Effect of Bromoethylamine Hydrobromide on Systemic Acid-Base Balance

YOSHIHIRO NAKAMURA; SEI SASAKI; TATSUO SHIIGAI; FUMIAKI MARUMO

doi:10.1620/tjem.156.23

YOSHIHIRO NAKAMURA, SEI SASAKI, TATSUO SHIIGAI, FUMIAKI MARUMO

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Keywords: renal tubular acidosis, papillary necrosis, collecting duct, bromoethylamine hydrobromide

JOURNAL FREE ACCESS

1988 Volume 156 Issue 1 Pages 23-32

DOI https://doi.org/10.1620/tjem.156.23

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Published: 1988 Received: April 27, 1988 Available on J-STAGE: August 31, 2006 Accepted: August 11, 1988 Advance online publication: - Revised: -
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Date of correction: August 31, 2006 Reason for correction: - Correction: ABSTRACT Details: Wrong : NAKAMURA, Y., SASAKI, S., SHIIGAI, T. and MARUMO, F. Effect of Bromoethylamine Hydrobromide on Systemic Acid-Base Balance. Tohoku J. exp. Med., 1988, 156 (1), 23-32-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 (25mg) or vehicle was injected to male Sprague-Dawley rats. Blood specimens and 24hr 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 1M NH₄Cl solution (1ml/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.
Right : 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 (25mg) 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 (1ml/100g) 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.

Date of correction: August 31, 2006 Reason for correction: - Correction: CITATION Details: Wrong : 1) Arruda, J.A.L., Savatini, S., Mehta, P.K., Sohdi, B. & Baranowski, R. (1979) Functional characterization of druginduced experimental papillary necrosis. Kidney Int., 15, 264-275.
2) Arruda, J.A.L. & Kurtzman, N.A. (1980) Mechanisms and classification of deranged distal urinary acidification. Amer. J. Physiol., 239, F515-F523.
3) Atkins, J.L. & Burg, M.B. (1985) Bicarbonate transport by isolated perfused rat collecting ducts. Amer. J. Physiol., 249, F485-F489.
4) Buerkert, J., Martin, D., Trigg, D. & Simon, E. (1983) Effect of reduced renal mass on ammonia handling and net acid formation by the superficial and juxtamedullary nephron of the rat. J. clin. Invest., 71, 1661-1675.
5) Finkelstein, F.O. & Hayslett J.P. (1974) Role of medullary structures in the functional adaptation of renal insufficiency. Kidney Int., 6, 419-425.
6) Garcia-Austt, J., Good, D.W., Burg, M.B. & Knepper, M.A. (1985) Deoxycorticosteron-stimulated bicarbonate secretion in rabbit cortical collecting ducts: Effects of luminal chrolide removal and in vivo acid loading. Amer. J. Physiol., 249, F205 F212.
7) Gottschalk, C.W., Lassiter, W.E. & Mylle, M. (1960) Localization of urine acidification in the mammalian kidney. Amer. J. Physiol., 198, 581-585.
8) Graber, M.L., Bengele, H.H., Schwartz, J.H. & Alexander, E.A. (1981) PH and pCO₂ profiles of the rat inner medullary collecting duct. Amer. J. Physiol., 241, F659 F668.
9) Higashihara, E., Carter, N.W., Puccaco, L. & Kokko, J.P. (1984) Aldosteron effects on papillary collecting duct pH profile of the rat. Amer. J. Physiol., 246, F725-F731.
10) Ishibashi, K., Sasaki, S., Yoshiyama, N., Shiigai, T. & Takeuchi, J. (1987) Generation of pH gradient across the rabbit collecting duct segments perfused in vitro. Kidney Int., 31, 930-936.
11) Kurtzman, N.A. (1983) Acquired distal renal tubular acidosis. Kidney Int., 24, 807-819.
12) Laski, M.E. & Kurtzman, N.A. (1983) Characterization of acidification in the cortical and medullary collecting tubule of the rabbit. J. clin. Invest., 72, 2050-2059.
13) Lombard, W.E., Kokko, J.P. & Jacobson, H.R. (1983) Bicarbonate transport in cortical and outer medullary collecting tubules. Amer. J. Physiol., 244, F289-F296.
14) Mckinney, T.D. & Burg, M.B. (1978) Bicarbonate secretion by rabbit cortical collecting tubules in vitro. J. clin. Invest., 61, 1421-1427.
15) Murray, G., Wyllie, R.G., Hill, G.S., Ramsden, P.W. & Heptinstall, R.H. (1972) Experimental papillary necrosis of the kidney. Amer. J. Path., 67, 285-302.
16) Sabatini, S., Mepta, P.A., Kurtzman, N.A. & Arruda, J.A.L. (1981) Drug induced papillary necrosis: Electrolyte excretion and nephron heterogeniety. Amer. J. Physiol., 241, F14-F22.
17) Sabatini, S., Alla, V., Wilson, A., Cruz-Soto, M., deWhite, A., Kurtzman, N.A. & Arruda, J.A.L. (1982) The effect of chronic papillary necrosis on acid excretion. Pflügers Arch., 393, 262-268.
18) Stone, D.K., Seldin, D.W., Kokko, J.P. & Jacobson, H.R. (1983) Mineralcorticoid modulation of rabbit medullary collecting duct acidification. J. clin. Invest., 72, 77-83.
19) Ullrich, K.J. & Papavassiliou, F. (1981) Bicarbonate reabsorption in the pappilary collecting duct of rats. Pflügers Arch., 389, 271-275.

