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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is generally believed that the reduction in plasma [HCO3] characteristic of chronic hypocapnia results from renal homeostatic mechanisms designed to minimize the alkalemia produced by.the hypocapneic state. To test this hypothesis, we have induced chronic hypocapnia in dogs in which plasma [HCO3] had previously been markedly reduced (from 21 to 15 meq/liter) by the prolonged feeding of HCl. The PaCO2 of chronically acid-fed animals was reduced from 32 to 15 mm Hg by placing the animials in a large environmental chamber containing 9% oxygen. In response to this reduction in PaCO2, mean plasma [HCO3] fell by 8.6 meq/liter, reaching a new steady-state level of 6.4 meq/liter. This decrement in plasma [HCO3] is almost identical to the 8.1 meq/liter decrement previously observed in normal (nonacid-fed) animals in which the same degree of chronic hypocapnia had been induced. Thus, in both normal and HCl-fed animals, the renal response to chronic hypocapnia causes plasma [HCO3] to fall by approximately 0.5 meq/liter for each millimeter of Hg reduction in CO2 tension. By contrast, the response of plasma [H+] in the two groups was markedly different. Instead of the fall in [H+] which is seen during chronic hypocapnia in normal animals, [H+] in HCl-fed animals rose significantly from 53 to 59 neq/liter (pH 7.28-7.23). This seemingly paradoxical response is, of course, an expression of the constraints imposed by the Henderson equation and reflects the fact that the percent fall in [HCO3] in the HCl-fed animals was greater than the percent fall in PaCO2. These findings clearly indicate that in chronic hypocapnia the kidney cannot be regarded as the effector limb in a homeostatic feedback system geared to the defense of systemic acidity.
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PMID:Regulation of acid-base equilibrium in chronic hypocapnia. Evidence that the response of the kidney is not geared to the defense of extracellular (H+). 0 88

As reported by Landau & Nachshen (1975), a decrease in extracellular pH at the frog neuromuscular junction leads to an increase in min.e.p.p. frequency. 2. Decreasing the extracellular pH still increases the min.e.p.p. frequency when the bathing Ringer contains 10 mM-Ca2+, in place of the usual 2-5 mM. At the mammalian neuromuscular junction, the elevated Ca2+ blocks the effect of the pH change on the min.e.p.p. frequency (Hubbard, Jones & Landau, 1968). 3. In Cl--free solution (isethionate or methylsulphate substitution) min.e.p.p. frequency is no longer a monotonic function of decreasing pH. Instead there is an optimum pH for spontaneous release between pH 6-6 and 8-6. 4. This suggests that in Cl- containing Ringer min.e.p.p. frequency increases with increasing extracellular acidity because there is a change in the PCl of the nerve terminal leading to a depolarization. In agreement with this idea,in low Ca2+ Ringer, acid pH has little effect on the min.e.p.p. frequency. 5. Decreasing the intracellular pH by raising PCO2 produces substantial increases in the min.e.p.p. frequency. The effects are much greater than the effects of equal changes of H+ in the extracellular solution. 6. Possible explanations for the effects of increased PCO2 are discussed. Although release of Ca2+ from mitochondria or other unknown effects of intracellular pH change or molecular CO2 are possible, the results do give some support to the hypothesis that an important step in transmitter release involves an electrostatic repulsion between fixed membrane surface charges on the transmitter containing vesicles and the inner face of the nerve terminal. The surface charge density would be decreased by a lower pH in the axoplasm, and this would increase the rate of spontaneous transmitter release, in agreement with the observations.
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PMID:The effects of pH changes on the frequency of miniature end-plate potentials at the frog neuromuscular junction. 1 40

