Slow postcapillary pH changes in blood in anesthetized animals

1978 ◽  
Vol 45 (5) ◽  
pp. 674-680 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Blood Cells ◽  
Ph Change ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillary ◽  
Before And After ◽  
Equilibration Process ◽  
Contact Surfaces ◽  
Electrode Chamber

To investigate the hypothesis that blood pH and PCO2 continue to change after the blood leaves an exchange capillary, we used a rapidly responding, pressure-insensitive, stopped-flow pH electrode apparatus. Arterial blood from an anesthetized dog or cat is drawn through the apparatus into a syringe. Syringe movement is then suddenly stopped. Temperature and pH of the blood in the electrode assembly are continuously monitored, both before and after blood withdrawal ceases. Hemolysis was reduced by coating all blood contact surfaces with silicone and fasting the animal overnight, anesthetizing it with crystalline pentobarbital sodium, and allowing it to ventilate spontaneously. After stopping withdrawal, pH of blood in the electrode chamber continued to change, rising 0.01 unit with t1/2 of 4.4 s. After lysed blood was returned to the animal to provide carbonic anhydrase to the plasma, no pH change was seen after stopping the flow. The small pH rise occurring in arterial blood in vivo is probably due in large part to disequilibrium of [H+] between red blood cells and plasma at the end of the pulmonary capillary, the equilibration process being rate-limited by the extracellular CO2 hydration-dehydration reaction.

Slow postcapillary changes in blood pH in vivo: titration with acetazolamide

1978 ◽  
Vol 45 (4) ◽  
pp. 565-573 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Carbonic Anhydrase ◽  
Transport Processes ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillaries ◽  
Before And After ◽  
Time Courses ◽  
Electrode Chamber ◽  
Good Agreement

A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.

Postcapillary changes in blood pH in vivo during carbonic anhydrase inhibition

1977 ◽  
Vol 43 (4) ◽  
pp. 582-590 ◽  
Author(s):  
E. D. Crandall ◽  
A. Bidani ◽  
R. E. Forster
Keyword(s):  
Carbonic Anhydrase ◽  
Carbonic Anhydrase Activity ◽  
Stopped Flow ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillary ◽  
Carbonic Anhydrase Inhibition ◽  
Glass Ph Electrode ◽  
Electrode Chamber

A rapidly responding stopped-flow glass pH electrode apparatus was used to investigate pH changes in blood in vivo after it exits from an exchange capillary. Arterial blood was drawn from anesthetized animals through the apparatus. Temperature and pH of the blood in the electrode chamber were continuously recorded, both during withdrawal and after flow was stopped. Blood pH did not change after stopping flow in control experiments. When benzolamide (2 mg/kg) was given to inhibit carbonic anhydrase activity available to plasma (e.g., due to lysis) while having less effect on intracellular activity, pH increased 0.02–0.04 (t1/2 approximately 8 s) after stopping flow. Administration of acetazolamide (50 mg/kg) resulted in pH decreasing 0.07–0.10 (t1/2 approximately 15 s) after stopping flow. Ventilation for 1 min with N2 resulted in an increased rise in pH for the benzolamide-treated animals but a decreased fall in pH for the acetazolamide-treated animals. These shifts in arterial blood pH after gas exchange are largely due to disequilibrium of [H+] between red cells and plasma at the end of the pulmonary capillary.

Adrenocortical response during corrected and uncorrected hypercapnic acidosis

1962 ◽  
Vol 202 (2) ◽  
pp. 334-336 ◽  
Author(s):  
Arnold Mittelman ◽  
Serge J. Dos ◽  
Harold G. Barker ◽  
Gabriel G. Nahas
Keyword(s):  
Flow Rate ◽  
Venous Blood ◽  
Concomitant Administration ◽  
Cortisol Secretion ◽  
Hypercapnic Acidosis ◽  
Sharp Reduction ◽  
Venous Flow ◽  
Arterial Blood ◽  
Blood Ph ◽  
Before And After

Adrenal venous flow rate and cortisol synthesis have been measured in dogs subjected to hypercapnic acidosis before and after intravenous administration of 0.34 mm/kg of tris (hydroxymethyl) amino methane (THAM). A comparison was made of adrenal venous, peripheral venous, and arterial blood, pH, pCO2 and O2 saturation. During uncorrected hypercapnic acidosis the concentration of cortisol increased while adrenal venous flow rate decreased, but there was a significant increase in the minute output of cortisol. With the concomitant administration of 0.34 mM/kg THAM, adrenal venous flow rate doubled. However, since this enhanced flow rate was accompanied by a sharp reduction in cortisol secretion, the minute output of cortisol returned to control levels. The possibility of a direct effect of THAM on the adrenal vascular bed and synthetic processes is discussed. Throughout all the above experiments adrenal venous blood resembled arterial blood rather than peripheral blood in its pCO2, O2 saturation and pH.

