Effects of metabolic arterial pH changes on medullary ecf pH, csf pH and ventilation in peripherally chemodenervated cats with intact blood-brain barrier

Teppema, L.J.; Barts, P.W.J.A.; Evers, J.A.M.

doi:10.1016/0034-5687(84)90050-1

Cited by 11 publications

(8 citation statements)

References 22 publications

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“…These values were taken to represent changes in pH ISF . When [HCO 3 − ] plasma was altered at nearly constant pCO 2 , Ahmad and Loeschcke [442], Teppema and coworkers [443, 444] and Davies and Nolan [445] all found rapid changes (e.g. within 30 s) in pH ISF and in one case also [Cl − ] ISF [442].…”

Section: Ph and Concentration Of Hco3− In The Extracellular Fluids Ofmentioning

confidence: 99%

“…ISF [HCO 3 − ] increased and [Cl − ] decreased by about 3 mM (pH increase of 0.07) with a half-time of about 20 s. This was interpreted as rapid exchange of HCO 3 − and Cl − between plasma and ISF. Teppema et al [443, 444] also saw rapid changes in pH. Davies and Nolan [445] using pH sensitive microelectrodes with pH sensitive tips about 1–2 µm diameter and 40 µm in length found that ISF pH responded to isocapnic, iv infusions of HCl or NaHCO 3 with lags of only a few minutes (ΔpH ISF was 40–80% of ΔpH arterial at the end of 30 min with no change in pH CSF ).…”

mentioning

confidence: 99%

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Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

Hladky

Barrand

2016

Fluids Barriers CNS

230

253

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The two major interfaces separating brain and blood have different primary roles. The choroid plexuses secrete cerebrospinal fluid into the ventricles, accounting for most net fluid entry to the brain. Aquaporin, AQP1, allows water transfer across the apical surface of the choroid epithelium; another protein, perhaps GLUT1, is important on the basolateral surface. Fluid secretion is driven by apical Na+-pumps. K+ secretion occurs via net paracellular influx through relatively leaky tight junctions partially offset by transcellular efflux. The blood–brain barrier lining brain microvasculature, allows passage of O2, CO2, and glucose as required for brain cell metabolism. Because of high resistance tight junctions between microvascular endothelial cells transport of most polar solutes is greatly restricted. Because solute permeability is low, hydrostatic pressure differences cannot account for net fluid movement; however, water permeability is sufficient for fluid secretion with water following net solute transport. The endothelial cells have ion transporters that, if appropriately arranged, could support fluid secretion. Evidence favours a rate smaller than, but not much smaller than, that of the choroid plexuses. At the blood–brain barrier Na+ tracer influx into the brain substantially exceeds any possible net flux. The tracer flux may occur primarily by a paracellular route. The blood–brain barrier is the most important interface for maintaining interstitial fluid (ISF) K+ concentration within tight limits. This is most likely because Na+-pumps vary the rate at which K+ is transported out of ISF in response to small changes in K+ concentration. There is also evidence for functional regulation of K+ transporters with chronic changes in plasma concentration. The blood–brain barrier is also important in regulating HCO3 − and pH in ISF: the principles of this regulation are reviewed. Whether the rate of blood–brain barrier HCO3 − transport is slow or fast is discussed critically: a slow transport rate comparable to those of other ions is favoured. In metabolic acidosis and alkalosis variations in HCO3 − concentration and pH are much smaller in ISF than in plasma whereas in respiratory acidosis variations in pHISF and pHplasma are similar. The key similarities and differences of the two interfaces are summarized.

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Section: Ph and Concentration Of Hco3− In The Extracellular Fluids Ofmentioning

confidence: 99%

mentioning

confidence: 99%

Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

Hladky

Barrand

2016

Fluids Barriers CNS

230

253

View full text Add to dashboard Cite

show abstract

“…continued increase in ventilation relative to the CO2 output (resulting in the continued decrease of Pa co, and increasing pH), must therefore result from another stimulatory mechanism. This is likely to reflect leak of hydrogen ions into the brain extracellular fluid at the site of central ventilatory chemosensitivity (Teppema, Barts & Evers, 1982;Eldridge, Kiley & Millhorn, 1985). In the hyperoxic condition, both P. co, and arterial hydrogen ion concentration were most elevated with respect to the other FI°, conditions, accounting, presumably, for the greatest rate of return in pHa under the condition in which peripheral chemosensitivity was the least.…”

Section: Discussionmentioning

confidence: 99%

Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans.

Rausch

Whipp

Wasserman

et al. 1991

The Journal of Physiology

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“…70 This would serve to provide a slowly developing additional source of respiratory compensation for the acidaemia (see following section). For example, during prolonged high intensity constant load exercise, a slow recovery of pHa was evident after the initial transient decrease, despite peripheral chemosensitivity being suppressed by hyperoxia.…”

Section: Central Chemosensory Mediationmentioning

confidence: 99%

Determinants and control of breathing during muscular exercise.

Whipp¹,

Ward²

1998

Br J Sports Med

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IntroductionExercise hyperpnoea is considered to be one of the major remaining challenges to understanding the control of human systemic function. The topic is currently in an exciting phase, both with respect to novel perspectives on its control and the application of novel techniques to investigate previously proposed mechanisms. However, despite this, the integrative aspects of the control that so closely regulates arterial PCO 2 (PaCO 2 ) and pH (pHa) during moderate exercise, and which constrains the fall in pHa at higher work rates, seem no less elusive.We attempt in this review to provide a current perspective on the mechanisms proposed to contribute to the exercise hyperpnoea in humans (typically under laboratory conditions) using, as a frame of reference, the diVerent regulatory demands of the diVerent temporal and intensity domains.

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Effects of metabolic arterial pH changes on medullary ecf pH, csf pH and ventilation in peripherally chemodenervated cats with intact blood-brain barrier

Cited by 11 publications

References 22 publications

Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans.

Determinants and control of breathing during muscular exercise.

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