Once ventilatory acclimatization begins in sea level residents sojourning at high altitude, abrupt restoration of normal oxygen tensions will not restore ventilation to normal. We have investigated the role of cerebrospinal fluid (CSF) [H(+)] in this sustained hyperventilation by measuring CSF acid-base status in seven men (lumbar) and five ponies (cisternal) in normoxia, first at sea level and then periodically over 13-24 h of "deacclimatization" after 3-5 d in hypoxia (P(B) = 440 mm Hg). After 1 h deacclimatization, hyperventilation continued at a level only slightly less than that obtained in chronic hypoxia (+1-2 mm Hg Pa(CO2)), whereas CSF pH was either equal (in man) or alkaline (in pony, +0.02, P < 0.01) to sea level values. Between 1 and 12-13 h deacclimatization in all humans and ponies Va fell progressively (Pa(CO2) increased 4-7 mm Hg) and CSF pH became increasingly more acid (-0.02 to -0.05, P < 0.01). Between 12 and 24 h of normoxic deacclimatization in ponies, Pa(CO2) rose further toward normal, coincident with an increasing acidity in CSF (-0.02 pH). Similar negative correlations were found between changes in arterial pH and Va throughout normoxic deacclimatization. We conclude that [H(+)] in the lumbar or cisternal CSF is not the mediator of the continued hyperventilation and its gradual dissipation with time during normoxic deacclimatization from chronic hypoxia. These negative relationships of Va to CSF [H(+)] in normoxia are analogous to those previously shown during acclimatization to hypoxia.
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PMID:Role of cerebrospinal fluid [H+] in ventilatory deacclimatization from chronic hypoxia. 3 11

Total and regional cerebral blood flow (CBF), and cerebrospinal fluid (CSF), and arterial blood acid-base status were measured in 26 chloralose-urethan-anesthetized dogs before and after 30 and 60 min of ventriculocisternal perfusion with artificial CSF equilibrated with 7% CO2 and containing either low (8.7 or 9.1 meq/l), normal (19.6 meq/l), or high (34.7 meq/l) bicarbonate ion concentration ([HCO3-]). An inverse linear relationship was observed between the CSF pH and total CBF. Regional blood flow changes were greater in structures that were closest to the ventricular system. In addition, regional blood flow changes were greater in all tissues studied after 60 min of perfusion than after 30. Perfusion with the control [HCO3-] caused no significant changes in either acid-base status or CBF. We believe that the regional cerebral blood flow changes are the result of changes in the H+ concentration gradient across the cerebral extracellular fluid (ECF) space due to the diffusional exchange of HCO3- between CSF and ECF. It is concluded that cerebral ECF acidity is important in the local regulation of cerebral blood flow.
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PMID:Effect of cerebral extracellular fluid acidity on total and regional cerebral blood flow. 4 28

Rats are made hypercapnic by breathing 8% CO2 for a week. Their stomachs, removed under anaesthesia in a hypercarbic atmosphere, are placed in a special chamber and the acidic secretion (free + titratable) is measured in vitro in relation to different parameters of the controlled atmosphere. The secretion depends on the gas composition. Under the same conditions (mucosa CO2 = 8%, serosa CO2 = 10%) the in vitro secretion of the hypercapnic subjects (n = 32) is lower than that in the normal rats (n = 27), the latter secretion decreasing more rapidly with the duration of the in vitro measurement. The differences between the hypercapnic and the control subjects are in the order of +/- 10% in titratable acidity (mEq/l/h/cm2) and +/- 20% in free acidity (muEq/l/h/cm2).
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PMID:[Effect of chronic hypercapnia on the gastric acid secretion in rats: a comparative study in vitro (author's transl)]. 45 65

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.
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PMID:Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism. 50 20

