Evolutionary determinants of normal arterial plasma pH in ectothermic vertebrates

2002 ◽  
Vol 205 (5) ◽  
pp. 641-650
Author(s):  
Richard F. Burton
Keyword(s):  
Cell Surface ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Surface Ph ◽  
Mean Values ◽  
Surface Sites ◽  
Arterial Ph ◽  
Arterial Plasma ◽  
Optimal Ph

SUMMARYMean values of normal arterial pH in different species of fish, amphibians and reptiles at 15 and 25°C, taken from the literature, are negatively correlated with arterial PCO2 and plasma [Na+]. At either temperature, the data accord with the hypothesis that extracellular acid–base homeostasis evolved to maintain an optimal pH at particular cell-surface sites that are similar in all species. These hypothetical sites bear fixed negative charges that attract H+, but which are partially screened by Na+; for the surface pH to be constant, the bulk interstitial pH should then vary inversely with [Na+], as is the case. At the same time, the bulk interstitial fluid must be more acid than arterial plasma by an amount that increases with decreasing arterial PCO2. With allowance made for additional screening by Ca2+ and Mg2+, the relevant cell-surface pH is probably approximately 6.2.

scholarly journals Damage to the gastric epithelium activates cellular bicarbonate secretion via SLC26A9 Cl−/HCO3−exchange

2010 ◽  
Vol 299 (1) ◽  
pp. G255-G264 ◽  
Author(s):  
Elise S. Demitrack ◽  
Manoocher Soleimani ◽  
Marshall H. Montrose
Keyword(s):  
Interstitial Fluid ◽  
Gastric Epithelium ◽  
Acid Base ◽  
Surface Ph ◽  
Two Photon ◽  
Acid Base Status ◽  
Genetic Deletion ◽  
Knockout Animals ◽  
Tissue Compartments

Gastric surface pH (pHo) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pHowith Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pHi) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 ± 0.03) after photodamage, compared with healthy surface cells both near (7.12 ± 0.06) and far (7.07 ± 0.04) from damage ( P < 0.05). This damaged cell acidification was further attenuated with 20 μM intravenous EIPA (6.34 ± 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H2DIDS (6.64 ± 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO3−secretion with 0.5 mM luminal H2DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl−/HCO3−exchanger blocked the pHoincrease normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE2significantly increased pHoin wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO3−secretion is fully mediated by SLC26A9. We conclude that cellular HCO3−secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage.

Effect of systemic acid-base disorders on ileal intracellular pH and ion transport

1986 ◽  
Vol 250 (5) ◽  
pp. G588-G593 ◽  
Author(s):  
J. D. Wagner ◽  
P. Kurtin ◽  
A. N. Charney
Keyword(s):  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Strong Correlations ◽  
Sprague Dawley ◽  
Acid Base ◽  
Ileal Mucosa ◽  
Arterial Pco2 ◽  
Co2 Partial Pressure ◽  
Arterial Ph ◽  
Acute Metabolic Acidosis

We previously reported that changes in ileal net Na absorption correlated with arterial pH, changes in net HCO3 secretion correlated with the plasma HCO3 concentration, and changes in net Cl absorption correlated with arterial CO2 partial pressure (PCO2) during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediated these effects, we measured pHi and calculated [HCO3]i in the distal ileal mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4,-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis, and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, mucosal pHi was not altered, but there were strong correlations between mucosal [HCO3]i and both arterial PCO2 (r = 0.97) and [HCO3] (r = 0.61). When we considered the rates of ileal electrolyte transport that characterized these acid-base disorders [A. N. Charney and L.P. Haskell, Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G230-G235, 1983], we found strong correlations between mucosal [HCO3]i and both net Cl absorption (r = 0.88) and net HCO3 secretion (r = 0.82). These findings suggest that the systemic acid-base disorders do not affect ileal mucosal pHi but do alter mucosal [HCO3]i as a consequence of altered arterial PCO2 and [HCO3]. The effects of these disorders on ileal net Cl absorption and HCO3 secretion may be mediated by changes in [HCO3]i. Arterial pH does not appear to alter ileal Na absorption through changes in the mucosal acid-base milieu.

