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Shunt Surgery, Right Heart Catheterization, and Vascular Morphometry in a Rat Model for Flow-induced Pulmonary Arterial Hypertension
Published on: February 11, 2017
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.
Abstract:
Cardiac hypertrophy is an early landmark during the clinical course of heart failure, and is an important risk factor for subsequent morbidity and mortality. The hypertrophy response to different types of cardiac overload is distinguished both at the molecular and cellular levels. These changes have been extensively characterized for pressure load hypertrophy; however, similar information for volume load hypertrophy is still needed. This study was undertaken to improve the existing method of producing experimental cardiac volume load. Previous investigators have employed surgical aorto-caval shunt (ACS) as a model for volume load hypertrophy (VO) in rats. The procedure is relatively simple and involves glue to seal the aortic hole after ACS. However, it has several limitations mostly related to the use of glue e.g. poor visualization due to hardening of tissues, imperfect sealing of the puncture site and glue seeping through the aortic hole resulting in shunt occlusion. We have modified the procedure using aortic adventitial suture instead of glue and 18G angiocatheter instead of 16G needle, which eliminated the technical difficulties from the former method. The ACS was visually confirmed at sacrifice, and the VO demonstrated by time-related changes in the heart weight/body weight ratio which increased from 78% at 4 weeks to 87% at 10 weeks and increased liver/body weight ratio by 22% at 10 weeks of post aorto-caval shunt. Cardiac expression of atrial natriuretic peptide (ANF) also demonstrated time-related increase in ANF mRNA (+275% increase at 4 weeks, p < 0.05, and +370% increase at 10 weeks, p < 0.001). This modified technique of aorto-caval shunt offers simpler, reproducible and consistent model for VO hypertrophy in rats.