Physiological studies on hypercapnic effects carried out on 13 Polaris patrols are summarized. The average CO2 concentrations ranged from 0.7-1% CO2; CO2 was identified as the only environmental contaminant of the submarine atmosphere that has a direct effect on respiration in the concentration range found in the submarine atmosphere. A comparison has been made of physiological effects produced during 42 days of exposure to 1.5% CO2 during laboratory studies (L.S.) with those observed during 50 to 60 days of exposure to 0.7-1% CO2 on patrols (P.S.). A close similarity was found in the effects on respiration and blood electrolytes under both conditions. Respiratory minute volume was elevated by 50-63% because of increased tidal volume. The physiological dead space increased 60%. Vital capacity showed a trend toward a decrease. Studies of acid-base balance carried out during patrols demonstrated cyclic changes in blood pH and bicarbonate; pH and blood bicarbonate fell during the first 17 days of exposure, rose during the subsequent 20 days, and decreased again after 40 days. These cycles cannot be explained on the basis of known renal regulations in CO2-induced acidosis and were not found during exposure to 1.5% CO2. The hypothesis is advanced that these changes in acid-base balance are caused by cycles in CO2 uptake and release in bones. The time constants of the bond CO2 stores fit the observed length of cycles in acid-base balance. Correlation with cycles of calcium metabolism provides further support for this hypothesis. Red cell electrolytes showed similar changes under 1.5% CO2 (L.S.) and 0.7-1% CO2 (P.S.). Red cell sodium increased and potassium decreased. Moreover, red cell calcium also increased under both conditions. The significance of these red cell electrolyte changes in regard to changes in permeability and active transport remains to be clarified. An increased gastric acidity was found during patrol (exposure to 0.8-0.95% CO2). The changes observed during patrols disappeared during the recovery periods.
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PMID:Physiological stresses related to hypercapnia during patrols on submarines. 50 22

The uptake of Ca2+ by liver mitochondria, when phosphate movement is inhibited, occurs when Co2 is present and not in its absence. Uptake of Ca2+ to form CaCO3 yields 2H+/Ca2+. Heart mitochondria, when phosphate movement is inhibited, will take up Ca2+ with the exact equivalent of hydroxybutyrate, lactate or acetate. By providing a carrier for Cl- with tributyltin, a stoicheiometric uptake of Cl- with the Ca2+ takes place. The uptakes appear to occur without significant pH change; there appears to be no CO2-dependent uptake into heart mitochondria. Oxygenation of anaerobic heart mitochondria, in the presence of an inhibitor of phosphate movement and of generation of phosphate from internal ATP, does not yield significant change of external acidity in relation to the amount of O2 added. Use of Bromothymol Blue as an indicator of the distribution of a weak acid anion confirms that the transient nature of the response of the dye distribution to Ca2+ is connected with movement of endogenous phosphate. Bromothymol Blue accumulated in response to Ca2+ is discharged when entry of the Ca2+ (in the presence of mersalyl) is mediated with nigericin. It is concluded that Ca2+ uptakes will occur alternatively with the equivalent of anions or in exchange for endogenous K+ and that proton production is connected with the changes of ionization of phosphate (unless phosphate movement is inhibited) and in liver mitochondria with the hydration of CO2.
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PMID:Anion/calcium ion ratios and proton production in some mitochondrial calcium ion uptakes. 74 66

Samples of freshly harvested corn and remoistened corn were inoculated with Asphergillus flavus and stored for 4 weeks at about 27 C in air and three modified atmospheres. Aflatoxins and fat acidity were determined weekly. Corn stored in the modified atmospheres did not accumulate over 15 mug of total aflatoxins per kg. Corn from the high CO2 treatment (61.7 per cent CO2, 8.7 per cent O2, and 29.6 per cent N2) was visibly molded at 4 weeks and had a higher fat acidity than the other treatments. In the N2 (99.7 per cent N2 and 0.3 per cent O2) and controlled atmosphere (13.5 per cent CO2, 0.5 per cent O2, 84.5 per cent N2) treatments, a fermentation-like odor was detected. When the corn was removed from the modified atmospheres it deteriorated rapidly and was soon contaminated with aflatoxins.
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PMID:Influence of modified atmosphere storage on aflatoxin production in high moisture corn. 80 17

Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
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PMID:The apparent buffer value of cerebrospinal fluid in acute hypercapnia. 82 71


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