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

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4

Samples of water and snails collected through aleatory scoops in a small dam were done to obtain data concerning the physical and chemical characteristics of the water and their possible influence on biological aspects of the life cycle of snails. Among the 17 analysed parameters, Alkalinity and Conductivity showed a positive correlation with the density of B. tenagophila (r = +0.224 and r = +0.290), while CO2 and Acidity were negatively correlated with this populacional parameter (r = -0.592 and 0.601). Alkalinity and Total Hardness values were slightly higher than 100 mg/l CaCO3. Chlorides and Conductivity showed means of 94.9 +/- 38.7 and 680.1 +/- 643 microS/cm; these values are very high for that region. Other factors like pH and OD are according to the pattern for provision untreated waters. The density of B. tenagophila declined in the 6th month after a long period of torrential rains and in the rainy summers. In the colder months of the following year the density was higher (until 124 individuals/months/90 scoops). The monthly mean of the diameters of the snails was always larger than 13 mm, reaching 21.4 +/- 4.1 mm, but the mode was about 17 mm. There was no correlation between diameter/density (r = 0.037) and density/temperature (r = 0.065).
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PMID:[Physical and chemical characteristics of the habitat of Biomphalaria tenagophila (Mollusca, Planorbidae)]. 383 31

Previous studies have shown that lymphocytic infiltrates of different mouse mammary tumors contain different proportions of the T cell subsets Lyt-1+ and Lyt-2+. These characteristic subset ratios may be established, at least in part, by differential locomotion of subsets in response to components of the tumor microenvironment, such as soluble chemotactic and chemokinetic factors, cell and stromal surfaces, oxygen tension, and pH. We describe a new in vitro assay for determining how such microenvironmental variables affect lymphocyte locomotion. Suspended lymph node cells, alone or mixed with other cell types, are sandwiched between two layers of type I collagen gel and bathed in culture medium. A halo of locomotory cells fans out around the flattened droplet. Locomotion requires energy and exogenous protein. After a 24-hr incubation at 37 degrees C, 10% CO2 in air, the cell density of the halo is analyzed optically and the subset ratios are characterized by immunofluorescence staining of the gel sandwich. Under standard culture conditions, the locomotory population is enriched 12% in Thy-1+ cells compared with the bulk population, and the ratio of Lyt-1+ to Lyt-2+ cells is significantly increased. Lymphocyte locomotion is inhibited by 1 microM PGE2, by decreased pH and oxygen tension, and by the presence of normal mammary cells or mammary adenocarcinoma cells. The Lyt-1+:2+ ratio in the locomotory population is not altered by PGE2 but is reduced by acidity and hypoxia. The ratio is also reduced by the presence of mammary cells and cells of one of the mammary adenocarcinoma cell lines tested (168) but not by two others (68H and 410). Our data support the hypothesis that the locomotion of T cell subsets is differentially responsive to the types of microenvironmental conditions that vary among tumors.
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PMID:T cell locomotion in the tumor microenvironment. I. A collagen-matrix assay. 387 12

To determine the effective stimulus to the central chemoreceptors, we measured CSF and medullary extracellular fluid (ECF) pH and phrenic activity in 11 anesthetized, paralyzed, vagotomized and glomectomized cats. Flat-tipped pH electrodes (2 mm diam.) were used to measure ECF pH on the ventral surface of the medulla and CSF pH 2 mm above the surface. Changes in alveolar/arterial PCO2 were produced by airway occlusions of 10-20 sec durations. Changes in CSF PCO2 and pH were made by infusing 100% CO2 or an acid buffer into the CSF. Airway occlusion caused an increase of alveolar/arterial PCO2. ECF pH began to fall 6-10 sec later, with a maximum decrease of 0.032 pH unit at 21.9 sec. Phrenic activity increased as ECF pH decreased, the greatest activity occurring when ECF pH was most acid. CSF pH decreased after a longer delay. Its maximum decrease at 54.1 sec was smaller (0.026 pH unit) than ECF pH and did not correlate with the increase of phrenic activity. Addition of 100% CO2 or an acid buffer into the CSF produced an acid shift in the CSF pH but no change in ECF pH or phrenic activity. Prolonged (greater than 30 min) increase of acidity of CSF did not alter phrenic activity until ECF pH developed a delayed acid shift. Even then, the change of ECF pH was much smaller than that of CSF. We conclude that medullary chemoreceptors do not respond to changes of CSF pH or PCO2 and that change of pH of CSF minimally affects ECF pH. On the other hand, respiratory responses are closely linked to changes in ECF pH.
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PMID:The roles of medullary extracellular and cerebrospinal fluid pH in control of respiration. 398 82

