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Abstracts for Bohr Effect and Cell Oxygenation: Healthy vs. Sick People

Aarnoudse JG, Oeseburg B, Kwant G, Zwart A, Zijlstra WG, Huisjes HJ, Influence of variations in pH and PCO2 on scalp tissue oxygen tension and carotid arterial oxygen tension in the fetal lamb, Biol Neonate 1981; 40(5-6): p. 252-263.

A description is given of the effect of hypercapnic acidaemia and hypocapnic alkalaemia on scalp tissue PO2 as measured with a subcutaneous needle-electrode and a transcutaneous electrode in 6 fetal lambs. The experiments were carried out under general anaesthesia with the fetus kept in utero. Hypocapnia was induced by hyperventilating the ewe and hypercapnia was achieved by administering extra CO2 to the ewe. Fetal carotid arterial, subcutaneous and transcutaneous PO2 were continuously recorded, and fetal and maternal arterial pH and arterial PCO2 were determined from blood samples taken at short intervals. In each experiment the H+ Bohr factor of fetal and maternal blood was measured. During hypocapnic alkalaemia, there was a fall in all fetal PO2 levels, whereas a marked rise was observed during hypercapnic acidaemia. The variations in fetal PO2 observed in vivo even exceeded the variations due to the H+ Bohr effect (measured in vitro). This was due to small variations in fetal carotid arterial oxygen saturation, which tended to fall during hypocapnic alkalaemia and to rise during hypercapnic acidaemia. The results of these findings strongly suggest that tissue PO2, as measured with the subcutaneous and transcutaneous electrodes, is dependent on the H+ Bohr effect. This adds to the uncertainty as to the value of subcutaneous and transcutaneous PO2 monitoring during labour as an early warning system for impending fetal asphyxia.

Braumann KM, Böning D, Trost F, Bohr effect and slope of the oxygen dissociation curve after physical training, J Appl Physiol. 1982 Jun; 52(6): p. 1524-1529.

Three O2 dissociation curves from venous blood [taken at rest (A), after in vitro acidification with lactic acid (B), and after exhaustive exercise (C)] were determined in eight athletes twice in a year in detrained and fully trained state. The steepness of the standard O2 dissociation curve becomes greater during the training period (increase in Hill's n from 2.68 +/- 0.10 to 2.96 +/- 0.15). There was a concomitant small rise in the intraerythrocytic organic phosphate concentrations. Bohr coefficients (BC) were calculated for blood O2 saturations ranging from 10 to 80% by comparing the dissociation curves A and B ("in vitro" BC) and curves A and C ("in vivo" BC). In detrained and trained state the in vivo BC show their maximal values at low saturation levels, in contrast the in vitro BC exhibit maximal values at middle saturations. During the training period there was an increase in the in vivo BC as well as in the in vitro BC at low saturations. These alterations may lead to augmented O2 extraction from a given volume of blood by up to 15% during heavy work in trained state. The reason for these observations could be an altered erythrocyte population.

Böning D, Schwiegart U, Tibes U, Hemmer B, Influences of exercise and endurance training on the oxygen dissociation curve of blood under in vivo and in vitro conditions, Eur J Appl Physiol Occup Physiol. 1975; 34(1): p. 1-10.

In experiments with graded exercise of 15 men (6 untrained, 3 semitrained, 6 endurance-trained) the trained subjects showed a massive shift to the right of the in vivo O2 dissociation curve (ODC) of femoral venous blood. At a saturation of 20 to 25% (18 mkp/sec) Po2 was about 9 mm Hg higher for the trained than for the untrained group. The following factors play a role: 1. The 2,3-diphosphoglycerate [2,3-DPG] concentration was increased by 15 to 20% in the trained group which explains about 2 mm Hg of the diffenence in Po2-2. Exercise acidosis in the femoral venous blood depends to a large extent on CO2 in the trained, but on lactic acid in the untrained group. At low saturations the CO2-Bohr effect increases sharply thus having a greater importance in the trained subjects. This factor can explain about 2 mm Hg of the difference. However, influence of chloride and 2,3-DPG on the Bohr effect must be taken into consideration. 3. Since the large ODC-shift to the right of the trained group was not reproducible under in vitro conditions, it is suggested that a rapidly decaying unknown substance accounts for the remaining difference in Po2.

