Possible role of garlic oil in ameliorating renal injury after liver ischemia/reperfusion in rats.

Acute liver failure induces renal injury by triggering inflammation and oxidative stress. The heme oxygenase system has a preventive role against reperfusion injury, while garlic oil has antioxidants and anti-inflammatory effects. This study investigated the protective effects of garlic oil pretreatment on remote renal functions after liver ischemia/reperfusion (I/R), and clarifying gene expressions of heme oxygenase 1 (HO1), autophagy-related 7 (Atg7) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) in renal tissues. Thirty six adult female Wistar rats were randomly divided into control, garlic oil-supplemented, liver I/R, and garlic oil-pretreated liver I/R groups. Liver ischemia was performed in anesthetized rats for 45 min, followed by reperfusion for 24 hours in metabolic cages. Serum samples were used for determination of liver enzymes and creatinine levels and total antioxidant capacity (TAC). Urine samples were assayed for albumin, volume and creatinine concentration. Right liver lobe and right kidney specimens were used for determination of oxidative stress markers (colorimeterically). Also, gene expressions of HO1, Atg7 and PGC1α were investigated in right kidney specimens using real time PCR. Left kidney specimens were used for histopathological studies. Liver I/R group exhibited higher liver enzymes and creatinine levels in serum, prominent oxidative stress in both liver and renal tissues, albuminuria, lowered GFR deranged renal structure, and upregulated HO1, Atg7 and PGC1α gene expressions in renal tissues. Garlic oil-pretreated I/R group restricted such detrimental changes in renal functions and structure, though it caused further upregulation of the studied gene expression in renal tissue to alleviate the oxidative stress. It is concluded that garlic oil exerted reno-protective effected against remote organ damage induced by liver I/R injury, through enhancing HO1, Atg7 and PGC1α gene expressions.

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

Metabolic acidosis could occur due to either endogenous acids accumulation or bicarbonate loss from the gastrointestinal tract or commonly from the kidney. This study aimed to investigate the possible underlying mechanism(s) of chronic acidosis-induced cardiac 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 NH(4)Cl 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 anesthetized by i.p. pentobarbitone (40 mg/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 group showed 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.