Intact rat diaphragms were exposed in vitro to varying CO(2) tensions and bicarbonate concentrations, and the steady-state citrate content of diaphragm muscle was measured to investigate the relationship between metabolism and extracellular pH, P(CO2), and (HCO(3) (-)). In addition, rat hemidiaphragms were incubated with 1,5-citrate-(14)C under different acid-base conditions, and (14)CO(2) production was determined as a measure of citrate oxidation. Acidification of the bathing medium achieved by raising CO(2) tension or lowering (HCO(3) (-)) was associated with a decrease in muscle citrate content. On the other hand, alkalinization of the medium induced by lowering CO(2) tension or raising (HCO(3) (-)) caused tissue citrate content to rise. At a physiologic extracellular pH value of approximately 7.40, citrate content was decreased or normal depending on the CO(2)/HCO(3) (-) combination employed to attain the pH. Under low bicarbonate and low P(CO2) conditions, citrate content was reduced. A similar result was found at external pH values of 7.15, implying that at these two extracellular pH levels (HCO(3) (-)) primarily determines citrate content. When changes in citrate content were compared with intracellular pH data reported earlier using the same intact diaphragm preparation, no simple relation between citrate content and intracellular pH was found. The effect of acidity on citrate content seems related to a change in citrate oxidation since the latter increased progressively with increasing degrees of medium acidity. These results show that cellular metabolism is not a simple function of extracellular pH but is dependent on the particular combination of P(CO2) and bicarbonate employed to achieve the pH value. These studies also suggest that accumulation or disposal of organic acids, such as citric acid, helps to regulate cellular acidity thereby contributing to the cells' defense against external acid-base disorders.
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PMID:The role of pH, PCO2, and bicarbonate in regulating rat diaphragm citrate content. 544 4

The high pH-maintaining capacity of yeast suspension after glucose-induced acidification, measured as its ability to neutralize added alkali, was found to be due mainly to actively extruded acidity (H+). The buffering action of passively excreted metabolites (CO2, organic acids) and cell surface polyelectrolytes contributed only 15--40% to the overall pH-maintaining capacity which was 10 mmol NaOH/l per pH unit between pH 3 and 4 and 3.5 nmol NaOH/l per pH unit between pH 4 and 7. The buffering capacity of yeast cell-free extract was still higher (up to 4.5-times) than that of glucose-supplied cell suspension; addition of glucose to the extract thus produced considerable titratable acidity but negligible net acidity. The glucose-induced acidification of yeast suspension was stimulated by univalent cations in the sequence K+ greater than Rb+ much greater than Li+ congruent to Cs+ congruent to Na+. The processes participating in the acidification and probably also in the creation of extracellular buffering capacity include excretion of CO2 and organic acids, net extrusion of H+ and K+ (in K+-free media; in K+-containing media this is preceded by an initial rapid K+ uptake), and movements of some anions (phosphate, chlorides). The overall process appears to be electrically silent.
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PMID:Processes involved in the creation of buffering capacity and in substrate-induced proton extrusion in the yeast Saccharomyces cerevisiae. 626 55