Acute Ammonia Toxicity and Ammonia Excretion in Rainbow Trout (Salmo gairdneri)

1979 ◽  
Vol 36 (6) ◽  
pp. 621-629 ◽  
Author(s):  
Betty A. Hillaby ◽  
David J. Randall
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Hydrogen Ion ◽  
Ammonia Toxicity ◽  
Salmo Gairdneri ◽  
Mean Values ◽  
Arterial Blood ◽  
Blood Ph ◽  
Before And After ◽  
Total Ammonia

Acute ammonia toxicity in rainbow trout (Salmo gairdneri) was studied by intraarterial injection of NH4Cl and NH4HCO3. Hydrogen ion and total ammonia concentrations were measured in blood sampled from the dorsal aorta both before and after injection. Although injection of NH4HCO3 increased arterial blood pH, and injection of NH4Cl decreased arterial blood pH, the same dose of each was required to kill fish. While the un-ionized form of ammonia in water has been shown to be toxic, in the blood either the ionized form or the total ammonia load is toxic to fish. Ammonia levels were measured in pre- and postbranchial blood. Mean values were not significantly different, but paired values indicated a fall in blood ammonia due to excretion across the gills. There appears to be a more rapid excretion of ammonia following NH4HCO3 infusions, which result in higher un-ionized ammonia levels in blood compared with those following NH4Cl infusions. These results are consistent with the hypothesis that ammonia is excreted in the un-ionized form. Key words: un-ionized ammonia, ionized ammonia, gills, pH, blood

An in vivo quantitative Raman-pH sensor of arterial blood based on laser trapping of erythrocytes

The Analyst ◽  
2016 ◽  
Vol 141 (10) ◽  
pp. 3027-3032 ◽  
Author(s):  
Manman Lin ◽  
Bin Xu ◽  
Huilu Yao ◽  
Aiguo Shen ◽  
Jiming Hu
Keyword(s):  
Ph Sensor ◽  
Laser Trapping ◽  
Arterial Blood ◽  
Blood Ph

A continuous and noninvasive approach is appliedin vivoto measure the arterial blood pH quantitatively.

scholarly journals Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

2007 ◽  
Vol 292 (3) ◽  
pp. G899-G904 ◽  
Author(s):  
Markus Sjöblom ◽  
Olof Nylander
Keyword(s):  
Base Excess ◽  
Ringer Solution ◽  
Bicarbonate Secretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
In Vivo Experiments ◽  
Arterial Blood ◽  
Blood Ph ◽  
Base Balance

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE2 was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15–7.21 and the base excess was about −8 mM at the end of experiments. The continuous infusion of Na2CO3 solution completely compensated for the acidosis. The blood pH was 7.36–7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE2-stimulated DMBS were markedly greater in animals treated with Na2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.

Perfusion of the Boar Testis with Androstenediol Sulfate in vivo and Studies on the in vitro Metabolism of Androgens by Porcine Blood Cells

1973 ◽  
Vol 51 (4) ◽  
pp. 390-396 ◽  
Author(s):  
M. A. Kraemer ◽  
J. I. Raeside
Keyword(s):  
Blood Cells ◽  
Dehydroepiandrosterone Sulfate ◽  
Spermatic Vein ◽  
In Vivo Studies ◽  
Similar Amount ◽  
Secretory Product ◽  
Arterial Blood ◽  
Almost All

An attempt was made to see if androstenediol sulfate, a normal secretory product of the boar testis, is important in testicular steroidogenesis in this species when perfused in vivo through the testis. Approximately 5 μCi of 7α-3H-androstenediol sulfate were administered via the spermatic artery to four, mature, anesthetized boars. Almost all of the radioactivity extracted from the spermatic vein blood and from the testis was associated with the unaltered substrate. Less than 0.2% of the substrate was isolated as 3H-dehydroepiandrosterone sulfate from the testicular extracts of one boar. An unsuccessful effort was made to characterize a similar amount of a metabolite present in extracts from spermatic vein blood of the same animal. The total amount of radioactivity which was associated with the free steroids represented about 0.2% of the administered dose of 3H-androstenediol sulfate given to each boar.17β-Hydroxysteroid dehydrogenase activity was demonstrated in a series of incubations of steroids with blood cells of the boar. Unconjugated Δ5-steroids were converted to a greater extent than were the Δ4-steroids (3.33 and 3.91% for DHA and androstenediol, respectively; 1.23 and 0.92% for androstenedione and testosterone, respectively). Androstenediol sulfate was converted to dehydroepiandrosterone sulfate (0.42%) but the reverse reaction was not observed. These findings were considered in relation to the in vivo studies. It was concluded that androstenediol sulfate in arterial blood entering the boar testis was not metabolized appreciably.

