The threshold response of neonatal rat cardiomyocytes to gradual enhancement of cryptosporidial invasion

One common cause of excessive cardiac loading in children is infectious gastroenteritis that produces malabsorption and tachyarrythmia. Our recent studies have shown that neonatal cryptosporidial gastroenteritis causes the long-term pathology of cardiomyocytes. In the present work, we studied how cryptosporidiosis of different degrees of severity is reflected on the heart anatomy and polyploidization and remodeling of cardiomyocytes of neonatal rats, as well as on the expression of their gene encoding factor sensitive to hypoxia (HIF-1α). By methods of Real-Time PCR, cytometry, immunocytochemistry, image analysis, and visual study of interatrial septum, we have established that gradual enhancement of infestation by cryptosporidiosis is accompanied by threshold changes in heart. With weak infection, the interatrial septum preserves integrity, while changes in cardiomyocytes are absent. With moderate and strong infection, the changes are expressed approximately equally: in the interatrial septum, foramen ovale appears and the heart becomes atrophied and elongated, while cardiomyocytes lose protein and become thinned and hyperpolyploid. In addition, an excessive level of mRNA of gene HIF-1α appears in the myocardium. It is important to note that the threshold response to the gradual increase of the action is a criterion of triggering of the developmental programming of cardiovascular diseases, as such response is based on irreversible disturbance of the anatomy of the organ and failure of cell differentiation. In our case, the disturbance of the heart is the patent foramen ovale in the interatrial septum, while the disturbance of differentiation is hyperpolyploidization of cardiomyocytes. Our data may be of interest to physicians, as they show for the first time a connection between gastroenteritis, disturbance of the integrity of the interatrial septum, and pathological alterations in cardiomyocytes.