1. The effect of heat-stable enterotoxin (ST) of Escherichia coli, cholera toxin (CT), and theophylline (a phosphodiesterase inhibitor) on ion and water transport was studied with an in vivo isolated loop system of the pig colon.2. All three agents abolished net Na absorption as a result of a decrease in the lumen to blood Na flux alone. With all three agents, net Cl absorption was reduced, but not abolished, and net HCO(3) secretion was elicited. Luminal p(CO2) was reduced with CT and theophylline from that observed in normal Ringer alone.3. Theophylline resulted in a prompt and sustained increase in both cyclic adenosine monophosphate (cyclic AMP) and cyclic guanosine monophosphate (cyclic GMP) levels in colonic mucosa studied in vitro. ST selectively elevated cyclic GMP, whereas CT selectively elevated cyclic AMP. These responses paralleled the time course and magnitude of response of the transepithelial electrical potential difference (psi(LB)) measured in vivo.4. Ion replacement studies in the presence or absence of theophylline showed that in the absence of Na, Cl absorption was slightly reduced and HCO(3) secretion was elicited; no further additive effects of theophylline in the absence of luminal Na were observed. In the absence of luminal Cl, net Na absorption was abolished and HCO(3) was absorbed; theophylline resulted in significant net Na and HCO(3) secretion. Theophylline also increased psi(LB) in the absence of either luminal Na or Cl.5. Results suggest that in the presence of theophylline or enterotoxin, the coupled Na-H and Cl-HCO(3) exchange processes that are normally responsible for at least half of the net NaCl absorption by this tissue are interrupted. Active HCO(3) secretion is observed and Cl absorption under these conditions can be entirely explained as a consequence of psi(LB). Thus, these studies indicate that the colon may participate in the production of diarrhoea of enterotoxigenic origin. They also suggest an important functional role of cyclic nucleotides in controlling the acidity and volume of colonic contents.
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PMID:Effect of Escherichia coli heat-stable enterotoxin, cholera toxin and theophylline on ion transport in porcine colon. 627 79

In the normal human body, the extracellular fluid pH of 7.40 is closely protected. Any increase in acidity or alkalinity summons forth three lines of defense, starting immediately with the blood buffers, followed soon by the respiratory system's control of CO2, and finally purged by the renal excretion of the excess acid or base. The complex interrelated processes of the renal responses require a few days to accomplish maximum compensation. We have presented the fundamental principles governing maintenance of the acid-base equilibrium to provide a conceptual framework for understanding the clinical disorders of hydrogen ion metabolism. The somewhat elusive concepts of endogenous acid production and net acid balance have also been reviewed to help reveal the pathophysiology of metabolic acidosis caused by renal tubular acidosis, chronic renal failure, certain infant feedings, and total parenteral nutrition. The development and perpetuation of metabolic alkalosis in relationship to chloride and potassium deficiency have been examined. In the delineation of a clinical acid-base disorder, the clinician must bear in mind the continual interactions of electrolytes and hormonal systems and should be prepared to reevaluate frequently the elected therapy against the changing responses, based on a thorough understanding of physiology. The various types of renal tubular acidosis have manifold facets but the basic understanding of their pathophysiology begins with the concept of the "anion gap," a point of reference that can be used in the differential diagnosis and treatment. In this chapter a number of new causes of type IV renal tubular acidosis--currently considered to be the most common form of renal tubular acidosis--have been pointed out, along with special reference to the mineral, electrolyte, and aldosterone metabolism in the various acidoses and current means of reversing growth failure in the child, especially through bicarbonate treatment. The mechanism of metabolic acidosis in chronic renal failure including metabolic acidosis in children undergoing dialysis and in recipients of kidney transplantation, and its relationships to mineral and electrolyte metabolism have been presented. The pathophysiology of the acidosis related to certain infant formulas and the acidogenic properties of some amino acid solutions employed in total parenteral nutrition have been briefly reviewed. Finally, the metabolic alkalosis seen in a variety of chloride deficiency syndromes, such as Bartter's syndrome and dietary chloride deprivation, has been discussed and a rational approach to evaluation and treatment outlined.
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PMID:Acid-base disorders and the kidney. 642 18