Bucci E, Fronticelli C, Anion Bohr effect of human hemoglobin, Biochemistry. 1985 Jan 15; 24(2): p. 371-376.

The pH dependence of oxygen affinity of hemoglobin (Bohr effect) is due to ligand-linked pK shifts of ionizable groups. Attempt to identify these groups has produced controversial data and interpretations. In a further attempt to clarify the situation, we noticed that hemoglobin alkylated in its liganded form lost the Bohr effect while hemoglobin alkylated in its unliganded form showed the presence of a practically unmodified Bohr effect. In spite of this difference, analyses of the extent of alkylation of the two compounds failed to identify the presence of specific preferential alkylations. In particular, the alpha 1 valines and beta 146 histidines appeared to be alkylated to the same extent in the two proteins. Focusing our attention on the effect of the anions on the functional properties of hemoglobin, we measured the Bohr effect of untreated hemoglobin in buffers made with HEPES [N-(2-hydroxyethyl)piperazine-N'-2-ethanesulfonic acid], MES [2-(N-morpholino)ethanesulfonic acid], and MOPS [3-(N-morpholino)propanesulfonic acid], which being zwitterions do not need addition of chlorides or other anions for reaching the desired pH. The shape acquired by the Bohr effect curves, either as pH dependence of oxygen affinity or as pH dependence of protons exchanged with the solution, was irreconcilable with that of the Bohr effect curves in usual buffers. This indicated the relevance of solvent components in determining the functional properties of hemoglobin. A new thermodynamic model is proposed for the Bohr effect that includes the interaction of hemoglobin with solvent components. The classic proton Bohr effect is a special case of the new theory.

Carter AM, Grønlund J, Contribution of the Bohr effect to the fall in fetal PO2 caused by maternal alkalosis, J Perinat Med. 1985; 13(4): p.185-191.

A decrease in the PO2 of fetal arterial blood is observed in maternal alkalosis caused by hyperventilation in labour or exercise. The contribution of altered blood oxygen affinity to this effect was studied experimentally and by computer simulation of placental gas exchange. Thirteen guinea pigs near term of pregnancy were anesthetized and the right atrium of the fetus was catheterized to enable continuous and simultaneous measurement of PO2 and PCO2 by mass spectrometry. An infusion of base was given through a catheter in the descending aorta of the dam and the effect on fetal respiratory gas tensions observed. The mean change in maternal arterial pH measured in blood taken from a femoral artery was 0.07 +/- 0.04 (mean +/- S. D.). There was an immediate decrease in PO2 in the right atrium of the fetus, but no consistent alteration in PCO2. Two minutes after the start of the infusion, PO2 had fallen by 3.2 +/- 1.6 Torr (p less than 0.001) and PCO2 had risen by 1.7 +/- 1.8 Torr (not significant). The experiments were simulated using a mathematical model of placental gas exchange in the guinea pig. The model was able to predict the change in fetal arterial PO2, given numerical values for the pH, PO2 and PCO2 of fetal and maternal arterial blood prior to infusion of base and for maternal blood during the infusion of base. These values were obtained from the experimental data. Other input variables of the model were maternal and fetal hematocrit and DPG concentration, and the rates of blood flow on the two sides of the placenta.(ABSTRACT TRUNCATED AT 250 WORDS)

diBella G, Scandariato G, Suriano O, Rizzo A, Oxygen affinity and Bohr effect responses to 2,3-diphosphoglycerate in equine and human blood, Res Vet Sci. 1996 May; 60(3): p. 272-275.

Lung Function Unit, Ospedale Cervello, Palermo, Italy.

