Distribution of the myocardial tissuePO2 in the rat and the inhomogeneity of the coronary bed

The structural inhomogeneity of the myocardial capillary bed is simulated by microcirculatory units (MCU's) in a diffusion model. This simulation is based on MCU's in which the arrangement of the capillary ends (concurrent structure, partial and total countercurrent structure, helical structure) as well as the structure and supply parameters are varied. The variation of these parameters is based on own measurements of the intracapillary HbO₂ saturation as well as on the following parameters from the literature: frequency distribution of capillary distance and capillary radius, mean capillary length or capillary section length respectively, arterial and mean venousPO₂, mean coronary blood flow, mean O₂ consumption and diffusion conductivity. The analysis of O₂ supply of the normoxic rat heart shows that an O₂ diffusion shunt is obligatory except for MCU's with an extremely large capillary distance or with a concurrent capillary structure. Therefore the minimal tissuePO₂ lies at the level of the capillary venousPO₂ of a MCU. The maximum of the totalPO₂ frequency distribution in the normoxic rat myocardium lies at 25±5 mm Hg, i.e. above the mean venousPO₂ (20 mm Hg). TissuePO₂ values between 0 and 5 mm Hg amount to 0.5%, i.e. they are extremely rare. TissuePO₂ values of 0–1 mm Hg represent less than 0.2%.List of Symbols a arterial capillary end - a branching point of a capillary near the arterial capillary end (branching point of an anastomosis) - A maximal O₂-consumption - A(P) O₂-consumption dependent uponPO₂ - AVDO₂ arterio-venous difference - AVDO₂; AVDO_{2 c} ^(j) arterio-venous difference of a capillary - c _j weighting factor of the capillary distance - c _Hb hemoglobin concentration in the blood - d, d ^j capillary distance - mean capillary distance - i index for the different MCU's (i=1...8) - i.e. PO₂ intracapillaryPO₂ - j index for the parameters of an MCU with the capillary distanced ^(j) (j=1...7) - K diffusion conductivity - l capillary length - l _s capillary section length - MCU microcirculatory unit - P, P(x,y,z), PO₂ O₂ partial pressure - P _a arterialPO₂ - P _a; P_a ^(j) PO₂ at the branching pointa - P _i; P_v ^(j) venousPO₂ - mean venousPO₂ - P ₅₀ PO₂ at half maximal O₂ consumption - P _min,P _min ^(j) minimal tissuePO₂ - r _c, r_c ^(j) capillary radius - mean capillary radius - s(P) relative HbO₂ saturation (HbO₂ dissociation curve) - s ^–1 inverse function of the HbO₂ dissorciation curve - S _v, S_v ^(j) capillary venous HbO₂ saturation - mean venous HbO₂ saturation - v venous capillary end - V volume of the tissue fragment of a MCU - V _c, V_c ^(j) capillary supply volume - W _c, W_c ^(j) blood flow of the supply volume of a capillary (local blood flow) - mean blood flow - x,y,z cartesian coordinates of thePO₂ in a MCU - Bunsen's solubility coefficient - _c . _c ^(J) capilary blood flow - , ^(j) blood flow of an MCU - _i ^(j) (P) relative frequency distribution of thePO₂ in thei-th MCU - (P) relative frequency distribution of thePO₂ of all MCU's, total frequency distribution of the myocardial tissuePO₂ - Laplace operator Supported by the DFG     

Secretin and VIP-stimulated adenylate cyclase from rat heart

The exact positions of microelectrodes used to measure thePO₂ in the cerebral cortex of the rat were determined by staining the tissue with Alcian Blue. The measurement sites were subsequently located under a light microscope and correlated with the capillary and cellular arrangement of the cortex. The microelectrodes used for thePO₂ measurements were made of gold glass fibers; the Alcian Blue was injected hydrostatically through a micropipette attached to thePO₂ microelectrode. The sites where dye had been deposited were seen under a light microscope as green blue spots about 100 m in diameter. The capillaries were visualized by silver nitrate perfusion. Differences between the localPO₂ values in the neo- and the archeocortex were found. In the neocortex the meanPO₂ was 31 mm Hg, capillary volume 1.6%, capillary surface area 980/mm², capillary length 13.5/mm; whereas in the archeocortex these values where 21 mm Hg, 0.9%, 820/mm² and 9.4/mm respectively. These data indicate a relationship between the microcirculatory transport system and the local oxygen tension and provide further evidence that the meanPO₂ level tends to decrease when moving from the surface into the archeocortex.Supported by the Deutsche ForschungsgemeinschaftReported in part at the 3rd Symposium of ISOTT, Cambridge, GB, 1977; and at the 27th International Congress of Physiological Sciences, Paris, France, 1977     

