Effects of cholecalciferol on cardiac electrical function autonomic regulation lipid peroxidation and myocardial injury in isoproterenol induced myocardial ischemia
Abstract
Myocardial ischemia is characterized by electrical instability, oxidative stress, and inflammation. This study investigated whether short-term cholecalciferol treatment attenuates cardiac electrical and autonomic dysfunctions and biochemical disturbances in a rat model of isoproterenol (ISO)-induced myocardial ischemia. Male Sprague–Dawley rats were allocated to Sham, cholecalciferol (CAL), ISO, and CAL + ISO groups. Cardiac electrical activity, autonomic function, and hemodynamics were assessed using electrocardiography, heart rate variability (HRV) analysis, and arterial pressure recordings under basal conditions, during phenylephrine-induced baroreflex activation and sustained elevation of arterial pressure, and following inhibition of endothelial nitric oxide synthase with L-NAME. Plasma malondialdehyde (MDA), NO metabolites, lactate dehydrogenase, total and differential leukocyte counts, and cardiac histopathology were also evaluated. ISO-induced myocardial ischemia increased heart rate, prolonged QT and QTc intervals, elevated the ST segment, and reduced HRV indices. These changes were accompanied by increased plasma MDA and NO metabolite levels, neutrophil percentage, and myocardial injury, along with decreased lymphocyte percentage and myocardial edema. Cholecalciferol treatment attenuated tachycardia and ST-segment elevation, reduced QTc prolongation during baroreflex activation, partially restored HRV responses during baroreflex activation, and altered autonomic balance. In addition, cholecalciferol reduced plasma MDA and NO metabolite levels and attenuated hematological alterations and myocardial structural damage. Short-term cholecalciferol administration improves cardiac electrical function and autonomic regulation and attenuates alterations in circulating leukocytes, plasma MDA and NO metabolite levels, and markers of myocardial injury. Our findings suggest that cholecalciferol may exert protective effects on cardiac electrical and autonomic function and mitigate biochemical and hematological alterations associated with isoproterenol-induced myocardial injury.
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BibTeX
@article{farokhipour2026effects,
title = {{Effects of cholecalciferol on cardiac electrical function autonomic regulation lipid peroxidation and myocardial injury in isoproterenol induced myocardial ischemia}},
author = {Maryam Farokhipour and Amirreza Dehghanian and Farzaneh Ketabchi},
journal = {Scientific Reports},
year = {2026},
month = oct,
doi = {10.1038/s41598-026-75746-z},
url = {https://www.nature.com/articles/s41598-026-75746-z},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Effects of cholecalciferol on cardiac electrical function autonomic regulation lipid peroxidation and myocardial injury in isoproterenol induced myocardial ischemia
AU - Maryam Farokhipour
AU - Amirreza Dehghanian
AU - Farzaneh Ketabchi
PY - 2026
DA - 2026/10/20
JO - Scientific Reports
DO - 10.1038/s41598-026-75746-z
UR - https://www.nature.com/articles/s41598-026-75746-z
AB - Myocardial ischemia is characterized by electrical instability, oxidative stress, and inflammation. This study investigated whether short-term cholecalciferol treatment attenuates cardiac electrical and autonomic dysfunctions and biochemical disturbances in a rat model of isoproterenol (ISO)-induced myocardial ischemia. Male Sprague–Dawley rats were allocated to Sham, cholecalciferol (CAL), ISO, and CAL + ISO groups. Cardiac electrical activity, autonomic function, and hemodynamics were assessed using electrocardiography, heart rate variability (HRV) analysis, and arterial pressure recordings under basal conditions, during phenylephrine-induced baroreflex activation and sustained elevation of arterial pressure, and following inhibition of endothelial nitric oxide synthase with L-NAME. Plasma malondialdehyde (MDA), NO metabolites, lactate dehydrogenase, total and differential leukocyte counts, and cardiac histopathology were also evaluated. ISO-induced myocardial ischemia increased heart rate, prolonged QT and QTc intervals, elevated the ST segment, and reduced HRV indices. These changes were accompanied by increased plasma MDA and NO metabolite levels, neutrophil percentage, and myocardial injury, along with decreased lymphocyte percentage and myocardial edema. Cholecalciferol treatment attenuated tachycardia and ST-segment elevation, reduced QTc prolongation during baroreflex activation, partially restored HRV responses during baroreflex activation, and altered autonomic balance. In addition, cholecalciferol reduced plasma MDA and NO metabolite levels and attenuated hematological alterations and myocardial structural damage. Short-term cholecalciferol administration improves cardiac electrical function and autonomic regulation and attenuates alterations in circulating leukocytes, plasma MDA and NO metabolite levels, and markers of myocardial injury. Our findings suggest that cholecalciferol may exert protective effects on cardiac electrical and autonomic function and mitigate biochemical and hematological alterations associated with isoproterenol-induced myocardial injury.
SN - 2045-2322
ER -