Controlled Hyperventilation and Its Effect on Brain Energy and Acid‐Base Parameters

Nilsson, L.; Busto, Raul

doi:10.1111/j.1399-6576.1973.tb00837.x

Cited by 14 publications

(7 citation statements)

References 31 publications

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“…These changes resemble those previously measured in normoglycemic animals (see Kjallquist et a\., 1969). However, hypocapnia induced greater changes in CSF pH (and smaller changes in [HC03D than in normoglycemic animals from previous reports (Kjallquist et aI., 1969;MacMillan and Siesj6, 1973;Nilsson and Busto, 1973). We would therefore con clude that hypoglycemia does not effect CSF pH regulation during hypercapnia but reduces CSF pH regulation during hypocapnia.…”

Section: Physiological Variables Plasma and Cs F Acid-base Changessupporting

confidence: 87%

“…It has been proposed that acid production and acid consumption provide an im portant mechanism of intracellular pH regulation in hypocapnia and hypercapnia, respectively (Siesjo, 1973). There is ample evidence that this mechanism is the primary reason for the almost complete regu lation of intracellular pH in acute hypocapnia (MacMillan and Siesjo, 1973;Nilsson and Busto, 1973;Arieff et aI., 1976;PeIIigrino et aI., 1981), and can account for about half of intraceIIular pH regu lation in acute hypercapnia (Siesjo et aI., 1972).…”

mentioning

confidence: 99%

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Regulation of Extra- and Intracellular pH in the Brain in Severe Hypoglycemia

Pelligrino

Siesjö

1981

J Cereb Blood Flow Metab

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Severe hypoglycemia is associated with a marked curtailment of cerebral glucose supply and with consumption of endogenous carbohydrate metabolites and amino acids, many of which exist as anions of acids. Since metabolic control of intracellular pH in acute hypo- and hypercapnia seems to be dependent on the production and consumption of metabolic acids, it must be suspected that intracellular pH in the brain is poorly regulated in hypoglycemic animals. We induced hypocapnia (Paco2 about 15 mm Hg) and hypercapnia (Paco2 about 90 mm Hg) in insulin-injected animals in “precoma” (EEG pattern of slow waves, polyspikes) and “coma” (cessation of EEG activity) and measured CSF and intracellular acid-base changes using the CO2 method. The induced hypoglycemia did not measurably alter CSF acid-base changes from the normal during hypercapnia, but it did impair CSF pH regulation in hypocapnia. Animals in precoma showed an unchanged cerebral energy state during both hypo- and hypercapnia. Regulation of intracellular pH was not measurably affected in hypercapnia but was reduced in hypocapnia. These results could be accounted for by a reduced ability of the hypoglycemic animals to produce metabolic acids in response to the decrease in Pco2, while the capacity to “consume” acids was largely retained. In comatose animals, cerebral energy state was held at normocapnic levels during hypercapnia but deteriorated during hypocapnia. In the latter condition, the reduction in adenylate energy charge correlated to a decrease in blood pressure. The capacity to alter metabolic acid levels was abolished. In spite of this, hypocapnia was associated with a marked rise in intracellular pH, in some animals to values of about 7.7 (control, 7.0), and hypercapnia caused only very moderate reduction in intracellular pH. It is proposed that the excessive increase in intracellular pH during hypocapnia was due to hypotension-induced energy failure with subsequent depolarization of cells and passive equilibration of HCO3− (or H+) across the cell membranes. In hypercapnia, the influx of HCO3− into cells was unrelated to further deterioration of cerebral energy state but could possibly have been caused by CO2-induced depolarization and/or increased cell membrane permeability to HCO3−/H+ ions. It is concluded that severe hypoglycemia disrupts intracellular pH regulation in the brain and that hypocapnia combined with moderate hypotension leads to an excessive intracellular alkalosis of potential importance for the development of cell damage.

