and consistent experimental model for inducing volume overload hypertrophy in rats.
  • This improved model facilitates further research into the molecular and cellular mechanisms of volume load hypertrophy and its role in heart failure.

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