The dependence of blood oxygen affinity and the Bohr effect on the concentration of 2,3-diphosphoglycerate (DPG) in erythrocytes was investigated in 24 trotter horses and 24 healthy men. The oxygen tension at half saturation and standard conditions (P50st at pH 7.4, PCO2(40) mmHg and 37 degrees C) and the carbon dioxide or fixed-acid-induced Bohr effect (dlogP50/dpH) were determined. Samples of fresh blood and blood depleted of or enriched with DPG were studied. In the absence of measurable DPG, the equine and human blood had similar mean (SD) values of P50st (16.6 [0.6] and 16.2 [0.7] mmHg, respectively). In both species these values increased with increasing DPG, but the response of equine blood was significantly lower, at least up to physiological values (P50st = 24.6 [0.6] and 26.2 [0.7]) mmHg; DPG = 14([1.8] and 12.8 [1.2] mumol gHb-1, respectively, in fresh blood). For concentrations above 20 to 25 mumol gHb-1 of DPG the difference between the values of P50st in the two species tended to decrease because the response in human blood reached a plateau. The interactions between the Bohr effect and the concentration of DPG showed that in the horses, as in the men, the level of DPG played an important role in governing the relative magnitude of carbon dioxide and fixed acid factors. The difference between them, which is associated with the oxylabile carbamino binding, was greatest in DPG-depleted blood, but whereas in the men the difference was suppressed by an above normal DPG concentration, in the horses it was still measurable.

Dzhagarov BM, Kruk NN, The alkaline Bohr effect: regulation of O2 binding with triliganded hemoglobin Hb(O2)3 [Article in Russian] Biofizika. 1996 May-Jun; 41(3): p. 606-612.

The processes of the proton concentration effect on the oxygen binding with triliganded human hemoglobin Hb(O2)3 have been studied by time resolved absorption spectroscopy. The pH-dependencies analysis carried out has shown that R-state alkaline Bohr effect was formed by two amino acid residues with pK = 7.3 +/- 0.1 and 9.1 +/- 0.1. It has been shown that oxygen affinity decrease at pH values above 8.5 could be caused by alpha 140-Tyr and beta 145-Tyr. The entrance and exit into/from the globin matrix is controlled by the same amino acid residues. On the strength of the experimental data the dynamics nature of the R-state alkaline Bohr effect has been proved.

Gersonde K, Sick H, Overkamp M, Smith KM, Parish DW, Bohr effect in monomeric insect haemoglobins controlled by O2 off-rate and modulated by haem-rotational disorder, Eur J Biochem. 1986 Jun 2; 157(2): p. 393-404.

The monomeric insect (Chironomus thummi thummi) haemoglobins CTT III and CTT IV show an alkaline Bohr effect. The amplitude of the Bohr effect curve of CTT IV is about twice as large as that of CTT III. In particular, at low pH a time-dependent 'slow' decrease in p50 upon cyclic oxygenation/deoxygenation is observed which is larger if dithionite, instead of ascorbate, is the reducing agent. The decrease of p50 (increase in affinity) correlates with the ratio of haem-rotational components exhibiting an increase of the 'myoglobin-like' haem-rotational component with high O2 affinity and high stability of the globin-haem complex. The replacement of protohaem IX by mesohaem IX and deuterohaem IX, respectively, causes an increase in O2 affinity following the order: proto less than meso less than deutero CTT Hbs. The Bohr effect, however, seems not to be affected by these porphyrin side-group substitutions. The O2 affinity is modulated by steric effects due to the substituents in position 2 and 4 via variation of the protein-haem interactions which influence the O2 release. The replacement of iron by cobalt in proto and meso CTT IV leads to an increase of the p50 by two to three orders of magnitude. Neither central metal nor vinyl replacement affect the Bohr effect. The natural CTT Hbs III and IV analyzed for mono-componential kinetic systems exhibit pH-dependent O2 off-rate constants: 300 s-1 (at pH 5.6) and 125 s-1 (at pH 9.7) for CTT III, and 550 s-1 (at pH 5.4) and 100 s-1 (at pH 9.0) for CTT IV. Inflection points and amplitudes of the log koff/pH plots correspond to those obtained from the Bohr effect curves indicating again a larger Bohr effect for CTT IV than for CTT III. In contrast, the O2 on-rate constants are pH-independent (kon = 1.15-1.26 X 10(8) M-1 s-1). Thus, the Bohr effect is completely controlled by the off-rate constants. Analysis for bi-componential kinetic systems employing the eigenfunction expansion method clearly identifies two kinetic components for proto-IX and deutero-IX CTT Hbs which can be attributed to the two haem-rotational components x and y (x and y differ due to an 180 degree rotation of the haem group about the alpha,gamma-meso axis; y is the myoglobin-like haem-rotational component).(ABSTRACT TRUNCATED AT 400 WORDS)

Grant BJ, Influence of Bohr-Haldane effect on steady-state gas exchange, J Appl Physiol. 1982 May; 52(5): p. 1330-1337.