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

Ventilation and CSF ions during hypocapnic HCl and HNO3 acidosis in conscious rabbits

1983 ◽  
Vol 55 (6) ◽  
pp. 1748-1757 ◽  
Author(s):  
E. E. Nattie ◽  
G. F. Birchard
Keyword(s):  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Production ◽  
Central Venous ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Mean Values ◽  
Frequency Responses ◽  
Ionic Mechanisms ◽  
Conscious Rabbits

In conscious rabbits with preimplanted arterial, central venous, and cisterna magna catheters, we infused HNO3 or HCl to lower and maintain arterial PCO2, pH, and plasma HCO-3 at the same mean values in both groups over 9 h. The hypothesis was that greater entry into cerebrospinal fluid (CSF) of the strong anion NO-3 vs. Cl- would result in a greater decrease in CSF [HCO-3] in the HNO3 vs. the HCl experiment, even though the acid-base stress as measured by arterial PCO2 and plasma [HCO-3] was the same. The results did not support the hypothesis. With HCl acidosis, delta CSF [HCO-3] was equal to delta CSF [Cl-]. With HNO3 acidosis, delta CSF [HCO-3] was equal to delta CSF [NO-3] + delta CSF [Cl-], as both CSF Cl- and HCO-3 decreased with NO-3 entry into CSF. The change in CSF [HCO-3] appeared tightly linked to the PCO2 or the plasma [HCO-3], it did not depend on the type of acid used. The ionic mechanisms that determine the CSF [HCO-3] in metabolic acidosis appear able to utilize changes in the strong anions NO-3 and Cl- to bring about CSF acid-base regulation. The change in alveolar ventilation per unit CO2 production as reflected by the arterial PCO2 was the same in both groups, although the expired minute ventilation and respiratory frequency responses were diminished in the HNO3 vs. the HCl groups. In both groups with acidosis, tidal volume increased, whereas respiratory frequency decreased.

Thermoregulation and acid-base status in the panting dehydrated fowl

1983 ◽  
Vol 54 (1) ◽  
pp. 234-243 ◽  
Author(s):  
Z. Arad
Keyword(s):  
Body Temperature ◽  
Heat Exposure ◽  
Regulatory System ◽  
Acid Base ◽  
Evaporative Water ◽  
Arterial Pco2 ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Stable Oxygen ◽  
Ph Level

This is the first study to report on thermoregulation and acid-base regulation in dehydrated and heat-exposed fowls. The dehydrated fowls (ca. 15% weight loss) panted at lower-than-normal panting frequencies, resulting in a reduced evaporative water loss and a relative hyperthermy. However, body temperature was effectively regulated below lethal levels, and heart rate remained stable. Oxygen consumption was slightly increased compared with normal hydration, when related to ambient temperature. However, when related to body temperature, a lower metabolism was evident at the higher range. Tidal and minute volumes were closely regulated, contributing to the avoidance of extreme acid-base disturbances. Arterial pH level indicated a relative metabolic acidosis compared with normal hydration. However, acid-base regulation during heat exposure had not deteriorated despite the lower arterial PCO2, due to a compensatory decrease in HCO-3 concentration. The inhibited evaporative cooling and the relative hyperthermy suggest a reduced responsiveness of the central regulatory system, possibly through an elevated hypothalamic set point. In spite of these changes, regulation of body temperature and acid-base status were not impaired.

Effect of chronic acetazolamide administration on gas exchange and acid-base control after maximal exercise

1994 ◽  
Vol 76 (3) ◽  
pp. 1211-1219 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones
Keyword(s):  
Gas Exchange ◽  
Muscle Power ◽  
Strong Ion Difference ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Lactate ◽  
Arterial Pco2 ◽  
Co2 Output ◽  
Base Balance ◽  
Arterial Plasma

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventral medullary extracellular fluid pH and PCO2 during hypoxemia

1987 ◽  
Vol 63 (4) ◽  
pp. 1567-1571 ◽  
Author(s):  
S. Javaheri ◽  
L. J. Teppema
Keyword(s):  
Steady State ◽  
Extracellular Fluid ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Mean Values ◽  
Designed Experiments ◽  
Ventilatory Depression ◽  
Spontaneously Breathing ◽  
Arterial Po2 ◽  
Made In

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].