The effect of a period of induced back diffusion of H+ on the isolated amphibian gastric mucosa was studied under various conditions. Under standard conditions (HCO3--buffered nutrient solution; 95% O2-5% CO2), passage of an electrical current of 500 microA/cm2 for 15 min from a secretory fluid of pH 2.10 across the mucosal resulted in a decrease of the transmucosal potential difference (PD) of 10.9 +/- 1.9 mV, a decrease of resistance (R) of 48 +/- 26 ogema cm2 and a decrease of short circuit current (Isc) of 18 +/- 7 microA/cm2. Flux of the neutral molecule, erythritol from secretory (S) to nutrient (N) fluid increased by 66% and the active transport of Cl- N lead to S decreased from 2.9 to 1.9 microeq/cm2/hr. With removal of HCO3- from the nutrient fluid and with inhibition of carbonic anhydrase activity the period of back diffusion induced significantly greater change in the electrical measurements than occurred when under standard conditions. This increased effect of back diffusion of H+ was not changed by change of the nutrient fluid pH from 7.20 to either 6.6 or 8.2. Increase of the HCO3- concentration of the nutrient fluid to 35 mM or decrease of the CO2 content of the aerating gas to 1% were associated with significantly less change of the electrical measurements than occurred with standard conditions. These studies support the proposal that the the neutralizing reaction HCO3- + H+ leads to CO2 + H2O plays a central role in the gastric mucosal handling of backing diffusing H+ and suggests that the capacity and poise of the HCO3-/CO2 buffer system is an important determinant of the ability of the mucosa to tolerate luminal acidity.
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PMID:Role of acid-base status in the response of the isolated amphibian gastric mucosa to back diffusion of H+. 677 1

Cerebrovascular responses to 30 min of isocapnic hypoxia [arterial O2 partial pressure (PaO2) = 33 +/- 1 Torr; means +/- SE] were examined in eight chloralose-urethan-anesthetized, paralyzed, and artificially ventilated New Zealand White rabbits. Cerebral blood flow (Q) was measured using the radioactive microsphere technique. Vascular resistance (R) was calculated from arterial pressure and Q. Brain extracellular fluid (ECF) pH was measured continuously in the same animals using pH microelectrodes (1- to 2-micrometers tip diameter) placed stereotaxically in the diencephalon. Diencephalon Q increased from 40 +/- 2 to 69 +/- 4 ml . 100 g-1 . min-1 (P less than 0.05) as R decreased (P less than 0.05) after 4-6 min of isocapnic hypoxia. Total brain Q and R changes resembled those of the diencephalon. The ECF pH of the diencephalon increased by 0.016 +/- 0.006 (P less than 0.05) after 1 min of isocapnic hypoxia and remained significantly elevated through the first 20 min of hypoxia. Ten minutes after the return of normoxia Q and R were at control levels, whereas diencephalon ECF pH was 0.043 +/- 0.006 below control (P less than 0.05). Five additional rabbits were prepared as described above then made hypocapnic [arterial CO2 partial pressure (PaCO2) = 21 +/- 0.3 Torr] for 18 min. Diencephalon and total brain Q and R remained at control levels through 12-14 min of hyperventilation, whereas diencephalon ECF pH was elevated by 0.03 +/- 0.006 (P less than 0.05). Hyperventilation was then continued with hypoxic gas to lower PaO2 to 35 +/- 4 Torr for 30 min. Both diencephalon and total brain R decreased (P less than 0.05), with no change in Q after 4-6 min of hypocapnic hypoxia. Diencephalon ECF pH was not significantly different from control throughout the hypocapnic-hypoxic period. We conclude that the early cerebral vasodilation during hypoxia is not mediated by increased brain ECF acidity.
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PMID:Brain extracellular fluid pH and blood flow during isocapnic and hypocapnic hypoxia. 681 24


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