Quantitative continuous measurement of partial oxygen pressure on the skin of adults and new-born babies

Summary It is possible to perform continuous quantitativeP _{O 2} measurements on vasodilated skin by means of surface Pt electrodes according to Clark when the electrode is fixed to the skin with a synthetic plastic material and in situ calibration is performed. A new in situ calibration of theP _{O 2} electrode is described. At first the skinP _{O 2} increases with O₂ inspiration. After perfusion stop the skinP _{O 2} shows a linear decrease because of the skin respiration, down to aP _{O 2} at which hemoglobin liberates chemically bound O₂. As thisP _{O 2} value of hemoglobin is known it is possible to use it for calibrating the electrode. TheP _{O 2} of normal skin is about 0–7 Torr. After vasodilation obtained by rubbing with a nicotinic acid derivate (Finalgon^®, Anasco, Wiesbaden),P _{O 2} increases to a mean value of 38.1 (±8.1) Torr (n=77). Under these conditions, skinP _{O 2} reaches arterial values never in adults and rarely in new-born babies.Part of the results have been reported during the Workshop on Oxygen Transport in Tissue, 19–22 July, 1971, in Dortmund and at the 4. Deutsche Kongress für Perinatale Medizin, 4–6 Nov. 1971, in Berlin. The study was carried out with partial support from the German Research Council (DFG).     

Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

Summary These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (P _a0₂) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO_2max) range = 65-77 ml·kg^–1·min^–1] performed a normoxic graded exercise test on a cycle ergometer toVO_2max at sea level. During incremental exercise atVO_2max 5 of the 12 subjects had ideal alveolar to arterial P02 gradients (P _A-aO₂) of above 5 kPa (range 5-5.7) and a decline from restingP _aO₂ (P _aO₂) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (P _A-aO₂) of 4.0-4.3 kPa with P _aO₂ of 0.4-1.3 kPa while the remaining 3 subjects hadP _A-aO₂ of 4.3-5 kPa with P _aO₂ between 1.7 and 2.0 kPa. The correlation between P_AO₂ andP _aO₂ atVO_2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSP _aO₂ and arterial partial pressure of carbon dioxide VSP _aO₂ atVO_2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

Transmural gradient of tissue gas tensions in the canine left ventricular myocardium during coronary clamping and reactive hyperemia

Mass spectrometry was used for the continuous, simultaneous and quantitative measurement of oxygen (PO₂) and carbon dioxide (PCO₂) partial pressures in the subendocardial and subepicardial layers of the left ventricle in 11 anaesthetized ventilated dogs. Under control conditions,PO₂ was significantly lower in the subendocardium (13.5±4.5 mm Hg) than in the subepicardium (20.7±2.3 mm Hg), whereasPCO₂ did not differ significantly (43±8.8 and 51±9.2 mm Hg respectively). These variables were not correlated with blood pressure or coronary blood flow. Subendocardial and subepicardialPO₂ decreased less than 5 s after coronary occlusion. These changes were more rapid and severe in the subendocardium. After occlusion for 90 s: subendocardialPO₂ was 4.1±6.3 mm Hg while subepicardialPO₂ was 6.7±15.0 mm Hg (P<0.05).PCO₂ reached peak values of 56±25 mm Hg subendocardial and 82±22 mm Hg subepicardial at 2.67±0.71 min and 3.43±0.93 min after coronary clamping. A reactive hyperemia occurred after coronary unclamping with different time courses and amplitudes for systolic and diastolic stroke flows whilePO₂ recovered with different kinetics. SubendocardialPO₂ increased with a lower initial slope, probably in relation with the delay in the diastolic hyperemia. The observed delayed subendocardial hyperoxia, unrelated to the hyperemia, may indicate a delay in the recovery of normal work and metabolism in the inner layers of the myocardium.     