Intracellular pH of brain: alterations in acute respiratory acidosis and alkalosis

1976 ◽  
Vol 230 (3) ◽  
pp. 804-812 ◽  
Author(s):  
AI Arieff ◽  
A Kerian ◽  
SG Massry ◽  
J DeLima
Keyword(s):  
Cerebral Cortex ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Metabolic Adaptations ◽  
Arterial Ph ◽  
Arterial Po2 ◽  
The Brain ◽  
Brain Extracellular Space

To evaluate the metabolic adaptations of the brain to acute respiratory acid-base disturbances, a method was developed to measure intracellular pH (pHi) in the brain of dogs under conditions in which arterial pH is rapidly altered. Brain pHi was determined by measuring the distribution of 14C-labeled dimethadione (DMO) in brain relative to cortical CSF. Brain extracellular space (ECS) was evaluated as the 35SO4 = space relative to cortical CSF, and arterial Po2 was maintained at 82-110 mmHg. In normal dogs, brain (cerebral cortex) pHi was 7.05, and after 1 h of hypercapnia (arterial pH = 7.07) it fell to 6.93. However, after 3 h with arterial Pco2 maintained at 85 mmHg brain pHi was normal (7.06), and during this time brain bicarbonate had risen from 11.3 to 24.4 meq/kg H2O. These changes were not prevented by intravenous doses of acetazolamide,

Cerebral interstitial fluid acid-base status follows arterial acid-base perturbations

1982 ◽  
Vol 53 (6) ◽  
pp. 1551-1555 ◽  
Author(s):  
D. G. Davies ◽  
W. F. Nolan
Keyword(s):  
Cerebrospinal Fluid ◽  
New Zealand ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Ph Probe ◽  
Arterial Blood ◽  
Blood Ph ◽  
New Zealand White Rabbits ◽  
Acid Base Status

Cerebral interstitial fluid (ISF) pH of ventral medulla or thalamus, cisternal cerebrospinal fluid (CSF) pH, and arterial blood pH, PCO2, and [HCO-3] were measured in chloralose-urethan-anesthetized, gallamine-paralyzed New Zealand White rabbits during 30-min episodes of either HCl or NaHCO3 intravenous infusions. ISF pH was measured continuously with glass microelectrodes (1- to 2-microns tip diameter). Cisternal CSF pH was measured continuously with an indwelling pH probe (1-mm tip diameter). Both ventral medullary and thalamic ISF [H+] changed significantly, whereas arterial PCO2 remained constant. CSF [H+] did not change. We conclude from these data that 1) changes in blood acid-base conditions are rapidly reflected in cerebral ISF and 2) transient differences in [H+] and [HCO-3] can exist between cerebral ISF and CSF.

Isolation of interstitial fluid from rat mammary tumors by a centrifugation method

2003 ◽  
Vol 284 (1) ◽  
pp. H416-H424 ◽  
Author(s):  
Helge Wiig ◽  
Knut Aukland ◽  
Olav Tenstad
Keyword(s):  
Interstitial Fluid ◽  
Tumor Tissue ◽  
Venous Blood ◽  
Lymphatic Drainage ◽  
Colloid Osmotic Pressure ◽  
Low Molecular Weight ◽  
Tissue Fluid ◽  
Arterial Plasma ◽  
Lower Ratio ◽  
Superficial Tumor

Access to interstitial fluid is of fundamental importance to understand tumor transcapillary fluid balance, including the distribution of probes and therapeutic agents. Tumors were induced by gavage of 9,10-dimethyl-1,2-benzanthracene to rats, and fluid was isolated after anesthesia by exposing tissue to consecutive centrifugations from 27 to 6,800 g. The observed51Cr-EDTA (extracellular tracer) tissue fluid-to-plasma ratio obtained from whole tumor or from superficial tumor tissue by centrifugation at 27–424 g was not significantly different from 1.0 (0.92–0.99), suggesting an extracellular origin only. However, fluid collected from excised central tumor parts had a significantly lower ratio (0.66–0.77) for all imposed G forces, suggesting dilution by fluid deriving from a space unavailable for51Cr-EDTA. The colloid osmotic pressure in tumor fluid was generally higher than in fluid isolated from the subcutis, attributable to less selective capillaries and impaired lymphatic drainage in tumors. HPLC analysis of tumor fluid showed that low-molecular-weight macromolecules not present in arterial plasma were present in tumor fluid obtained by centrifugation and in venous blood draining the tumor, most likely representing proteins derived from tumor cells. We conclude that low-speed centrifugation may be a simple and reliable method to isolate interstitial fluid from tumors.

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