Metabolic Acidosis

Metabolic Acidosis

682 METABOLISM, ENDOCRINOLOGY AND IMMUNOLOGY vasive method of imaging the scrotal contents. It is reliable and helpful in differentiating scrotal he...

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vasive method of imaging the scrotal contents. It is reliable and helpful in differentiating scrotal hernia from a primary scrotal pathological condition. F. T. A. 7 figures, 13 references


M. FINKEL, Section of Nephrology, Lahey Clinic, Boston, Massachusetts

Lahey Clin. Found. Bull., 31: 1-7 (Jan.-Mar.) 1982 The pathophysiology and principles of treatment of metabolic acidosis are reviewed. The Henderson-Hassel back equation is the basis for evaluating the relationship among body pH, bicarbonate ion and carbon dioxide pressure. Changes in bicarbonate ion reflect metabolic acidosis on alkalosis. Metabolic acidosis can result from loss of bicarbonate ion (gastrointestinal tract fistula and renal tubular acidosis), excess generation of nonvolatile or fixed acids (lactic acidosis and ketoacidosis) or inability of the kidney to eliminate normally produced body hydrogen ion (renal failure). The normal body response to acidosis is increased renal excretion of hydrogen ion or increased pulmonary release of carbon dioxide. A bicarbonate ion level ~12 mEq. strongly suggests metabolic acidosis, since respiratory alkalosis rarely will lower it to that degree. Blood gas determinations (pH and carbon dioxide pressure) can help to establish definitively the status. Determination of the blood anion gap (difference between serum sodium and chloride+ bicarbonate should be lOto 12 mEq.), if>12 mEq. can define overproduction of organic acids, ingestion of toxins or impaired excretion of acids. Chronic states of metabolic acidosis can be managed by oral sodium bicarbonate ion administration. In more acute situations more rapid bicarbonate ion administration should not be too vigorious since secondary alkalosis (metabolic and/ or respiratory) can result with neuromuscular irritability, tetany or central nervous system depression. Finally, excess sodium bicarbonate ion administration can result in fluid overload. Hemodialysis can be useful in selected instances to correct acidosis and to protect against fluid overload. J. H. N. 1 table, 30 references

lesterol and steroidogenesis in the presence or absence of adrenocorticotropic hormone in the rat adrenal cortex. The adrenal mitochondria in the rats treated with aminoglutethimide were elongated and organelles tended to surround the lipid droplets. It also produced blockage of cholesterol side chain cleavage enzyme system and caused accumulation of cholesterol in the adrenal gland and decrease in serum testosterone concentration. When aminoglutethimide was administered with adrenocorticotropic hormone the effects were more apparent. However, there was no difference in serum testosterone concentration in the presence or absence of adrenocorticotropic hormone. The testosterone level in the castrated animals is significantly increased by adrenocorticotropic hormone, suggesting that the low level of testosterone in the castrated animals results in a reflex increase in luteinizing hormone, which interacts with adrenocorticotropic hormone to enhance the adrenal steroid secretion. N. V. R. 3 figures, 2 tables, 27 references

Novel Calcium Channels Used for Lanthanide Ion-Induced Adrenal Catecholamine Release M. SHANBAKY AND J. L. BoROWITZ, Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana

D. NG, N.

Res. Comm. Chem. Path. Pharm., 37: 259-265 (Aug.) 1982 Adrenal medullary catecholamine secretion is stimulated by lanthanum ion Laa+, Cea+, Pra+ or Nda+. This effect is calciumdependent and the catecholamine release is enhanced at low pH and only slightly inhibited by pre-treatment with a calcium channel blocker, such as verampamil. Since the calcium channels in the adrenal medulla used by the lanthamum ions are not blocked by low pH or verapmil it is suggested that the lanthanum ion opens a calcium channel distinct from ~hat opened by acetylcholene in the adrenal medulla to allow calcium influx and subsequent catecholamine release. N. V. R. 5 figures, 11 references

Cyclosporin A-Induced Increases in Renin Storage and Release

s. WILLIS, B. M. HALL, J. s. J. TILLER, Renal Unit, Royal Prince Alfred Hospital, Sydney, N.S. W Australia


G. G.



Effect of Aminoglutethimide on the Structure and Function of Rat Adrenals K. W. CHUNG, Department of Anatomical Sciences, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma Res. Comm. Chem. Path. Pharm., 37: 215-226 (Aug.) 1982 Aminoglutethimide has been used as an anticonvulsant, and for the treatment of carcinoma of the breast and prostate gland, and also for fertility. This drug inhibits adrenal steroidogenesis by interfering with enzymatic conversion of cholesterol to pregnenolone, a step required for the biosynthesis of all steroid hormones. It blocks the activity of 38 hydroxysteroid dehydrogenase and isomerase enzyme complex, inhibits the metabolism of androgens to estrogens and alters the pattern of peripheral metabolism of testosterone. The author attempted to study the effect of aminoglutethimide on mitochondrial morphology, the accumulation of cho-

Res. Comm. Chem. Path. Pharm., 37: 305-312 (Aug.) 1982 N ephrotoxicity is a frequent and clinically important side effect in patients receiving the new immunosuppressive drug, cyclosporin A. The mechanism of cyclosporin A nephrotoxicity is unknown. Since the renin-angiotensin system is considered to have a role in the intrarenal control of glomerular filtration rate the authors studied the effect of cyclosporin A on the renal and plasma renin in rats. Slice renin release, tissue renin level and plasma renin levels were elevated significantly in rats treated with 20 to 50 mg./kg. cyclosporin A daily for 3 to 7 days. Slices pre-mixed with cyclosporin A in vitro did not show increased renin release. These results indicated that there is an increase in the synthesis of renin in the kidney. It is possible that these increases in renin are related to the nephrotoxicity of cyclosporin A. Further studies are required to determine the activity of renin in humans taking cyclosporin A. N. V. R. 2 figures, 12 references