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Section: Physiological Variables Plasma and Cs F Acid-base Changessupporting

confidence: 87%

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confidence: 99%

Regulation of Extra- and Intracellular pH in the Brain in Severe Hypoglycemia

Pelligrino

Siesjö

1981

J Cereb Blood Flow Metab

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“…This possibility was previously described with respect to the involvement of K ATP channels in the pH-mediated relaxation/contraction of cerebral vessels (Rosenblum, 2003). In addition, experimental parameters or inherent differences between preparation types may also result in ambiguity with regards to pCO 2 - and pH-dependent mechanisms, as follows: Non-physiologic pH: Hypercapnia and hypocapnia can lower and elevate CSF pH by ~0.3 pH units, i.e., to ~7.1 and ~7.6, respectively (Plum and Posner, 1967; Adaro et al, 1969; Nilsson and Busto, 1973). Thus, non-physiologic mechanisms may be elicited by solutions with pH values outside of this range.…”

Section: Physiologic and Non-physiologic Parametersmentioning

confidence: 99%

“…Non-physiologic pH: Hypercapnia and hypocapnia can lower and elevate CSF pH by ~0.3 pH units, i.e., to ~7.1 and ~7.6, respectively (Plum and Posner, 1967; Adaro et al, 1969; Nilsson and Busto, 1973). Thus, non-physiologic mechanisms may be elicited by solutions with pH values outside of this range.…”

Section: Physiologic and Non-physiologic Parametersmentioning

confidence: 99%

pCO2 and pH regulation of cerebral blood flow

Yoon¹,

Zuccarello²,

Rapoport³

2012

Front. Physio.

116

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CO2 serves as one of the fundamental regulators of cerebral blood flow (CBF). It is widely considered that this regulation occurs through pCO2-driven changes in pH of the cerebral spinal fluid (CSF), with elevated and lowered pH causing direct relaxation and contraction of the smooth muscle, respectively. However, some findings also suggest that pCO2 acts independently of and/or in conjunction with altered pH. This action may be due to a direct effect of CSF pCO2 on the smooth muscle as well as on the endothelium, nerves, and astrocytes. Findings may also point to an action of arterial pCO2 on the endothelium to regulate smooth muscle contractility. Thus, the effects of pH and pCO2 may be influenced by the absence/presence of different cell types in the various experimental preparations. Results may also be influenced by experimental parameters including myogenic tone as well as solutions containing significantly altered HCO3− concentrations, i.e., solutions routinely employed to differentiate the effects of pH from pCO2. In sum, it appears that pCO2, independently and in conjunction with pH, may regulate CBF.

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“…bicarbonate concentration during altered ventilation reveals certain consistent differences. Plasma bicarbonate concentration decreased during the first 15 min (Nilsson & Busto, 1973;Ponten, 1966) but then remained constant during the remainder of 4-6 hr of hyperventilation (Arieff, Kerian, Massry & DeLima, 1976;Kazemi, Shannon & Carvallo-Gil, 1967;Wichser & Kazemi, 1975). Ponten (1966) (Kazemi et al 1967).…”

Section: Discussionmentioning

confidence: 99%

Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus.

Husted¹,

Reed²

1977

The Journal of Physiology

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1. The regulation of cerebrospinal fluid (c.s.f.) bicarbonate concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. Decreases in plasma bicarbonate concentration caused relatively small changes in the c.s.f. bicarbonate concentration. 3. Alterations in c.s.f. bicarbonate concentration (c.s.f. HCO3‐=9 or 28 m‐equiv/l.) were countered by changes in the bicarbonate concentration of the fluid produced by the plexus or in the rate of bicarbonate transport which returned c.s.f. bicarbonate towards normal. 4. There was significant regulation of pH in the choroid plexus fluid during hypocapnia and hypercapnia. 5. Alterations of plasma acid‐base status did not significantly alter the potential difference across the choroid plexus. However, the potential difference increased when c.s.f. bicarbonate was increased and decreased when c.s.f. bicarbonate was decreased. 6. The data indicate that the bicarbonate concentration in the c.s.f. is actively regulated by the choroid plexus during acid‐base disturbances occurring either systemically or in the c.s.f.

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Controlled Hyperventilation and Its Effect on Brain Energy and Acid‐Base Parameters

Cited by 14 publications

References 31 publications

Regulation of Extra- and Intracellular pH in the Brain in Severe Hypoglycemia

Regulation of Extra- and Intracellular pH in the Brain in Severe Hypoglycemia

pCO2 and pH regulation of cerebral blood flow

Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus.

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