Influence of hypothermia at different arterial CO2 pressures and local cooling of the spinal cervical cord on the activity of single phrenic motoneurons

Summary In anesthetized guinea pigs the action of acetylcholine, norepinephrine, epinephrine, isoproterenol, and reactive hyperaemia on arterial blood pressure, blood flow in the lower leg (measured by venous occlusion plethysmography), and distribution ofpO₂-values a platinum-O₂-microelectrode was used. By continuous recording of thepO₂ the electrode was moved slowly through the muscle tissue by constant velocity (33 /sec).During the action of norepinephrine, epinephrine, isoproterenol, and following temporary arterial occlusion a linear proportion was found between meanpO₂-values or meanpO₂-gradients and mean blood flow values (between 1.3 and 7.8 ml/min ·100 ml tissue). During the action of acetylcholinepO₂-values decreased in spite of increased blood flow.The reduced number of higherpO₂-values and the decreasedpO₂-gradients appear to indicate a relatively small number of open (perfused) capillaries during the action of acetylcholine. The reduced tissue oxygen delivery is due to enlarged diffusion distances and smaller capillary surface areas.     

APCO2 surface electrode working on the principle of electrical conductivity

APCO₂ electrode working on the principle of electrical conductivity is described. The calibration curve can be linearized according to the formula . This linearity has been tested in thePCO₂ range of 0.93–9.33 kPa (7–70 Torr). For the experiments electrodes are used which have conductivity values of about 50 nS and drifts of maximally 5%/h at aPCO₂ of 5.33 kPa (40 Torr). The response time (T ₉₀) is about 20 s. The temperature sensitivity is 2.4 nS/1 K between 298K–310K. The standard error of the measurements is =0.33 nS. With these electrodes tissuePCO₂ can be measured on the surface of various organs.     

Effect of an increase in{\text{Hb}}_{{\text{O}}_{\text{2}} } affinity on the calculated capillary recruitment of an isolated rat heart

The effect of an increase in hemoglobin O₂ affinity on myocardial O₂ delivery was studied in a blood perfused working rat heart preparation. In a first series of experiments P₅₀ ( for which saturation is 50%) was lowered by use of carbon monoxide. The heart was alternatively perfused with the blood sample of P₅₀=32 mm Hg and the blood sample of P₅₀=17 mm Hg. O₂ capacity of both samples was kept the same by appropriate hemodilution. In a second serie of experiments change of P₅₀ was obtained by the use of adult human erythrocytes containing hemoglobin creteil with a P₅₀ of 13.6 mm Hg. As P₅₀ decreased from 25 to 10 mm Hg, coronary sinus ( ) diminished from 26±2 to 18±2 mm Hg (–29±2%), coronary sinus O₂ content ( ) increased by 15±3%, myocardial oxygen consumption did not change significantly. The percentage of increase of coronary flow was 23±4%.Analysis of these results with a simple mathematical model of O₂ delivery suggest that increase in affinity is corrected by a simultaneous increase in coronary flow and capillary recruitment.This study was supported by contracts 74-7-0274 from D.G.R.S.T., 76-1-1755 from I.N.S.E.R.M. and a grant from the University of Paris VII     

Einstellzeit der Pt-Elektrode bei Messungen nicht stationärer O2-Partialdrucke

Zusammenfassung Das Meßsignal bei sprunghaftenpO₂-Änderungen wird anhand des Diffusionsfeldes der Elektrode beschrieben. Es wird das zeitliche Verhalten des Meßsignals von blanken und membranbespannten Elektroden in gasförmigen und nicht gasförmigen Meßmedien betrachtet. Aus dem Verhalten des Meßsignals kann jeweils die Einstellzeit alssystematischer Meßfehler abgeleitet werden. In nicht gasförmigen Medien (z. B. biologisches Gewebe) übersteigt das Meßsignal nach einempO₂-Sprung zu höheren Werten das stationäre Endsignal. Daraus ergibt sich eine besondere Betrachtung der Einstellzeit in solchen Medien.Die Einstellzeit für Pt-Elektroden mit einfacher und doppelter Membran wird explizit angegeben. Schließlich wird für biologische Medien die Einstellzeit mit dem Diffusionsfehler [8] verglichen. Die Forderungen an eine Membran der Pt-Elektrode mit kleiner Einstellzeit und gleichzeitig kleinem Diffusionsfehler sind zusammengestellt.