The influence of the Bohr-Haldane effect (BH) on steady-state gas exchange has previously been described by its effect of gas transfer from the blood when arterial and venous blood gas tensions were held constant. This report quantifies by computer analysis the effects of BH when either or both arterial and venous blood gas tensions are subject to change. When mixed venous blood gas composition is held constant, elimination of BH from a single lung unit typically reduces CO2 output by 6.5% and O2 uptake by 0.5%. Similar effects occur in a two-compartment lung model whether alveolar ventilation-perfusion (VA/Q) mismatch occurs in a parallel or series ventilatory arrangement. When arterial blood gas composition is held constant, elimination of BH increases systemic venous CO2 partial pressure, but O2 partial pressure is hardly affected in the absence of metabolic acidosis. When both mixed venous and arterial blood gas tensions vary and gas exchange is stressed by VA/Q inequality, altitude, anemia, or exercise, elimination of BH predominantly affects mixed venous rather than arterial blood gas tensions. it is concluded that BH may act primarily to reduce tissue acidosis.

Gottstein U, Zahn U, Held K, Gabriel FH, Textor T, Berghoff W, Effect of hyperventilation on cerebral blood flow and metabolism in man; continuous monitoring of arterio-cerebral venous glucose differences (author's transl) [Article in German], Klin Wochenschr. 1976 Apr 15; 54(8): p. 373-381.
CBF decreases when arterial PCO2 is lowered by physiological, pathological or therapeutically induced hyperventilation. This is accompanied by an undelayed compensatory increase of oxygen-av-differences. Continuous monitoring of enzymatically determined glucose-av-differences of the brain during hyperventilation has for the first time shown that there is an undelayed fall of the cerebral venous glucose content, too. This indicates that the brain cells extract an augmented amount of glucose per ml blood during decreased CBF. Therefore glucose metabolism of the brain is not impaired during non-critical CBF reduction. However, when arterial PCO2 falls below 25 mmHg a detrimental effect on CBF and cerebral metabolism has to be expected. CBF will then decrease below the critical threshold for an undisturbed oxygen supply, and the respiratory alcalosis will lead to a disturbed oxygen delivery due to the Bohr-effect. As a consequence both of these factors will reduce the energy-yielding oxydative glycolysis and augment the little energy producing anaerobic glycolysis with a concomitant increase of lactate formation, resulting in a tissue and spinal fluid lactate acidosis. From our results it is therefore concluded that induced hyperventilation should be avoided, and that central hyperventilation in diseased states has to be considered as an additional threat to the brain.

Grubb B, Jones JH, Schmidt-Nielsen K, Avian cerebral blood flow: influence of the Bohr effect on oxygen supply, Am J Physiol. 1979 May; 236(5): p. H744-749.

To clarify the problems of altitude tolerance in birds, we studied the combined effect of hypocapnia and hypoxia on cerebral blood flow (CBF) in ducks. CBF was measured by the xenon clearance method. Normocapnic hypoxia causes CBF to increase when the arterial O2 tension (PaO2) falls below 60--70 mmHg. Hypocapnic hypoxia significantly shifts the blood flow curve so that blood flow does not increase until a lower PaO2 (50--60 mmHg) is reached. This gives the appearance that hypocapnia suppresses the hypoxia-induced increase in CBF. However, due to the Bohr effect, the hypocapnic blood contains significantly more O2 than does the normocapnic blood at the same PaO2. Therefore, when CBF is expressed as a function of O2 content, rather than PO2, CBF in the hypocapnic group does not differ significantly from the CBF in the normocapnic group. We interpret this to mean that because of the significantly greater oxygen content of the hypocapnic blood at a given PaO2, the degree of hypoxia experienced by these brains is not as severe as that experienced by the normocapnic brains.

Hlastala MP, Woodson RD, Bohr effect data for blood gas calculations, J Appl Physiol. 1983 Sep; 55(3): p. 1002-1007.

