Disease relevance of Alkalosis, Respiratory

• Both metabolic and respiratory alkalosis develop in all subjects during lactate infusion, but only hyperventilation-induced hypocapnia differentiates patients at the point of lactate-induced panic from nonpanicking patients and normal controls [1].
• IL-2 therapy produced a syndrome similar to endotoxemia with the development of respiratory alkalosis (pH = 7.44 +/- .2, pCO2 = 30 +/- 2) and hypotension (mean BP, 71.3 mm Hg) [2].
• In this model an early respiratory alkalosis developed, followed by a metabolic acidosis with increased levels of blood lactate [3].
• CONCLUSIONS: Acute metabolic and respiratory alkalosis markedly decreased PTH values during normocalcemia and delayed the PTH response to hypocalcemia [4].
• Effects of respiratory alkalosis on thromboxane-induced pulmonary hypertension in piglets [5].

Psychiatry related information on Alkalosis, Respiratory

• The patient shows the following symptoms not previously emphasized in the Rett syndrome: deceleration of head growth (rather than acquired microcephaly), fall-off in linear growth in infancy, early hypotonia, precocious puberty and respiratory alkalosis [6].
• A 2 month old male infant, a product of a consanguineous marriage (Suphanburi province); developed poor feeding on day 7, lethargy, convulsion, hepatomegaly and respiratory alkalosis leading to respiratory failure and coma [7].

High impact information on Alkalosis, Respiratory

• This study evaluated whether progesterone and estradiol contribute to the respiratory alkalosis common in cirrhotic patients [8].
• Direct suppressive effect of acute metabolic and respiratory alkalosis on parathyroid hormone secretion in the dog [4].
• It is characterized by abrupt alteration in mental status and respiratory alkalosis associated with markedly elevated plasma ammonium levels in the absence of any identifiable cause, and frequently results in intractable coma and death [9].
• Cerebral dysfunction and respiratory alkalosis during peritoneal dialysis with D-lactate-containing dialysis fluids [10].
• From an initial state of hyperventilated respiratory alkalosis (FIO2 = 0.21, VT = 18 ml/kg, RR = 35), we studied the changes in VA/Q distributions, respiratory gas exchange, and hemodynamics when the acid-base status of the dogs was manipulated by combinations of acid or alkali infusion with or without CO2 inhalation [11].

Chemical compound and disease context of Alkalosis, Respiratory

• Five hours after induction of respiratory alkalosis, mean CSF [HCO3-] decreased significantly by 4.4 +/- 1.2 mEq/L (mean +/- SD) [12].
• Respiratory alkalosis decreases the phosphaturic response to parathyroid hormone (PTH). beta-adrenoreceptor blockade by propranolol infusion restores the phosphaturic effect of PTH in respiratory alkalotic rats; however, the nephron site of these changes in phosphate reabsorption by propranolol is not known [13].
• Site of restoration of the effect of PTH by propranolol in respiratory alkalosis [13].
• It results in impaired generation of adenosine triphosphate and produces a primary respiratory alkalosis [14].
• The principal toxic manifestations of respiratory alkalosis and metabolic acidosis, altered glucose availability and depletion, fluid and electrolyte losses, and hypermetabolism result in serious morbidity and are potentially fatal [15].

Biological context of Alkalosis, Respiratory

• Lactic acid kinetics in respiratory alkalosis [16].
• We conclude that respiratory alkalosis increases myocardial O2 extraction but does not produce hemodynamically significant coronary vasoconstriction in CAD patients [17].
• In spite of extreme panting body temperature rose to 42.2 degrees C. Exposure to 40 degrees C/50% relative humidity with 4% CO2 in the climatic chamber inhibited the respiratory alkalosis and the increase of plasma enzymes [18].
• Also, high levels of NaHCO3 and CaCl2 intake can produce abnormal acid-base equilibrium conditions during the heat stress-induced respiratory alkalosis [19].
• The effects of respiratory alkalosis and dehydration on the pharmacokinetics of sufentanil have been determined [20].

Anatomical context of Alkalosis, Respiratory

• Arterial and cerebrospinal fluid lactate was elevated in association with a marked respiratory alkalosis in 13 patients studied 5 to 12 hours after the seizure [21].
• High-HCO3- metabolic alkalosis protects the mucosa against this ulceration, whereas low-HCO3- respiratory alkalosis does not, suggesting that lack of systemic and intramucosal HCO3-, rather than tissue acidosis per se, renders the mucosa susceptible to ulceration [22].
• Hypoxia produces respiratory alkalosis leading to an increased erythrocyte oxygen affinity Ep secretion followed by an increase in 2,3 DPG in erythrocytes and an increased flow of oxygen to tissues [23].

Gene context of Alkalosis, Respiratory

• The aim of the study was to determine whether respiratory alkalosis is characteristic of patients with LS due to SURF1 mutations [24].
• It may be that in Fahr disease some factors, such as chronic respiratory alkalosis, could lead to hypoparathyroidism-like changes in the brain tissue [25].
• All durations of oxygen exposure resulted in significant respiratory alkalosis and elevated pulmonary and blood glutathione peroxidase concentrations [26].
• On the other hand, in respiratory alkalosis glycolytic intermediates shift to the opposite direction and forward crossover at PFK step appears, being associated with an elevation of 2,3 DPG [27].
• Respiratory alkalosis was present in varying degrees in most patients with either tachypnea or prominent CSR [28].

Analytical, diagnostic and therapeutic context of Alkalosis, Respiratory

• However, the maximal PTH response was observed after a decrease in ionized calcium of 0.20 mM in the control group but not until a decrease of 0.40 mM in the metabolic and respiratory alkalosis groups [4].
• The effects of acutely induced metabolic and respiratory alkalosis with reduction of serum potassium concentration as well as chronic total body potassium depletion induced by furosemide treatment were evaluated and correlated with alteration of neuromuscular blockade induced by d-tubocurarine, pancuronium, and succinylcholine in 12 mongrel dogs [29].

References