Frontiers in cardiovascular medicine · 2026
A cost-effective proof-of-concept ex vivo perfusion model for myocardial ischemia-reperfusion injury in wistar rats: enhancing accessibility in resource-constrained settings.
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P Sainath, Satyam Shakta Mani, Rehman Abdul, Bharati Sanjay, Shetty Prakashchandra, El-Tanani Mohamed, Ahmed Akheruz Zaman, Kumari Rashmi, Albadawi Muaweya Sufian, Assaf Firas, Hashemi Seyed Mohammad Seyed Morteza, Khan Faisal Aslam, Doukarli Mohmed Krem Adnan, Robari Marwan Mohamed Hassan Rustom, Paryani Murk Jai Pal, Singh Varun Kumar, S Ganesh Kamath
Аннотация
INTRODUCTION: Myocardial ischemia-reperfusion injury (IRI) continues to impede the advancement of effective cardioprotective therapies. Experimental limitations, particularly the lack of accessible and cost-effective ex vivo platforms, restrict mechanistic and translational research. This study aimed to develop a simplified, resource-conscious proof-of-concept ex vivo rat heart perfusion model capable of inducing key features of myocardial IRI, rather than establishing a fully validated replacement for conventional Langendorff systems.
METHODS: Twelve adult male Wistar rats were randomly assigned to a non-ischemic control group (n = 6) or an IRI group (n = 6). Following a 10 min stabilization period, hearts in the IRI group underwent 30 min of global ischemia using potassium-based Krebs-Henseleit buffer (KHB) cardioplegic solution, followed by 60 min of reperfusion. Control hearts received continuous perfusion without ischemic insult. Coronary flow was assessed to evaluate functional changes. Myocardial injury was quantified using triphenyl tetrazolium chloride (TTC) staining, and structural alterations were examined through histopathological analysis.
RESULTS: The IRI group demonstrated an approximately 4.7-fold reduction in coronary flow during early reperfusion, reflecting acute vascular dysfunction. TTC staining revealed significant infarct development compared to controls. Histopathological examination confirmed cardiomyocyte degeneration, cytoplasmic vacuolization, inflammatory cell infiltration, and interstitial edema. Functional impairment strongly correlated with structural myocardial injury, demonstrating consistent induction of myocardial injury within the experimental setting.
DISCUSSION: This simplified ex vivo model reproduces fundamental features of myocardial IRI within a resource-conscious framework. However, it should be interpreted as a proof-of-concept platform rather than a replacement for conventional Langendorff systems.
METHODS: Twelve adult male Wistar rats were randomly assigned to a non-ischemic control group (n = 6) or an IRI group (n = 6). Following a 10 min stabilization period, hearts in the IRI group underwent 30 min of global ischemia using potassium-based Krebs-Henseleit buffer (KHB) cardioplegic solution, followed by 60 min of reperfusion. Control hearts received continuous perfusion without ischemic insult. Coronary flow was assessed to evaluate functional changes. Myocardial injury was quantified using triphenyl tetrazolium chloride (TTC) staining, and structural alterations were examined through histopathological analysis.
RESULTS: The IRI group demonstrated an approximately 4.7-fold reduction in coronary flow during early reperfusion, reflecting acute vascular dysfunction. TTC staining revealed significant infarct development compared to controls. Histopathological examination confirmed cardiomyocyte degeneration, cytoplasmic vacuolization, inflammatory cell infiltration, and interstitial edema. Functional impairment strongly correlated with structural myocardial injury, demonstrating consistent induction of myocardial injury within the experimental setting.
DISCUSSION: This simplified ex vivo model reproduces fundamental features of myocardial IRI within a resource-conscious framework. However, it should be interpreted as a proof-of-concept platform rather than a replacement for conventional Langendorff systems.