Independent and dependent variables of acid-base control

Stewart, Peter A.

doi:10.1016/0034-5687(78)90079-8

Cited by 353 publications

(217 citation statements)

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“…Kraig et al (1983) have analyzed their pH data using the formalism of Stewart (1978Stewart ( , 1981. In the case of brain interstitial fluid devoid of weak acids or bases, pH is determined only by Peo2 and the strong ion difference, which is the sum of all strong cations minus all strong anions, this value being equal to 'buffer base' or base excess (Siesjo, 1972).…”

Section: Discussionmentioning

confidence: 99%

Extracellular pH Changes during Spreading Depression and Cerebral Ischemia: Mechanisms of Brain pH Regulation

Mutch

Hansen

1984

J Cereb Blood Flow Metab

298

186

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Summary:We have examined the extracellular pH (pH e) during spreading depression and complete cerebral isch emia in rat parietal cortex utilizing double-barrelled H + liquid ion exchanger microelectrodes. The baseline pHe of the parietal cortex was 7.33 at a mean arterial Peoz of 38 mm Hg. Following spreading depression and cerebral ischemia, highly reproducible triphasic changes in pHe occurred, which were intimately related to the negative deflection in tissue potential (Ye). The changes in pHe for spreading depression (n = 23) were a small initial acidic shift, beginning before the rapid change in Ye, followed by a rapid transient alkaline shift of 0.16 pH units, the onset of which coincided with the negative deflection in Ye• A prolonged acidic shift of 0.42 pH units then oc curred. The maximal decrease in pHe was to 6.97 and the mean duration of the triphasic pHe change was 7.8 min. The lactate concentration in brain cortex increased fromThe adaptive response by the brain microenvi ronment to altered extracellular pH (pHe) remains poorly understood, partially due to the difficulty in directly measuring the interstitial hydrogen ion con centration. Now, however, high-fidelity recordings of pH changes in mammalian brain interstitium can be obtained with double-barrelled H+ liquid ion ex changer (LIX) microelectrodes (Ammann et aI., 1981; Kraig et aI., 1983). The use of similar LIX microelectrodes has greatly facilitated study of Dr. Mutch's present address is Department of Anesthesia, St. Boniface General Hospital, 40 9 Ta che Avenue, Winnipeg, Man itoba, Canada R2H 2A6.Address correspondence and reprint requests to Dr. Hansen at Department of Medical Physiology A, University of Copen hagen, The Panum Institute, B1egdamsvej 3, DK-22 00, Copen hagen N, Denmark.Abbreviations used: DIDS, 4,4'-Diisothiocyanostilbene-2,2' disulfonic acid; DNDS, 4, 4' -dinitrostilbene-2,2' -disulfonic acid; EH+, potential derived from H+ activity; LlX, liquid ion ex changer; pHe, extracellular pH; Ve, tissue potential. 17 baseline 1.2 mM to 7.0 mM (n = 6) during the maximal acidic change in spreading depression. In addition, lactate levels correlated well with resolution of the pHe changes during spreading depression. The triphasic pHe changes following complete cerebral ischemia were an initial acidic shift of 0.43 pH units which developed over 2 min, then an alkaline shift of 0.10 pH units coincident with the negative deflection in Ye, and a final acidic shift of 0.26 pH units. The terminal pHe was 6.75. Superfusion of the cortex with inhibitors of carbonic anhydrase (acetazol amide), Na+/H+ counter transport (amiloride), and Cl-/ HC03' countertransport (4,4' -diisothiocyanostilbene-2,2' disulfonic acid) altered the triphasic pHe changes in a similar fashion for both spreading depression and cerebral ischemia, providing insights into the pHe regulatory mechanisms in mammalian brain.

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Section: Discussionmentioning

confidence: 99%

Extracellular pH Changes during Spreading Depression and Cerebral Ischemia: Mechanisms of Brain pH Regulation

Mutch

Hansen

1984

J Cereb Blood Flow Metab

298

186

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Section: Pharmacology Of Sodium Acetatementioning

confidence: 99%

“…In vitro, the Brønsted-Lowry concept would describe acetate as a proton acceptor; in vivo, the increase in serum pH by sodium acetate infusion is more completely understood by Stewart's approach to acid-base homeostasis [14,15]. In brief, a solution that increases the body's strong ion difference (the concentration of strong cations minus strong anions) will increase serum pH [15]. After injection and cellular uptake, the two-carbon acetate anion forms acetyl CoA and enters the citric acid cycle; the final by-products, carbon dioxide and water, are in a rapid equilibrium with bicarbonate through the catalyst activity of carbonic anhydrase [16,17].…”

Section: Pharmacology Of Sodium Acetatementioning

confidence: 99%

Sodium Acetate as a Replacement for Sodium Bicarbonate in Medical Toxicology: a Review

et al. 2013

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Sodium bicarbonate is central to the treatment of many poisonings. When it was placed on the FDA drug shortage list in 2012, alternative treatment strategies to specific poisonings were considered. Many hospital pharmacies, poison centers, and medical toxicologists proposed sodium acetate as an adequate alternative, despite a paucity of data to support its use in medical toxicology. The intention of this review is to educate the clinician on the use of sodium acetate and to advise them on the potential adverse events when given in excess. We conducted a literature search focused on the pharmacology of sodium acetate, its use as a buffer in pathologic acidemia and dialysis baths, and potential adverse events associated with excess sodium acetate infusion. It appears safe to replace sodium bicarbonate infusion with sodium acetate on an equimolar basis. The metabolism of acetate, however, is more complex than bicarbonate. Future prospective studies will be needed to confirm the efficacy of sodium acetate in the treatment of the poisoned patient.

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“…This was appreciated by Gamble in the 1930s, A,B and it was quantitatively formalized by Peter Stewart over 30 years ago. 16 The consequence of non-linear system interconnectivity to patient care in the clinical setting is that it will likely not be possible to ascertain causality between fluid and electrolyte management and increased mortality. It is probable that the linkage between hospital mortality and acquired disturbances in volume and electrolyte status will remain undefined for the foreseeable future of critical care medicine.…”

mentioning

confidence: 99%

“…Ce phénomène a été décrit par Gamble dans les années 1930, A,B et il a été formalisé de façon quantitative par Peter Stewart il y a plus de 30 ans. 16 clinique est qu'il sera vraisemblablement impossible d'établir un lien de causalité entre la prise en charge liquidienne et électrolytique et une augmentation de la mortalité. Les dérèglements au niveau du Na?…”

unclassified

Unappreciated aspects of fluid and electrolyte physiology and implications to patient recovery

Wilkes

Akbari

2010

Can J Anesth/J Can Anesth

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Independent and dependent variables of acid-base control

Cited by 353 publications

References 1 publication

Extracellular pH Changes during Spreading Depression and Cerebral Ischemia: Mechanisms of Brain pH Regulation

Extracellular pH Changes during Spreading Depression and Cerebral Ischemia: Mechanisms of Brain pH Regulation

Sodium Acetate as a Replacement for Sodium Bicarbonate in Medical Toxicology: a Review

Unappreciated aspects of fluid and electrolyte physiology and implications to patient recovery

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