alkalosis/hypoxia

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The influence of hypoxia and hyperoxia during metabolic acidosis and alkalosis on pulmonary haemodynamics.

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In anaesthetised, mechanically ventilated Beagle dogs a moderate metabolic acidosis increased the pulmonary vascular resistance to a greater extent than moderate hypoxia. Alkalosis and hyperoxia did not alter the pulmonary vascular tone.

Ventilatory acclimatization to hypoxia is not dependent on cerebral hypocapnic alkalosis.

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We previously demonstrated that, in awake goats, 6 h of hypoxic carotid body perfusion during systemic normoxia produced time-dependent hyperventilation that is typical of ventilatory acclimatization to hypoxia (VAH). The hypocapnic alkalosis that occurred could have produced VAH by inducing

Intracellular alkalosis during hypoxia in newborn mouse brain in the presence of systemic acidosis: a phosphorus magnetic resonance spectroscopic study.

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We investigated the in vivo changes in cerebral energy metabolism and pHi in newborn mice noninvasively during 8 h of hypoxia with FiO2 = 5%, using phosphorus magnetic resonance spectroscopy continuously. The intracellular brain pH (pHi) increased from 7.20 +/- 0.03 to 7.36 +/- 0.03 (P < 0.05) at 1

Fentanyl-induced block of hERG channels is exacerbated by hypoxia, hypokalemia, alkalosis, and the presence of hERG1b.

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Human ether-a-go-go-related gene (hERG) encodes the pore-forming subunit of the rapidly activating delayed rectifier potassium channel (I_Kr) important for repolarization of cardiac action potentials. Drug-induced disruption of hERG channel function is a main cause of acquired long

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.

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Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated

Polymodal regulation of hTREK1 by pH, arachidonic acid, and hypoxia: physiological impact in acidosis and alkalosis.

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Expression of the human tandem P domain K+ channel, hTREK1, is limited almost exclusively to the central nervous system, where ambient Po2 can be as low as 20 Torr. We have previously shown that this level of hypoxia evokes a maximal inhibitory influence on recombinant hTREK1 and occludes the

QUANTITATIVE ALTERATIONS IN THE HYPEREMIA RESPONSES TO LOCAL ISCHEMIA OF THE SMALLEST BLOOD VESSELS OF THE HUMAN SKIN FOLLOWING SYSTEMIC ANOXEMIA, HYPERCAPNIA, ACIDOSIS, AND ALKALOSIS.

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The responsiveness of the smallest blood vessels of the human skin was measured in systemic anoxemia, hypercapnia, acidosis, and alkalosis. A method was used which measured quantitatively the reactive hyperemia produced by a standardized period of local ischemia of these fine vessels. By timing the

Metabolic alkalosis and the response of the trout, Salmo fario, to acute severe hypoxia.

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Trout (Salmo fario) were acutely transferred from seawater to freshwater in order to induce blood metabolic alkalosis (cf. Maxime et al., J. Comp. Physiol. 160: 31-39, 1990). After 2 weeks, the fish were exposed to severe environmental hypoxia (final water oxygen partial pressure, PWO2 = 25-45 Torr,

Involvement of lipoxygenase and cyclo-oxygenase pathways in hypoxia and metabolic alkalosis produced by canatoxin in rats.

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This paper reports on the metabolic alkalosis produced in rats by canatoxin, a neurotoxic principle extracted from Canavalia ensiformis seeds. Rats receiving canatoxin showed increased blood bicarbonate concentration with alkaline pH and no change in pCO2. A fall in pO2 was also seen. A

The effect of alkalosis on hypoxia-induced pulmonary vasoconstriction in lungs of newborn rabbits.

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The purpose of this study was to determine whether metabolic and respiratory alkalosis reduce hypoxia-induced pulmonary vasoconstriction in lungs of newborn rabbits. To accomplish this, we isolated and perfused with blood the lungs from 33 newborn rabbits, 3-14 d old. In all pairs of lungs, we first

Differential effect of metabolic alkalosis and hypoxia on high-intensity cycling performance.

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The purpose of this study was to investigate the effects of sodium bicarbonate (NaHCO3) ingestion and acute hypoxic exposure on repeated bouts of high-intensity cycling to task failure. Twelve subjects completed 4 separate intermittent cycling bouts cycling bouts to task failure (120% peak power

Determinants of curvature constant (W') of the power duration relationship under normoxia and hypoxia: the effect of pre-exercise alkalosis.

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OBJECTIVE This study investigated the effect of induced alkalosis on the curvature constant (W') of the power-duration relationship under normoxic and hypoxic conditions. METHODS Eleven trained cyclists (mean ± SD) Age: 32 ± 7.2 years; body mass (bm): 77.0 ± 9.2 kg; VO2peak: 59.2 ± 6.8 ml·kg-1·min-1

Effect of ischemia, hypertrophy, hypoxia, acidosis, and alkalosis on canine defibrillation.

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Our purpose was to assess the effect of myocardial ischemia, left ventricular hypertrophy, and systemic hypoxia and acid-base abnormalities on the energy requirements for defibrillation. We determined the defibrillation threshold (DFT), the minimum energy required to defibrillate. DFT was not

Elevation of arterial potassium during acute systemic hypoxia is abolished by alkalosis.

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BACKGROUND Small elevations in plasma potassium evoke vasodilation in the peripheral circulation. Systemic hypoxia elevates arterial potassium and also modifies arterial pH. OBJECTIVE We examined the interaction between pH and potassium in blood during systemic hypoxia and the effect of pH on the

Hypoxia silences retrotrapezoid nucleus respiratory chemoreceptors via alkalosis.

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In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exerting opposite effects on central respiratory chemoreceptors (CRCs). We tested this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nucleus (RTN), a putative CRC and

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