Related Experiment Video
Updated: Jun 21, 2025
Standardized Rat Coronary Ring Preparation and Real-Time Recording of Dynamic Tension Changes Along Vessel Diameter
Published on: June 16, 2022
Graphene Oxide Significantly Modifies Cardiac Parameters and Coronary Endothelial Reactivity in Healthy and
Marcin Z Krasoń1,2, Anna Paradowska1, Sławomir Boncel3,4
1Silesian Park of Medical Technology Kardio-Med Silesia, Marii Skłodowskiej-Curie 10C, 41-800 Zabrze, Poland.
Insights
Graphene oxide (GO) interactions with rat hearts depend on its structure. Fewer layers and higher oxygen content in GO are safer for cardiac function, especially in hypertensive hearts.
Area of Science:
- Biomaterials Science
- Cardiovascular Research
- Nanotoxicology
Background:
- Graphene oxide (GO) interactions with ex vivo rat hearts and coronary vessels remain uncharacterized.
- Conflicting structure-property data hinder GO's biomedical applications.
- Understanding GO's impact on cardiac function is crucial for safe use.
Purpose of the Study:
- To investigate the cardiotoxicity of various graphene oxide (GO) structural variants on isolated rat hearts.
- To assess the influence of GO on cardiac function under normotensive and hypertensive conditions.
- To elucidate the role of GO structure in NO-dependent vasodilation.
Main Methods:
- Utilized four distinct GO variants differing in layer number, oxygen content, and functionalization.
- Employed ex vivo working heart and Langendorff perfusion models with normotensive and hypertensive rat hearts.
- Assessed cardiotoxicity via histopathology, Raman spectroscopy, cardiac function parameters, and bradykinin-induced coronary flow response.
Main Results:
- GO variants with fewer layers and higher oxygen content (e.g., GO2) showed differential effects, impacting coronary flow and aortic pressure.
- GO variants with more layers and lower oxygen content (e.g., GO3) significantly reduced cardiac function and vasodilation responses.
- Hypertensive hearts exhibited increased susceptibility to GO-induced cardiotoxicity, particularly with low-oxygen content variants.
- Higher GO concentrations (30 mg/L) blocked the coronary response to bradykinin in normotensive hearts.
Conclusions:
- Graphene oxide (GO) cardiotoxicity is critically dependent on its structural characteristics, specifically layer number and oxygen content.
- Fewer GO layers and higher oxygen content are associated with improved cardiac safety profiles.
- Hypertensive hearts are more vulnerable to adverse effects from specific GO structures.
- Strict structural control of GO and personalized medicine approaches are essential for safe biomedical applications.
Abstract:
Interactions of graphene oxide (GO) with an ex vivo rat heart and its coronary vessels have not been studied yet. Moreover, the conflicting data on the "structure-properties" relationships do not allow for biomedical applications of GO. Herein, we study the impact of GO on the ex vivo isolated rat heart, normotensive and hypertensive, under the working heart and the constant-pressure perfusion (Langendorff) regimes. Four structural GO variants of the following initial morphology were used: few-layer (below 10-layer) GO1, O < 49%; predominantly single-layer GO2, O = 41-50%; 15-20-layer GO3, O < 11%; and few-layer (below 10-layer) NH4 +-functionalized GO4, O < 44%, N = 3-6%. The aqueous GO dispersions, sonicated and stabilized with bovine serum albumin in Krebs-Henseleit-like solution-uniformized in terms of the particle size-were eventually size-monodisperse as revealed by dynamic light scattering. To study the cardiotoxicity mechanisms of GO, histopathology, Raman spectroscopy, analysis of cardiac parameters (coronary and aortic flows, heart rate, aortic pressure), and nitric oxide (NO-)-dependent coronary flow response to bradykinin (blood-vessel-vasodilator) were used. GO1 (10 mg/L) exerted no effects on cardiac function and preserved an increase in coronary flow in response to bradykinin. GO2 (10 mg/L) reduced coronary flow, aortic pressure in normotensive hearts, and coronary flow in hypertensive hearts, and intensified the response to bradykinin in normal hearts. GO3 (10 mg/L) reduced all parameters in hypertensive hearts and coronary response to bradykinin in normal hearts. At higher concentrations (normotensive hearts, 30 mg/L), the coronary response to bradykinin was blocked. GO4 (10 mg/L) reduced the coronary flow in normal hearts, while for hypertensive hearts, all parameters, except the coronary flow, were reduced and the coronary response to bradykinin was blocked. The results showed that a low number of GO layers and high O-content were safer for normal and hypertensive rat hearts. Hypertensive hearts deteriorated easier upon perfusion with low-O-content GOs. Our findings support the necessity of strict control over the GO structure during organ perfusion and indicate the urgent need for personalized medicine in biomedical applications of GO.