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Erklärung der Symbole a Verhältnis der Diffusionskoeffizienten zweier Membranen - Bunsenscher Löslichkeitskoeffizient des Mediums - _m Bunsenscher Löslichkeitskoeffizient der Membran - b Verhältnis der Diffusionsleitfähigkeiten von Membran und Medium - C ₁,C ₂ Proportionalitätskonstanten zwischen Meßsignal und O₂-Partialdruck - D Diffusionskoeffizient des Mediums - D _m,D _m Diffusionskoeffizienten der Membranen - Diffusionskoeffizient der effektiven Membran - DF Diffusionsfehler - DGl Differentialgleichung - d _m,d _m Dicke der Membranen - Dicke der effektiven Membran - dimensionsloser Parameter des Diffusionsfehlers - erf Fehlerfunktion - exp Exponentialfunktion - F Faradaykonstante - grad Gradient - I stationäres Meßsignal vor dempO₂-Sprung - I stationäres Meßsignal nach dempO₂-Sprung - I(t), I(),I() instationäres Meßsignal als Funktion der Zeit bzw. zeitabhängiger dimensionsloser Parameter - K Diffusionsleitfähigkeit des Mediums - K _m Diffusionsleitfähigkeit der Membran - Diffusionsleitfähigkeit der effektiven Membran - dimensionsloser Parameter - n Summationsindex - pO₂ O₂-Partialdruck - pO₂ als Funktion von Ort und Zeit bzw. zeitabhängiger dimensionsloser Parameter; Diffusionsfeld der Elektrode - p _c konstanterpO₂ vor dempO₂-Sprung - p _c konstanterpO₂ nach dempO₂-Sprung - p(r ₀+d _m , ) pO₂ an der Grenze Membran/Medium in Abhängigkeit des Zeitparameters - p(r,o) Diffusionsfeld zum Zeitpunkt (t=0) despO₂-Sprunges - p(r₀+d_m, o) pO₂ an der Grenze Membran/Medium zum Zeitpunkt despO₂-Sprunges - R Radius der ebenen, kreisförmigen Elektrode - r ₀ Radius der Elektrode mit halbkugelförmiger Pt-Oberfläche - r Kugelkoordinate - ₁,₂ dimensionslose ortsabhängige Parameter - T ₉₀,T ₉₅ Zeit, bis 90% bzw. 95% des Signalunterschiedes nach dempO₂-Sprung ausgeglichen sind (Einstellzeit) - T ₉₀,T ₉₅ Einstellzeit der Elektrode mit Doppelmembran - T _90*,T _95* Zeit, bis sich das Signal nach Übersteigen des stationären Endwertes diesem auf 10% bzw. 5% angenähert hat - dimensionslose Parameter zu den vorangegangenen Einstellzeiten - t Zeitkoordinate - , dimensionslose zeitabhängige Parameter - t _max, _max Zeit maximaler Signalhöhe nachpO₂-Sprung und zugehöriger dimensionsloser Parameter - V(t) Diffusionsgesamtfluß zur Pt-Oberfläche - Stromdichtevektor der diffundierenden O₂-Moleküle - x, y, z Kartesische Koordinaten - Integrationsvariable - ² Laplace-Operator - partielle Ableitung nach der Zeit - Integral über eine Fläche - gerichtetes Flächenelement     

A novel,remote-controlled suspension device for brain tissue PO2 measurements with multiwire surface electrodes

A new device was developed for rapid assessment of PO₂ values in viable tissue, such as the brain, using a multiwire surface electrode. The instrument utilizes a phonograph-like construction with weightless suspension of the electrode which thus minimizes surface pressure and allows for compensation of brain movements. The new and original component of the present device is the motor-driven, servo-controlled rotation of the PO₂ electrode around its vertical axis. This enables PO₂ measurements from precisely defined locations. From values measured on rabbit brain surface a PO₂ histogram was constructed. The mean PO₂ and distribution histogram were similar to those obtained with a needle electrode. The novel device, therefore, enables accurate and fast tissue PO₂ measurements with minimal risk of brain damage.     

Diffusionsfehler und Eigenverbrauch der Pt-elektrode beipO2-Messungen im steady state

Zusammenfassung Im steady state beeinflussen Diffusionsfehler und Eigenverbrauch der Pt-Elektrode als systematische Fehler O₂-Partialdruckmessungen. Sie sind abhängig von den geometrischen Eigenschaften der Elektrode, den Diffusionseigenschaften der Membran sowie den Diffusions- und Konvektionseigenschaften des Meßmediums. Das Diffusionsfeld vor der Pt-Oberfläche und das dadurch bestimmte stationäre Meßsignal werden für gasförmige und nicht gasförmige Medien mit und ohne Konvektion berechnet. Daraus resultieren quantitative Aussagen über die systematischen Fehler. Speziell für Messungen in durchbluteten Geweben (z. B. Hirnrinde und Myokard) wird der Einfluß des Eigenverbrauchs von Pt-Elektroden auf den intracapillärenpO₂-Abfall in Durchblutungsrichtung und das intercapillärepO₂-Feld am Meßort der Elektrode ermittelt. Diese Berechnungen erfolgten mit Hilfe eines Digitalmodells.

