Metabolic acidosis could occur due to either endogenousm acids accumulation or bicarbonate loss from the gastrointestinal tract or commonly from the kidney. This study aimed to investigatethe possible underlying mechanism(s) of chronic acidosis-inducedcardiac contractile and electrical
changes in rats. Twenty four adult Wistar rats, of both sexes, were randomly divided into control group and chronic metabolic acidosis group, which received orally 0.28 M NH4Cl in the drinking water for 2 weeks. At
the end of experimental period, systolic and diastolic blood pressure values
were measured. On the day of sacrifice, rats were an esthetized by i.p. pentobarbitone (40mg/kg b.w.), transthoracic echocardiography and ECG
were performed. Blood samples were obtained from abdominal aorta for complete blood count and determination of pH, bicarbonate, chloride,
sodium, potassium, troponin I, CK-MB, IL-6, renin and aldosterone levels.
Hearts from both groups were studied for cardiac tissue IL-6 and
aldosterone in addition to histopathological examination.
Compared to control group, chronic metabolic acidosis groupshowed anemia, significant systolic and diastolic hypotension accompanied by significant reduction of ejection fraction and fraction of shortening, significant bradycardia, prolonged QTc interval and higher widened T wave
as well as significantly elevated plasma levels of renin, aldosterone, troponin
I, CK-MB and IL-6, and cardiac tissue aldosterone and IL-6. The left
ventricular wall of the acidosis group showed degenerated myocytes
with fibrosis and apoptosis. Thus, chronic metabolic acidosis induced negative inotropic and chronotropic effects and cardiomyopathy, possibly by elevated aldosterone and IL-6 levels released from the cardiac tissue.