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of metabolic acidosis on proximal tubular total CO2 absorption

1985 ◽  
Vol 249 (1) ◽  
pp. F62-F68 ◽  
Author(s):  
R. T. Kunau ◽  
J. I. Hart ◽  
K. A. Walker
Keyword(s):  
Metabolic Acidosis ◽  
Proximal Tubule ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Co2 Absorption ◽  
Arterial Blood ◽  
Blood Ph ◽  
In Series ◽  
Proximal Tubular

In vivo microperfusion studies of the proximal convoluted tubule of the rat were performed to determine the effect of metabolic acidosis on total CO2 (tCO2) absorption. In series I, tubular perfusion was performed in control and acidotic rats in a manner by which similar mean total CO2 concentrations in the proximal tubule were maintained. Comparable ranges of perfusion rate were studied in both groups. Following 3 days of HCl ingestion, plasma tCO2 was 20.0 +/- 0.9 mM in the acidotic rats whereas it was 29.6 +/- 0.53 mM in control rats. The arterial blood pH values were 7.25 +/- 0.02 vs. 7.43 +/- 0.01. Starting tCO2 perfusate concentrations were identical in both groups, 29.3 and 29.7 mM, as were the concentrations at the end of the perfused segments, 21.2 and 21.9 mM. The absorption of tCO2 (JtCO2, pmol X mm-1 X min-1) was significantly greater in the acidotic rats than in the controls, 576 +/- 39 vs. 256 +/- 21. At all perfusion rates studied, proximal tubular JtCO2 was higher in the acidotic than in the control rats. In series II, similar lengths of the late proximal tubule were perfused at the same rate in control and acidotic rats. Again, JtCO2 was higher in the acidotic rats, 352 +/- 19 vs. 198 +/- 13. The results indicate that at comparable luminal tCO2 concentration and tubular fluid flow rates, tCO2 absorption is significantly increased in the acidotic state. Although other mechanisms cannot be excluded, the finding of an increase in proximal tCO2 absorption in the acidotic rats is in agreement with the presence of an accelerated Na+/H+ exchange rate in brush border membrane vesicles obtained from the renal cortex of animals with metabolic acidosis.

The effects of softwater acclimation on respiratory gas transfer in the rainbow trout Oncorhynchus mykiss

1995 ◽  
Vol 198 (12) ◽  
pp. 2557-2567 ◽  
Author(s):  
A M Greco ◽  
K M Gilmour ◽  
J C Fenwick ◽  
S F Perry
Keyword(s):  
Oncorhynchus Mykiss ◽  
Respiratory Alkalosis ◽  
Soft Water ◽  
Gas Transfer ◽  
O2 Uptake ◽  
Ventilation Frequency ◽  
Arterial Blood ◽  
Blood Ph ◽  
Co2 Excretion

Gill O2 uptake, CO2 excretion, ventilation and blood respiratory/acid­base variables were evaluated in control and softwater-acclimated trout (Oncorhynchus mykiss) to test the hypothesis that gill chloride cell (CC) proliferation, elicited by 2 weeks of softwater exposure, impairs the diffusion of respiratory gases across the gill. The proliferation of CCs in softwater fish was verified using light microscopy, and its impact on respiratory gas transfer was assessed in vivo by continuous monitoring of arterial blood PO2 (PaO2), PCO2 (PaCO2) and pH (pHa) using an extracorporeal blood circulation under conditions of normoxia and graded hypoxia [water PO2 (PwO2) was lowered from 20.0 kPa to 5.3 kPa within 20 min]. During normoxia, ventilation frequency was significantly higher in the softwater trout (78±4 versus 57±4 breaths min-1; mean ± s.e.m.), while ventilation amplitude was similar in both groups (1.0­1.1 cm opercular displacement). PaCO2 and plasma HCO3- concentration were significantly lower in the softwater fish and the blood acid­base status was characterized by a mixed respiratory alkalosis and metabolic acidosis such that blood pH was not statistically different between the two groups. CO2 excretion (2.5­2.8 mmol kg-1 h-1) and O2 uptake rates (2.3­5.1 mmol kg-1 h-1), as measured during normoxia, were unaffected by acclimation to soft water. During hypoxia, ventilation frequency and amplitude increased in the control trout, whereas only ventilation amplitude increased in the softwater-acclimated fish. The rate of PaO2 reduction during hypoxia was significantly greater in the softwater fish (0.84±0.06 versus 0.65±0.06 kPa PaO2 kPa-1 PwO2) and, at the most severe level of hypoxia (PwO2=5.3 kPa), PaO2 was significantly lower in the softwater fish. The rate of PaCO2 reduction (caused by hyperventilation) was significantly lower in the softwater-acclimated fish (0.002±0.001 versus 0.005±0.001 kPa PaCO2 kPa-1 PwO2; mean ± s.e.m.; P<0.06) and, indeed, was not statistically different from zero. Blood pH did not change significantly during hypoxia in either group but, through much of the hypoxic period (7­15 kPa PwO2), pHa was statistically lower in the softwater-acclimated fish. These results demonstrate that exposure of trout to soft water for 2 weeks is associated with proliferation of lamellar CCs and impaired branchial gas transfer. Hyperventilation was identified as a compensatory physiological adjustment.

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