The effect of sodium bicarbonate on CBF and intracellular pH in man: Stable Xe-CT and<sup>31</sup>P-MRS

Nakashima, Kazuya; Yamashita, Tetsuo; Kashiwagi, Shiro; Nakayama, Naoto; Kitahara, Tetsuhiro; Ito, Hiroki

doi:10.1111/j.1600-0404.1996.tb00561.x

Cited by 34 publications

(34 citation statements)

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“…In previous studies, single measurements of CBF after NaHCO 3 infusion showed confl icting data. In healthy adults, NaHCO 3 administration resulted in an increased CBF [7] , whereas NaHCO 3 infusion did not lead to changes in CBF in animal studies [9,10] . Lou et al [34] reported a decrease in CBF after NaHCO 3 infusion in distressed preterm infants with severe metabolic acidosis.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Rapid versus Slow Infusion of Sodium Bicarbonate on Cerebral Hemodynamics and Oxygenation in Preterm Infants

Velden¹,

Hopman²,

Klaessens³

et al. 2006

Neonatology

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Background: Sodium bicarbonate (NaHCO₃) is often used for correction of metabolic acidosis in preterm infants. The effects of NaHCO₃ administration on cerebral hemodynamics and oxygenation are not well known. Furthermore, there is no consensus on infusion rate of NaHCO₃. Objectives: To evaluate the effects of rapid versus slow infusion of NaHCO₃on cerebral hemodynamics and oxygenation in preterm infants. Methods: Twenty-nine preterm infants with metabolic acidosis were randomized into two groups (values are mean ±SD): In group A (GA 30.5 ± 1.7 weeks, b.w. 1,254 ± 425 g) NaHCO₃ 4.2% was injected as a bolus. In group B (GA 30.3 ± 1.8 weeks, b.w. 1,179 ± 318 g) NaHCO₃ 4.2% was administered over a 30-min period. Concentration changes of oxyhemoglobin (cO₂Hb) and deoxyhemoglobin (cHHb) were assessed using near infrared spectrophotometry. Changes in HbD (= cO₂Hb – cHHb) represent changes in cerebral blood oxygenation and changes in ctHb (= cO₂Hb + cHHb) reflect changes in cerebral blood volume. Cerebral blood flow velocity was intermittently measured using Doppler ultrasound. Longitudinal data analysis was performed using linear mixed models (SAS procedure MIXED), to account for the fact that the repeated observations in each individual were correlated. Results: Administration of NaHCO₃ resulted in an increase of cerebral blood volume which was more evident if NaHCO₃was injected rapidly than when infused slowly. HbD and cerebral blood flow velocity did not show significant changes in either group. Conclusion: To minimize fluctuations in cerebral hemodynamics, slow infusion of sodium bicarbonate is preferable to rapid injection.

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Section: Discussionmentioning

confidence: 99%

“…NaHCO 3 administration provokes hypercapnia [7][8][9] , hyperosmolarity [7,10,11] and changes in hemodynamics [12][13][14] which can lead to changes in cerebral blood fl ow (CBF) when auto-regulation is impaired. Fluctuating CBF is a known risk factor for IVH in preterm infants [15] .…”

Section: Sodium Bicarbonate In Preterm Infantsmentioning

confidence: 99%

Effects of Rapid versus Slow Infusion of Sodium Bicarbonate on Cerebral Hemodynamics and Oxygenation in Preterm Infants

Velden¹,

Hopman²,

Klaessens³

et al. 2006

Neonatology

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“…In a rabbit model of hypoxic lactic acidosis, brain intracellular acidosis was partially corrected by bicarbonate administration56; however, in a study of five normal adult humans, intravenous sodium bicarbonate resulted in a reduction in brain intracellular pH, measured by magnetic resonance imaging spectroscopy 57. Despite all this, it is not known whether the therapeutic correction of intracellular acidosis is without adverse effects, and one experimental study shows that intracellular acidosis might protect against reperfusion injury 8…”

