Effect of bromoethylamine hydrobromide on systemic acid-base balance.

Abstract

Intravenous administration of bromoethylamine hydrobromide (BEA) has been shown to induce papillary necrosis of the kidney. We used this model to clarify the role of the medullary structure in acid-base homeostasis. BEA (25 mg) or vehicle was injected to male Sprague-Dawley rats. Blood specimens and 24 hr urine were collected once a week totaling 4 weeks. Blood bicarbonate significantly decreased in BEA treated rats with no change in plasma creatinine or creatinine clearance at 3 and 4 weeks, we noted that these parameters did not change in control rats. Administration of 1 M NH4Cl solution (1 ml/100 g) into the peritoneal space resulted in a significant reduction in urine pH by 0.41 +/- 0.05 in control rats, whereas it did not induce any change in BEA treated rats. Ammonia excretion rates were significantly lower in BEA treated rats than in control rats. Histological examination showed that in BEA treated rats there was necrosis of epithelial cells of papillary collecting ducts at 1 week. Observation showed they recovered at 4 weeks with only mild interstitial edema and slight dilatation of collecting ducts. The present results suggested that tissue damages in the papillary structure caused metabolic acidosis due to a decreased renal acidification.