The oxygen dissociation curve (ODC) and Bohr effect of human blood were measured over a wide range of acid-base conditions and blood-O2 saturations at normal and low 2,3-diphosphoglycerate (DPG) concentrations. The fixed-acid Bohr factor (H+ titration) was relatively constant as a function of O2 saturation. At normal DPG levels, the H+ Bohr factor was not dependent on PCO2 except for a modest increase (in absolute magnitude) at very low PCO2 (7 Torr). For low DPG blood, the H+ Bohr factor decreased markedly with increasing PCO2 such that at PCO2 101 Torr, delta log PO2/delta pH varied between 0 and -0.13. The CO2 Bohr factor (CO2 titration) was strongly dependent on O2 saturation, being greatest at low O2 saturation. For normal DPG blood, this factor did not differ significantly at base excess (BE) +0.1 and +19.5 mmol/l, but decreased slightly at BE -20.3 mmol/l. For low DPG blood this factor showed a modest decrease with BE from -0.5 to +19.5 mmol/l but increased appreciably at BE -18.6 mmol/l. The data indicate that the Bohr factor may vary from unmeasurable levels to -0.93 under physiological and pathophysiological conditions. Results allow calculation of the shape and position of the ODC under the diverse conditions which may attend gas exchange.

Jensen FB, Red blood cell pH, the Bohr effect, and other oxygenation-linked phenomena in blood O2 and CO2 transport, Acta Physiol Scand. 2004 Nov; 182(3): p. 215-227.

Institute of Biology, University of Southern Denmark, Odense, Denmark.

The discovery of the S-shaped O2 equilibrium curve and the Bohr effect in 1904 stimulated a fertile and continued research into respiratory functions of blood and allosteric mechanisms in haemoglobin (Hb). The Bohr effect (influence of pH/CO2 on Hb O2 affinity) and the reciprocal Haldane effect (influence of HbO2 saturation on H+/CO2 binding) originate in the Hb oxy-deoxy conformational change and allosteric interactions between O2 and H+/CO2 binding sites. In steady state, H+ is passively distributed across the vertebrate red blood cell (RBC) membrane, and intracellular pH (pHi) changes are related to changes in extracellular pH, Hb-O2 saturation and RBC organic phosphate content. As the Hb molecule shifts between the oxy and deoxy conformation in arterial-venous gas transport, it delivers O2 and takes up CO2 and H+ in tissue capillaries (elegantly aided by the Bohr effect). Concomitantly, the RBC may sense local O2 demand via the degree of Hb deoxygenation and release vasodilatory agents to match local blood flow with requirements. Three recent hypotheses suggest (1) release of NO from S-nitroso-Hb upon deoxygenation, (2) reduction of nitrite to vasoactive NO by deoxy haems, and (3) release of ATP. Inside RBCs, carbonic anhydrase (CA) provides fast hydration of metabolic CO2 and ensures that the Bohr shift occurs during capillary transit. The formed H+ is bound to Hb (Haldane effect) while HCO3- is shifted to plasma via the anion exchanger (AE1). The magnitude of the oxylabile H+ binding shows characteristic differences among vertebrates. Alternative strategies for CO2 transport include direct HCO3- binding to deoxyHb in crocodilians, and high intracellular free [HCO3-] (due to high pHi) in lampreys. At the RBC membrane, CA, AE1 and other proteins may associate into what appears to be an integrated gas exchange metabolon. Oxygenation-linked binding of Hb to the membrane may regulate glycolysis in mammals and perhaps also oxygen-sensitive ion transport involved in RBC volume and pHi regulation. Blood O2 transport shows several adaptive changes during exposure to environmental hypoxia. The Bohr effect is involved via the respiratory alkalosis induced by hyperventilation, and also via the pHi change that results from modulation of RBC organic phosphate content. In teleost fish, beta-adrenergic activation of Na+/H+ exchange rapidly elevates pHi and O2 affinity, particularly under low O2 conditions.

Kister J, Marden MC, Bohn B, Poyart C, Functional properties of hemoglobin in human red cells: II. Determination of the Bohr effect, Respir Physiol. 1988 Sep; 73(3): p. 363-378.

INSERM U 299, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France.