Section: Management Of Lactic Acidosismentioning

confidence: 99%

Dysoxia and lactate

Duke

1999

Archives of Disease in Childhood

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Disturbances of oxygen supply or cellular oxygen metabolism are common in critically ill patients. An understanding of dysoxia, or oxygen limited energy depletion, requires an understanding of the normal physiology of cell oxygen metabolism, and the compensatory mechanisms that supply high energy molecules under conditions of hypoxia. Understanding disorders associated with hyperlactataemia requires consideration of the cellular response in dysoxia, and pathology specific derangements in lactate metabolism. Much has recently been discovered about the causes of lactic acidosis in sepsis, and about the role of lactate in monitoring critically ill children.This review discusses how cells produce energy for metabolism under normal and hypoxic conditions; what happens to lactate produced during these processes; the clinical situations in which lactic acidosis has been described; the reasons why excess lactate may occur in sepsis; the evidence that a high lactate concentration is not simply a surrogate for tissue dysoxia; the relevance of lactate in the management of critically ill children; and suggested strategies to manage high blood lactate. Normal cellular oxygen metabolismCells require oxygen for the production of ATP, the principal energy source. ATP is hydrolysed to ADP and high energy phosphate by adenosine triphosphatases in the cytosol. Energy released is used for the maintenance of membrane integrity, ionic pumps, and other specialised functions, such as contractility of muscle cells, and impulse transmission in neurons. The body's stores of ATP will last no more than a few minutes, so it must be synthesised continuously as it is being used. Under physiological conditions, most ATP is generated from the metabolism of glucose, by the process of oxidative phosphorylation. The first stage of oxidative phosphorylation is the conversion of glucose to pyruvic acid; this occurs in the cytoplasm. The second stage, the oxidation of pyruvic acid, can only occur in the mitochondria as part of the Krebs (citric acid) cycle. Oxidative phosphorylation produces a net 36 molecules of ATP (or 1270 kJ of available energy) for every glucose molecule oxidised.Under normal conditions some tissues, such as myocytes, preferentially use free fatty acids, rather than glucose, as the substrate for ATP generation. In myocytes, palmitate forms about 60% of the total substrate metabolised, glucose 10%, and lactate 30%. During cellular hypoxia the consumption of lactate ceases, and that of glucose increases to 90% of the total substrate consumed.2 The brain, on the other hand, under any conditions can use only glucose or ketone bodies for ATP production. Thresholds of hypoxia and cell (dys)functionOxidative phosphorylation can only occur when the partial pressure of oxygen (PO 2 ) within the mitochondrion is above a critical level, thought to be in the order of 1 mm Hg (0.13 kPa).3 Although the PO 2 of dry air at sea level is 159 mm Hg, and the alveolar PO 2 is about 100 mm Hg, the mean capillary blood PO 2 is 50 mm Hg. From the capill...

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“…A study on neonatal dogs found that infusion of hypertonic sodium bicarbonate caused a significant reduction in brain water content [16]. Several human studies have demonstrated an increase in cerebral blood flow after sodium bicarbonate infusion [17,18].…”

Section: Discussionmentioning

confidence: 98%

Sodium Bicarbonate Lowers Intracranial Pressure After Traumatic Brain Injury

Bourdeaux

Brown

2010

Neurocrit Care

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The effect of sodium bicarbonate on CBF and intracellular pH in man: Stable Xe-CT and³¹P-MRS

Cited by 34 publications

References 10 publications

Effects of Rapid versus Slow Infusion of Sodium Bicarbonate on Cerebral Hemodynamics and Oxygenation in Preterm Infants

Effects of Rapid versus Slow Infusion of Sodium Bicarbonate on Cerebral Hemodynamics and Oxygenation in Preterm Infants

Dysoxia and lactate

Sodium Bicarbonate Lowers Intracranial Pressure After Traumatic Brain Injury

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The effect of sodium bicarbonate on CBF and intracellular pH in man: Stable Xe-CT and31P-MRS

Cited by 34 publications

References 10 publications

Effects of Rapid versus Slow Infusion of Sodium Bicarbonate on Cerebral Hemodynamics and Oxygenation in Preterm Infants

Effects of Rapid versus Slow Infusion of Sodium Bicarbonate on Cerebral Hemodynamics and Oxygenation in Preterm Infants

Dysoxia and lactate

Sodium Bicarbonate Lowers Intracranial Pressure After Traumatic Brain Injury

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The effect of sodium bicarbonate on CBF and intracellular pH in man: Stable Xe-CT and³¹P-MRS