Lactic acidosis.

A H Harken

Home/Archive/PubMed

PubMed · 816021

Lactic acidosis.

A H Harken

View original source ↗Export metadata ↓

Abstract

Many assumptions and compromises must be made in order to establish blood lactate as a reliable parameter of tissue oxygenation. One must think not only of reactions and cells as having oxidation-reduction potentials, but the concept of the redox potential of tissues, organs and even whole patients becomes applicable. Blood lactate concentrations probably are not an accurate measure of intracellular lactate. Thermodynamic equilibrium of the intracellular lactic acid dehydrogenase system cannot be assumed and, in fact, is probably not compatible with life. Clinically, however, the lactate-pyruvate system appears to establish a dynamic equilibrium that is responsive both to oxygen supply and substrate pyruvate availability. The diagnostic and prognostic values of blood lactate with both a stable and increased lactate to pyruvate ratio have been established empirically by numerous investigators. If evaluated within the constraints of available knowledge, blood lactate concentration is a valuable indicator of tissue perfusion and an effective surgical tool.

Explore related subjects

Acid-Base Equilibrium Acidosis Catecholamines Diabetic Ketoacidosis Energy Metabolism Ethanol Humans Lactates Neoplasms Oxidation-Reduction Oxidative Phosphorylation Oxygen Consumption Phenformin Pyruvates Shock Thiamine Deficiency Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

A H Harken. 1976. Lactic acidosis.. https://pubmed.ncbi.nlm.nih.gov/816021/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

ATP-driven Ca2+/H+ antiport in acid vesicles from Dictyostelium.

Amoebae of the cellular slime mold Dictyostelium discoideum possess an extensive and dynamic endomembrane system that includes many types of acidic vacuoles. A light membrane fraction from Dictyostelium, rich in vacuolar-type H(+)-ATPase, has been described [Padh, H., Lavasa, M. & Steck, T.L. (1989) J. Cell Biol. 108, 865-874]. Here, we show that this "acidosomal" fraction also contains a high-affinity vanadate-sensitive Ca2+ uptake activity that is stimulated by the pH gradient formed by the H(+)-ATPase. We attribute this Ca2+ uptake to the presence of a H(+)-countertransporting Ca(2+)-ATPase, pumping Ca2+ into an acidic compartment.

Acid-Base Equilibrium↗

PubMed1992

Episodic weakness associated with exertional lactic acidosis and myopathy in Old English sheepdog littermates.

Two Old English Sheepdog littermates were evaluated for weakness that developed during periods of minimally intense exercise. Lactic acidosis accompanied by increased muscle enzyme activity, an increased lactate/pyruvate ratio, and increased venous PO2 supported the possibility of defective mitochondrial oxygen use. Electromyographic abnormalities included increased insertional activity and complex repetitive discharges. Muscle alterations included scattered myofiber necrosis, abundant endomysial connective tissue, excessive glycogen accumulation, and greater than normal numbers and vacuolation of mitochondria. A distinctive pattern of subsarcolemmal mitochondrial aggregates, referred to as "ragged red fibers" in human mitochondrial myopathies, was observed in muscle biopsy samples from 1 dog. Several features of the disease in these dogs, including onset of weakness during early life, simultaneous disease in littermates, subtle nonprogressive weakness of at least 3 years' duration, and partial reversibility of lactic acidosis following rest were suggestive of an inborn error of metabolism, consistent with mitochondrial myopathy.

Acid-Base Equilibrium↗

PubMed1992

Mechanisms of ion and acid-base regulation at the gills of freshwater fish.

This review examines the branchial mechanisms utilized by freshwater fish to regulate internal acid-base status and presents a model to explain the underlying basis of the compensatory processes. Rainbow trout, Oncorhynchus mykiss, and brown bullhead, Ictalurus nebulosus, were examined under a variety of experimental treatments which induced respiratory and metabolic acid-base disturbances. Acid-base regulation was achieved by appropriate adjustments of Na+ and Cl- net fluxes across the gills which, in turn, were accomplished by variable contributions of three different branchial mechanisms: 1) differential changes in Na+ and Cl- diffusive effluxes, 2) changes in internal substrate (H+, HCO3-) availability, and 3) morphological adjustments to the gill epithelium. Differential diffusive efflux of Na+ over Cl- was involved only during periods of metabolic alkalosis. The importance of internal substrate availability was demonstrated using a two-substrate model. According to the model, ionic flux rates (J(in)Cl-, J(in)Na+) are determined not only by the concentration of the external ion (Na+, Cl-) but also by the concentration of the internal counterion (H+, HCO3-). This system provides for an "automatic negative feedback" to aid in the compensation of metabolic acid-base disturbances. Morphological alteration of the gill epithelia and the associated regulation of chloride cell (CC) fractional area is an essential third mechanism which is especially important during respiratory acid-base disturbances. Specifically, fish vary the availability of the CC associated Cl-/HCO3- exchange mechanism by physical covering/uncovering of CCs by adjacent pavement cells.

Acid-Base Equilibrium↗