Document Type


First Advisor

Dr. Dwight Ginn

Publication Date


Scholarship Domain(s)

Scholarship of Discovery



Current animal models of human cardiac disease may be similar in anatomy and physiology but are often expensive and tedious to work with. The current need is for a model organism that is more efficient to work with in the lab but that still provides an accurate model of human cardiac disease. Drosophila melanogaster (D. mel) is such a candidate. While 74% of the genes coding for protein are conserved between D. mel and human hearts, it is unknown if cardiac medication used in humans, such as atropine and propranolol hydrochloride, similarly affect heart rate. I hypothesized that administration of atropine and propranolol hydrochloride to third instar larvae would cause an increase and decrease respectively in the heart rates of D. mel.


After larvae hatched and reached the second instar larval phase, they were moved to fresh vials. The control group larvae were transferred to vials containing no medication, and the experimental group larvae were transferred to vials with 1mM atropine or 1mM propranolol hydrochloride. The larvae inhabited the new vials for twenty-four hours to reach the third instar larvae stage. Larvae were removed, placed individually on a microscope slide, and observed using the 4X objective lens of a Leica compound microscope. Heart rates of fifty larvae per group were recorded in triplicate over fifteen second intervals.


We observed elevated heart rates of 406 ± 3.18 beats per minute in atropine treated larvae when compared to rates of 388 ± 2.07 in control larvae, a 4.83% increase. Moreover, heart rates were slowed to an average of 274 ± 2.70 beats per minute in propranolol hydrochloride treated hearts, a 29.18% decrease. Both changes in heart rate when compared to the control were found to be statistically significant (p<0.001).


Administration of propranolol hydrochloride and atropine increased and decreased the heart rates of D. mel respectively. This data supports the hypothesis that D. mel can serve as an experimental model for human cardiovascular disease. Future work should build on this study and focus on the use of D. mel in preliminary pharmaceutical testing for new medication treating cardiovascular conditions.


Honors Cohort 8

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Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.