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Prenatal exposure to cyclosporine impair cardiac function in neonates
Author(s) -
ElMas Mahmoud,
ElBassossy Hany,
Awan Zuheir
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.997.1
Subject(s) - medicine , cardiotoxicity , pregnancy , cardiac function curve , blood pressure , prenatal exposure , diastole , adverse effect , qt interval , cardiology , pr interval , gestation , heart rate , anesthesia , heart failure , chemotherapy , genetics , biology
Although cardiotoxicity has been recognized as an adverse effect of cyclosporine A (CSA), limited or no information exists regarding effect of prenatal exposure on the cardiac function in the newborn. We tested the hypothesis that prenatal exposure to CSA impair cardiac function in neonates. Prenatal exposure to CSA (15 mg/kg/day sc) from the day 6 of pregnancy till delivery resulted in a sex‐dependent impairment in ventricular systolic functions in neonates as reflected by a tenfold decrease in ESPVR slope in male neonates while two‐fold decreases in female neonates. In addition, prenatal exposure to CSA led to a significant rise in systolic and diastolic blood pressure in male neonates but not in female neonates. prenatal exposure to CSA caused significant increases in JT interval and tendency to increase in QTc interval in male neonates, but not in females, indicating LV ischemia and arrhythmogenesis. On the other hand, prenatal exposure to CSA resulted in a delay in AV conduction in female neonates, but not in male, rats as reflected by the significant prolongation in P duration and tendency to increase in PR interval In conclusion, In summary, the current study establishes the importance of the rat sex in defining the magnitude of cardiotoxicity due to CSA prenatal exposure Support or Funding Information This work was funded by the Deanship of Scientific Research (DSR), King Abdulaziz University, Jeddah, under grant No. (166 ‐ 110 ‐ D1437).