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Erklärung der Symbole A O₂-Verbrauch des Gewebes - Bunsenscher Löslichkeitskoeffizient des Mediums - _m Bunsenscher Löslichkeitskoeffizient der Membran - C ₁,C ₁,C ₂,C ₂,C ₃ Konstanten - D Diffusionskoeffizient des Mediums - DF, DF Diffusionsfehler bei einfacher und doppelter Membran - DGl Differentialgleichung - d Capillarabstand - d _h Dicke der hydrodynamischen Grenzschicht - d _m ,d _m Dicke der Membranen - , , , , , dimensionslose Parameter - exp Exponentialfunktion - F Faradaykonstante - grad Gradient - I _o stationäres Meßsignal in Medien ohne Konvektion - I stationäres Meßsignal in Gasen - I _o stationäres Meßsignal in Flüssigkeiten mit Konvektion - J _o nullte Bessel-Funktion - K Diffusionsleitfähigkeit des Mediums - KE, KE Konvektionseffekt bei einfacher und doppelter Membran - K _m ,K _m Diffusionsleitfähigkeit der Membranen - l Capillarlänge - l Capillarabschnitt - Viscosität des Mediums - p, pO₂,p(r), p(r,z) O₂-Partialdruck - p mittlerer Partialdruck - P _a O₂-Partialdruck am arteriellen Capillarende - p _c konstanter Partialdruck - P/r _o +d _m O₂-Partialdruck an der Grenze Membran/Medium - P _v O₂-Partialdruck am venösen Capillarende - P _g relativer O₂-Partialdruckabfall im Gewebe - P _v relativer O₂-Partialdruckabfall am venösen Capillarende - R Radius der ebenen kreisförmigen Elektrode - RB Randbedingung - RDF, RDF restlicher Diffusionsfehler einfacher und doppelter Membranen - r _o Radius der Elektrode mit halbkugelförmiger Pt-Oberfläche - r, z Zylinderkoordinaten - r _K Capillarradius - S Sättigungsabfall im Capillarblut ohne Elektrode - S Sättigungsabfall im Capillarblut mit Elektrode - u O₂-Konzentration - V Diffusionsgesamtfluß - V _K Diffusionsfluß aus einem Capillarabschnitt - v _r ,v _z Komponenten des Stromdichtevektors inr- bzw.z-Richtung (Zylinderkoordinaten) - mittlere Stromdichte - Stromdichtevektor des Flusses der O₂-Moleküle - v _c konstante Geschwindigkeit des bewegten Mediums - x, y, z Kartesische Koordinaten - Integrationsvariable - ² Laplace-Operator - partielle Ableitung nach der Zeit     

The oxygen supply of the rat kidney: Measurements of intrarenalpO2

Summary Using a newly developed platinum-O₂-microeletrode [30] based on the design ofSilver [37] the construction and properties of which are described,pO₂-measurements in the parenchyma of the blood-perfused and the cell-free perfused rat kidney were carried out.By continuous recording of thepO₂ during slow (150 ×min^–1) insertion of the O₂-electrode into the respiring tissue two regions of distinctly different meanpO₂-values were found. In the outer region which extends from the renal surface to a depth of about 3–4 mm (corresponding anatomically with the renal cortex) largepO₂-differences exist close to each other. In the blood-perfused kidney the maximum corticalpO₂-values lie in the range of arterialpO₂ the lowest values at about 10 Torr. In the cortex of the cell-free perfused kidney the maximumpO₂-values lie considerably below the arterialpO₂.In both the blood perfused and in the cell-free perfused kidney at centripetal movement of the O₂-electrode the cortical region of high and fluctuatingpO₂ is followed by a narrow zone (200 radial extension) of a steep decrease of the meanpO₂. At further insertion in both preparations thepO₂ remains at lowpO₂-values of ca. 10 Torr. Anatomically, this latter region of low and constantpO₂ corresponds to renal medulla and pelvis.By recording the decrease of parenchymalpO₂ after sudden stop of the perfusion attempts were made at measuring the critical local O₂-supply pressure. In the cortex of the cell-free perfused kidney critical local O₂-supply pressures between 6 and 28 Torr with a maximum abundance at 8 Torr were found.The qualitative and quantitative implications of the presented data on the conditions of parenchymal O₂-supply are discussed. The results are interpreted as an indication for the arteriovenous shunt (bypass)-diffusion of considerable amounts of oxygen, especially under the conditions of the cell-free perfusion. Furthermore, it follows from the data presented that even at high venous O₂-pressures and high meanpO₂-values in the parenchyma regions of local anoxia may exist.     