Parameters of the Bohr effect (delta log P50/delta pHi) for human normal red blood cell suspensions have been calculated between intracellular pH (pHi) 5.5 and 8.5, in order to test how these quantities compare with those measured in dilute human hemoglobin solution (Hb). For a precise comparison between red cell and Hb solutions data, the cells were fractionated to reduce cellular heterogeneity and depleted of their 2,3-diphosphoglycerate (DPG) content. The P50 values were related to pHi. From the value of the Donnan equilibrium factor rH+ and the cellular water content at each extracellular pH (pHe), the variations of the intracellular chloride concentration were calculated. This quantity exhibited a three fold change between pHi 5.5 and 8.5, with extracellular chloride concentration [Cl-]e fixed at 140 mM. In the absence of DPG, chloride is the main allosteric effector of Hb and increases the alkaline Bohr effect. When all these interacting factors are accounted for, the oxygen affinity and Bohr parameters for red cell suspensions become identical to those observed for dilute Hb solutions. These results indicate that the hydration of the Hb molecules in the highly concentrated red cell milieu is not much different from that of nearly ideal solutions.

Kobayashi H, Pelster B, Piiper J, Scheid P, Significance of the Bohr effect for body oxygen level in a model with counter-current blood flow, Respir Physiol. 1989 Jun; 76(3): p. 277-288.

Institut für Physiologie, Ruhr-Universität, Bochum, F.R.G.

Counter-current arrangement of afferent and efferent blood flow in tissues is commonly considered to be detrimental to tissue oxygenation, since O2 diffusion would shunt O2 away from the tissue. We have investigated the combined effects of counter-current CO2 and O2 exchange in a simple model, paying particular attention to the Bohr effect. We have obtained the following main results. (1) Back-diffusion of CO2 leads to increasing CO2 partial pressure (PCO2) and CO2 content along the afferent vessel. This is enhanced when fixed acid is released by the tissue into the venous blood, e.g. during hypoxia, which leads to a further PCO2 increase therein. (2) The increasing PCO2, with concomitant decrease in pH, in the afferent blood leads to a decrease in blood O2 affinity (Bohr effect) and thus results in increased PO2. (3) The resulting O2 diffusion shunt diminishes the O2 content in afferent blood, but for most conditions its PO2 remains higher than without the Bohr effect. (4) During hypoxia, both the PO2 in blood reaching the tissue (Pta) as well as in that leaving it (Ptv) are significantly elevated above the level without the Bohr effect. Moreover, with fixed acid release both Pta and Ptv for O2 can be higher than the arterial PO2 value. (5) During hyperoxia, O2 diffusion shunt prevents the tissue PO2 levels from increasing to levels that might be regarded as toxic. It is concluded that a diffusion shunt in tissues stabilizes the O2 partial pressure at the tissue when it varies in arterial blood (hypoxia or hyperoxia).

Lapennas GN, The magnitude of the Bohr coefficient: optimal for oxygen delivery, Respir Physiol. 1983 Nov; 54(2): p.161-172.

This paper examines relationships between the magnitude of the blood Bohr coefficient and arterial-venous changes in blood pH, PCO2 and oxygen affinity during steady-state, aerobic gas exchange. The physical-chemical linkage of the Bohr and Haldane effects is taken into account. It is concluded that for blood in which there is negligible oxygen-linked carbamate formation: (a) arterial-venous pH and PCO2 changes would be minimized if the Bohr coefficient were approximately equal to the respiratory quotient, with opposite sign, and (b) the rightward shift of the oxygen equilibrium curve in the tissues, relative to the curve at arterial pH, would be maximal if the Bohr coefficient were about one half the respiratory quotient (Bohr coefficient -0.35 to -0.5 for RQ 07-1.0). Actual Bohr coefficients in several mammals maximize the right shift of the oxygen equilibrium curve and are therefore optimal for oxygen delivery. Actual Bohr coefficients do not minimize pH or PCO2 changes. These results suggest that the contribution of the Bohr-Haldane effect to oxygen transport is more important than its contribution to pH homeostasis or CO2 transport.

Matthew JB, Hanania GI, Gurd FR, Electrostatic effects in hemoglobin: Bohr effect and ionic strength dependence of individual groups, Biochemistry. 1979 May 15; 18(10): p.1928-1936.

