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At least 1,495 records · Page 83Linked to original sources
PubMed1993

The role of the octanoic fatty acid in the pathogenesis of the metabolic alkalosis in experimental liver failure.

Octanoate was found to stimulate the muscle proteins catabolism in rats with portacaval anastomosis thus increasing the amounts of 3-methylhistidine, creatinine, ammonium and urea in the excreted urine. The intensive decomposition of the endogenous proteins also produced great amounts of HCO3- whose levels increased in both the urine and blood. It is suggested that in hepatic insufficiency octanoate causes metabolic acidosis through: a) more intensive catabolism of the muscle proteins whose decomposition results in greater amounts of HCO3-, b) metabolization of octanoate to HCO3-, and c) inhibition of the ornithine cycle.

Alkalosis↗
PubMed1976

Cerebral blood flow determinations by radioactive microspheres in the subhuman primate: influence of unilateral internal carotid ligation, hypercapnic acidosis, and hypocapnic alkalosis.

Cerebral blood flow (CBF) was measured by electromagnetic and radioactive microsphere (RMS) techniques in the anubis baboon. Regional cerebral blood flows were calculated by distribution of intracardiac injections of RMS, labeled with one of three radionuclides: 51Cr, 85Sr, or 141Ce. In Group I (six animals, normocapnia), CBF's as estimated by electromagnetic measurement of internal carotid blood flow, were 65 +/- 10 and 74 +/- 4 (S.E.M.) ml. per minute per 100 Gm. for the right (RH) and left (LH) cerebral hemispheres, respectively; whereas CBF's as estimated by the RMS technique were 65 +/- 5 and 70 +/- 4 ml. per minute per 100 Gm., respectively, and these values were not significantly (p greater than 0.05) different. CBF, as determined by RMS techniques in Group 1, was not altered by unilateral internal carotid arterial ligation. In Group 2 (seven animals), arterial PCO2 was varied randomly from a low range (18 +/- 2 mm. Hg, L), to a middle range (PCO2 36 +/- 2, M), and a high range (PCO2 64 +/- 2, H), and CBF was measured by the RMS technique. During L, M, and H, CBF's were 44 +/- 10, 75 +/- 15, and 159 +/- 27 ml. per minute per 100 Gm., respectively, for RH, whereas CBF's were 44 +/- 10, 75 +/- 15, and 160 +/- 26 ml. per minute per 100 Gm., respectively, for LH. During H, RH and LH were significantly (p less than 0.05) greater than during L and M. Changes in regional CBF were uniform throughout the brain. These data demonstrate the correlation between CBF, as estimated by electromagnetic and RMS techniques, as well as confirm the adequacy of collateral cerebral circulation during unilateral carotid arterial ligation in the baboon. The usefulness of the RMS technique for hemispheric and regional CBF measurements is prevented also.

Acidosis, Respiratory↗
PubMed1995

[Hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria; Bartter's syndrome in Gitelman's variant--case report].

A case is presented of a 30-year old man with long-term history of painful muscle cramps, episodes of tetany, general malaise and persistent hypokaliemia. On the ground of clinical appearance and biochemical data the Bartter's syndrome in Gitelman's variant was diagnosed. In differential diagnosis we considered renal tubular acidosis, other tubular defects (Liddle's syndrome), primary and secondary hyperaldosteronism. Other possible causes of hypokaliemia were excluded such as surreptitious diuretic and lexative abuse, persistent vomiting and diarrhea. Good therapeutic effect were achieve using spironolacton, indomethacin, propranolol and potassium supplementation.

Adult↗