In vivo measurement of carbon dioxide tension with a miniature electrode

A commercially available catheter type electrode with whichP _CO2 can be continuously measured in vivo and in vitro gave progressively less accurate results the longer the measuring period was extended. This proved to be due to temperature effects and a change in sensitivity with time. A correction procedure for these effects was developed which was based on two observations. 1. The relationship between temperature and the logarithm of the sensitivity of the electrodeamplifier combination was linear and virtually identical for 9 electrodes: 8% change in sensitivity for a deviation of 1° C from the temperature during calibration. 2. The change in sensitivity due to drift of the electrode output is approximately a logarithmic function of time: 1 h after calibration all electrodes exhibited a decreased sensitivity, varying between 0.3 and 16.7%. The drift effect can be dealt with by repeated calibrations, preferably at 1^1/2 h intervals.The adequacy of the correction procedure was assessed in in vivo measurements in cats and dogs. The meanP _CO2 difference between the in vivo measurement, corrected for temperature and drift, and samples analyzed with a conventional electrode, was 0.005 kPa (0.04 mm Hg) with a standard deviation of 0.187 kPa (1.39 mm Hg).     

Fixed acid and carbon dioxide bohr effects as functions of hemoglobin-oxygen saturation and erythrocyte pH in the blood of the frog,Rana temporaria

Using a thin film, dynamic recording technique, the pH sensitivity of the oxygen equilibrium (Bohr effect) of whole blood in the frogRana temporaria, and its dependence on CO₂ and fixed acids and on plasma and erythrocyte pH values were measured. Under standard conditions (20°C,P _{CO 2}=14.7 mm Hg, pH=7.65) the oxygen equilibrium could be described by a P₅₀ value of 38 mm Hg andn ₅₀ of 1.8. Hill plots of the oxygen equilibria showed increased cooperativity in oxygen binding with increasing saturation (n ₂₀ 1.2,n ₈₀ 4.0). Values of the fixed acid and CO₂ Bohr factors ({ie7-1} and {ie7-2}, respectively) were similar at specific saturations (S_{20, 50, 80}) but showed saturation dependence with high values occurring at high saturation. The same statements also hold for the intracellular Bohr factors (derived from the relation between blood P₅₀ and erythrocyte pH) although the values of both {ie7-3} and {ie7-4} now were greater than those related to blood pH.     

Comparison of arterial,end-tidal and transcutaneous PCO2 during moderate exercise and external C02 loading in humans

Summary Static relationships between arterial, transcutaneous[/p] and end-tidal PCO₂ (P _aCO₂, P _tc CO ₂, P _etCO₂) as well as the dynamic relationship between P _etCO₂ and P _tcCO₂ were studied during moderate bicycle ergometer exercise with and without external C0₂ loading. The exercise pattern consisted of 5-min intervals of constant power at 40 W and 100 W and 900 s of randomised changes between these two power levels. The external CO₂ loading was achieved by means of controlled variations of inspiratory gas compositions aimed at a constant P _etCO₂ of 6.5 kPa (49 mm Hg). The P_etO2 was regulated at 17.3 kPa (130 mm Hg). Under steady-state conditions all PCO₂ parameters showed close linear relationships. P _aCO₂/P _tcCO₂ was near to identity while the P _etCO₂ systematically overestimated changes in P _aCO₂. No relationship showed a significant influence of the exercise intensity. Transients of P _tcCO₂ are considerably slower than P _etCO₂ transients. The dynamic relationship between both parameters was found to be independent of whether internal or external C0₂ loadings were applied. It is concluded that the combination of P _etCO₂ and P _tcCO₂ measurements allows an improved non-invasive assessment of P _aCO₂. While P _etC0₂ better reflects the transients, P _tcCO₂ can be employed to determine slow changes of the absolute P _aCO₂.     

