Possible mechanisms of cardiac contractile dysfunction and electrical changes in ammonium chloride induced chronic metabolic acidosis in Wistar rats

Title:

Possible mechanisms of cardiac contractile dysfunction and electrical changes in ammonium chloride induced chronic metabolic acidosis in Wistar rats

Creator:

Lasheen, N.N. and Mohamed, G.F.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:4c9fb7a3-1cda-4544-872a-dd2f182b7b8c
uuid:4c9fb7a3-1cda-4544-872a-dd2f182b7b8c

Subject:

Aldosterone, Cardiac, Chronic metabolic acidosis, ECG, and IL-6

Type:

article, model:article, and TEXT

Description:

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.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:6

Harvested from:

CDK

Metadata only:

false