The electrostatic treatment applied in the preceding paper in this issue [Matthew, J. B., Hanania, G.I.H., & Gurd, F.R.N. (1979) Biochemistry (preceding paper in this issue)] to the titration behavior of individual groups in human deoxyhemoglobin and oxyhemoglobin was applied to the computation of the alkaline Bohr effect at various values of ionic strength. The enhanced proton binding of deoxyhemoglobin in the pH range of 6--9 was accounted for at ionic strength 0.01 M by the effects of the unique charge distributions of ionizable groups in the two quaternary states. At ionic strength 0.10 M the effects of 2--4 bound anions had to be considered in addition in the deoxyhemoglobin charge configuration. At the higher ionic strength 10 groups per tetramer contributed to the Bohr effect, whereas 28 groups were contributory at the lower ionic strength. The ionic strength dependence of individual groups in the two tetrameric structures as well as in the alpha-chain monomer was explained in terms of the electrostatic treatment. This examination showed that the differences in electrostatic behavior of deoxy- and oxyhemoglobin follow from particular dissymmetries in their configurations with respect to charge and static solvent accessibility.

Meyer M, Holle JP, Scheid P, Bohr effect induced by CO2 and fixed acid at various levels of O2 saturation in duck blood, Pflugers Arch. 1978 Sep 29; 376(3): p. 237-240.

The Bohr factor, phi = delta log Po2/deltapH, was determined at various levels of hemoglobin O2 saturation (SO2) in fresh whole blood of the duck. Plasma pH was varied by either changing PCO2 of the blood at constant base excess (CO2 Bohr factor, phiCO2) or by addition of NaHCO3 and HCl at constant PCO2 (fixed acid BOHR factor, phiAH). No differences were found between phiCO2 and phiAH at SO2 levels between 20 and 85%, and there was no saturation dependence of the Bohr factor, its average value being -0.44. It is concluded that in whole blood of this bird species CO2 exerts no direct effect on the O2 affinity of hemoglobin.

Monday LA, Tétreault L, Hyperventilation and vertigo, Laryngoscope 1980 Jun; 90(6 Pt 1): p.1003-1010.

An electronystagmographic study was conducted on 19 normal subjects, in order to observe whether the subjective sensation of dizziness provoked by hyperventilation could be confirmed objectively by nystagmus. Each of them had two electronystagmograms, the first being a routine ENG and the second a repetition of the first, but with additional periods of 90 sec. of hyperventilation at certain precise pre-determined moments of the test. Hyperventilation was not shown to have significant effect on the slow phase of post caloric nystagmus; however, it increased significantly (p = 0.061) the number of positions in which nystagmus was elicited. Hyperventilation would have such an effect in producing a certain degree of cerebral hypoxia through cerebral vasoconstriction and the Bohr effect.

Tyuma I, The Bohr effect and the Haldane effect in human hemoglobin, Jpn J Physiol. 1984; 34(2): p.205-216.

Protons and carbon dioxide are physiological regulators for the oxygen affinity of hemoglobin. The heterotropic allosteric interaction between the non-heme ligands and oxygen, collectively called the Bohr effect, facilitates not only the transport of oxygen but also the exchange of carbon dioxide. Several types of interactions can be thermodynamically formulated. The Bohr and Haldane coefficients and the classical Bohr and Haldane coefficients are thus explicitly defined, which will save confusion about the use of the term "Bohr effect" seen in the literature. Molecular mechanism and the physiological significance of the classical Bohr and Haldane effects are outlined. The latter effect seems to play a far greater physiological role than the reciprocal influence of carbon dioxide on oxygen transport--the classical Bohr effect.

Winslow RM, Monge C, Winslow NJ, Gibson CG, Whittembury J, Normal whole blood Bohr effect in Peruvian natives of high altitude, Respir Physiol. 1985 Aug; 61(2): p. 197-208.

Measurements of whole blood O2 affinity were made with an automatic technique that allowed recording of O2 saturation continuously over a range of PO2 of 1 to 150 torr at constant pH and PCO2 with fresh samples of blood obtained from 5 natives of high altitude at Morococha, Peru (altitude, 4540 m). The results were not significantly different from those obtained with controls living at sea level with regard to the dlog P50/dpH slope at constant PCO2 or at constant base excess. Both results also agree with previous studies with normal sea-level blood. Thus earlier claims of an increased Bohr in Peruvian high-altitude natives is not supported.

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