Physiological responses to intermittent and continuous exercise at the same relative intensity in older men

We investigated the physiological responses in older men to continuous (CEx) and intermittent (IEx) exercise. Nine men [70.4 (1.2) years, O_2peak: 2.21 (0.20) l min^–1; mean (SE)] completed eight exercise tests (two CEx and six IEx) on an electronically braked cycle ergometer in random order. CEx and IEx were performed at 50% and 70% O_2peak. IEx was performed using 60sE:60sR, 30sE:30sR and 15sE:15sR exercise to rest ratios. The duration of exercise was adjusted so that the total amount of work completed was the same for each exercise test. Oxygen uptake (O₂), minute ventilation (_E) and heart rate (HR) were measured at the mid-point of each exercise test. Arterialised blood samples were obtained at rest and during exercise and analysed for pH and PCO₂. At the same relative intensity (50% or 70% O_2peak), IEx resulted in a significantly lower (P<0.01) O₂, _E and HR than CEx. There were no significant differences (P>0.05) in O₂, _E and HR measured at the mid point of the three exercise to rest ratios at 50% and 70% O_2peak. pH and PCO₂ during CEx and IEx at 50% O_2peak were not significantly different from rest. CEx performed at 70% O_2peak resulted in significant decreases (P<0.05) in pH and PCO₂. There was a significant decrease (P<0.05) in pH only during the 60sE:60sR IEx at 70% O_2peak. Changes in arterialised PCO₂ during the 60sE:60sR, 30sE:30sR and 15sE:15sR at both 50% and 70% O_2peak exercise tests were not significant. When exercising at the same percentage of O_2peak and with the total amount of work fixed, IEx results in significantly lower physiological responses than CEx in older men. All results are given as mean (SE).     

Effect of variations in blood hydrogen ion concentration on pulmonary gas exchange of artificially ventilated dogs

The effect of variation of blood hydrogen ion concentration on arterial and mixed venousP _{O 2},ideal alveolar-arterial O₂ pressure difference (P _AiO₂–P _aO₂),venous admixture (Q _s/Q _t), arterio-alveolar CO₂ pressure difference (a–A)D _{CO 2},physiological dead space to tidal volume ratio (V _D/V_T),cardiac output (Q _t) and mean pulmonary arterial pressure ( ) has been studied. Arterial and mixed venousP _{O 2}increased and (P _AiO₂–P _aO₂)decreased with increasing blood hydrogen ion concentration. No change in (Q _s/Q _t), (a–A)-D _{CO 2},V _D/V_T,Q _t and was observed.The effect of hydrogen ion concentration on arterial and mixed venousP _{O 2}and on (P _AiO₂–P _aO₂)is mainly due to a shift of the blood oxyhemoglobin dissociation curve (ODC), i.e. due to the Bohr effect. The upper part of the ODC is more flat in alkalosis (shift to the left) than in acidosis (shift to the right). Therefore the same end-capillary to arterial O₂ content difference results in a greater (P _AiO₂–P _aO₂)in alkalosis than in acidosis. Any factor influencing the slope of the upper part of the ODC is expected to affect the arterialP _{O 2}and the (P _AiO₂–P _aO₂)by this mechanism. Similarly any factor shifting the steep part of the ODC is expected to affect theP _{O 2}of the mixed venous blood.     

Absence of long-term modulation of ventilation by dead-space loading during moderate exercise in humans

The stability of arterial PCO₂ (P_aCO₂) during moderate exercise in humans suggests a CO₂-linked control that matches ventilation (_E) to pulmonary CO₂ clearance (CO₂). An alternative view is that _E is subject to long-term modulation (LTM) induced by hyperpnoeic history. LTM has been reported with associative conditioning via dead-space (V_D) loading in exercising goats (Martin and Mitchell 1993). Whether this prevails in humans is less clear, which may reflect differences in study design (e.g. subject familiarisation; V_D load; whether or not _E is expressed relative to CO₂; choice of P_aCO₂ estimator). After familiarisation, nine healthy males performed moderate constant-load cycle-ergometry (20 W-80 W-20 W; <lactate threshold, _L): day 1, pre-conditioning, n=3; day 2, conditioning (V_D=1.59 l, doubling _E at 20 W and 80 W), n=8 with 10 min rest between tests; and, after 1 h rest, post-conditioning, n=3. Gas exchange was determined breath-by-breath. Post-conditioning, neither the transient [phase 1, phase 2 (1, 2)] nor steady-state _E exercise responses, nor their proportionality to CO₂, differed from pre-conditioning. For post-conditioning trial 1, steady-state _E was 28.1 (4.7) l min^–1 versus 29.1 (3.8) l min^–1 pre-conditioning, and mean-alveolar PCO₂ (a validated P_aCO₂ estimator) was 5.53 (0.48) kPa [41.5 (3.6) mmHg] versus 5.59 (0.49) kPa [41.9 (3.7) mmHg]; the 1 _E increment was 4.2 (2.9) l min^–1 versus 5.2 (1.9) l min^–1; the 2 _E time-constant () was 64.4 (24.1) s versus 64.1 (25.3) s; _E/CO₂ was 1.12 (0.04) versus 1.10 (0.04); and the _E-CO₂ slope was 21.7 (3.4) versus 21.2 (3.2). In conclusion, we could find no evidence to support ventilatory control during moderate exercise being influenced by hyperpnoeic history associated with dead-space loading in humans.     