Right : 1) Arruda, J. A. L., Savatini, S., Mehta, P. K., Sohdi, B. & Baranowski, R. (1979) Functional characterization of druginduced experimental papillary necrosis. Kidney Int., 15, 264-275.
2) Arruda, J. A. L. & Kurtzman, N. A. (1980) Mechanisms and classification of deranged distal urinary acidification. Amer. J. Physiol., 239, F515-F523.
3) Atkins, J. L. & Burg, M. B. (1985) Bicarbonate transport by isolated perfused rat collecting ducts. Amer. J. Physiol., 249, F485-F489.
4) Buerkert, J., Martin, D., Trigg, D. & Simon, E. (1983) Effect of reduced renal mass on ammonia handling and net acid formation by the superficial and juxtamedullary nephron of the rat. J. clin. Invest., 71, 1661-1675.
5) Finkelstein, F. O. & Hayslett J. P. (1974) Role of medullary structures in the functional adaptation of renal insufficiency. Kidney Int., 6, 419-425.
6) Garcia-Austt, J., Good, D. W., Burg, M. B. & Knepper, M. A. (1985) Deoxycorticosteron-stimulated bicarbonate secretion in rabbit cortical collecting ducts: Effects of luminal chrolide removal and in vivo acid loading. Amer. J. Physiol., 249, F205-F212.
7) Gottschalk, C. W., Lassiter, W. E. & Mylle, M. (1960) Localization of urine acidification in the mammalian kidney. Amer. J. Physiol., 198, 581-585.
8) Graber, M. L., Bengele, H. H., Schwartz, J. H. & Alexander, E. A. (1981) PH and pCO₂ profiles of the rat inner medullary collecting duct. Amer. J. Physiol., 241, F659-F668.
9) Higashihara, E., Carter, N. W., Puccaco, L. & Kokko, J. P. (1984) Aldosteron effects on papillary collecting duct pH profile of the rat. Amer. J. Physiol., 246, F725-F731.
10) Ishibashi, K., Sasaki, S., Yoshiyama, N., Shiigai, T. & Takeuchi, J. (1987) Generation of pH gradient across the rabbit collecting duct segments perfused in vitro. Kidney Int., 31, 930-936.
11) Kurtzman, N. A. (1983) Acquired distal renal tubular acidosis. Kidney Int., 24, 807-819.
12) Laski, M. E. & Kurtzman, N. A. (1983) Characterization of acidification in the cortical and medullary collecting tubule of the rabbit. J. clin. Invest., 72, 2050-2059.
13) Lombard, W. E., Kokko, J. P. & Jacobson, H. R. (1983) Bicarbonate transport in cortical and outer medullary collecting tubules. Amer. J. Physiol., 244, F289-F296.
14) Mckinney, T. D. & Burg, M. B. (1978) Bicarbonate secretion by rabbit cortical collecting tubules in vitro. J. clin. Invest., 61, 1421-1427.
15) Murray, G., Wyllie, R. G., Hill, G. S., Ramsden, P. W. & Heptinstall, R. H. (1972) Experimental papillary necrosis of the kidney. Amer. J. Path., 67, 285-302.
16) Sabatini, S., Mepta, P. A., Kurtzman, N. A. & Arruda, J. A. L. (1981) Drug induced papillary necrosis: Electrolyte excretion and nephron heterogeniety. Amer. J. Physiol., 241, F14-F22.
17) Sabatini, S., Alla, V., Wilson, A., Cruz-Soto, M., deWhite, A., Kurtzman, N. A. & Arruda, J. A. L. (1982) The effect of chronic papillary necrosis on acid excretion. Pflügers Arch., 393, 262-268.
18) Stone, D. K., Seldin, D. W., Kokko, J. P. & Jacobson, H. R. (1983) Mineralcorticoid modulation of rabbit medullary collecting duct acidification. J. clin. Invest., 72, 77-83.
19) Ullrich, K. J. & Papavassiliou, F. (1981) Bicarbonate reabsorption in the pappilary collecting duct of rats. Pflügers Arch., 389, 271-275.

Date of correction: August 31, 2006 Reason for correction: - Correction: PDF FILE Details: -

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 (25mg) 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 (1ml/100g) 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.

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