Respiratory gas exchange indices used to detect the blood lactate accumulation threshold during an incremental exercise test in young athletes

Summary The time course of changes in blood lactate concentration and ventilatory gas exchange was studied during an incremental exercise test on a cycle ergometer to determine if the lactate accumulation threshold (LT₂) could be accurately estimated by the use of respiratory indices (VT₂) in young athletes. LT₂ was defined as the starting point of accelerated lactate accumulation. VT₂ was identified by the second exponential increase in _E and the ventilatory equivalent for O₂ uptake with a concomitant nonlinear increase in the ventilatory equivalent for CO₂ output. Twelve trained subjects, aged 18–22 years, participated in this study. The initial power setting was 30 W for 3 min with successive increases of 30 W every minute except at the end of the test when the increase was reduced. Ventilatory flow ( _E), oxygen uptake ( O₂), carbon dioxide output ( CO₂), and ventilatory equivalents of O₂ and CO₂ were determined during the last 30 s of every minute. Venous blood samples were drawn at the end of each stage of effort and analysed enzymatically for lactate concentration. After each test, LT₂ and VT₂ were determined visually by two investigators from the graphic results using a double-blind procedure. The results [mean (SEM)] indicate no significant difference between LT₂ and VT₂ expressed as O₂ [43.98 (1.70) vs 44.93 (2.39) ml - min^– - kg^–], lactataemia [4.01 (0.28) vs 4.44 (0.37) mM - 1^–], or heart rate [171 (3.36) vs 173 (3.11) min^–]. In addition, strong correlations were noted between the two methods for O₂ (r=0.90,P<0.001), lactataemia (r=0.75,P<0.01), and heart rate (r=0.96,P<0.001). It is concluded that VT₂ coincides with LT₂ determination and that the ventilatory gas exchange method can thus satisfactorily evaluate the lactate accumulation threshold in young athletes.     

Effect of alteration of peripheral blood flow on the central circulation in man during supine cycling in different ambient temperatures

Summary Whether the alteration of peripheral circulation caused by changing ambient temperature (T_a) affects central circulatory changes in man during supine cycling was investigated in four well-trained men, who exercised at two levels (117.7 or 176.6 W). Exercise metabolic rate (VO₂) in cold (0 C or 10 C) was the same as it was at 20 C, whereas the cardiac output (CO; CO₂ rebreathing technique) and heart rate were significantly lower (e.g., 176.6 W at 0 C, both p<0.01). In heat (30 C or 40 C), the VO₂ reduced with falling CO and mean arterial blood pressure from those at 20 C (e.g., 176.6 W at 40 C, all cases p<0.01), whereas the peak post-exercise calf blood flow (CBF_p) increased (p<0.01). The VO₂ and stroke volume (SV) were inversely proportional to the ratio of CBF_p to CO/kg body weight (CBF_p/CO) (r>–0.78, p<0.001). Total peripheral resistance (TPR) was related to arteriovenous oxygen difference (A-VO₂ difference) (r>0.78, p<0.001). The TPR and A-VO₂ difference decreased as T_a rose, while CBF_p/CO was almost the same. As CBF_p/CO had exceeded 50 and further progressed, however, the two parameters elevated until the same level as that at 0 C. The present results suggest that during moderately prolonged (16–60 min) supine cycling in different T_a's the central circulatory changes are mainly affected by the altered peripheral blood flow in competing between skin and muscle for blood flow.