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.     

Effect of exposure to oxygen at 101 and 150 kPa on the cerebral circulation and oxygen supply in conscious rats

Hyperbaric oxygen at pressures of 300 to 500 kPa has been shown to induce changed distribution of cerebral blood flow ( _CBF) in rats, in places reducing the supply of the supplementary O₂. Thus, in the present study, the effect of hyperoxia at 101 (group 1, n = 9) and 150 (group 2, n = 9) kPa OZ on cerebral blood flow distribution and central haemodynamics was tested in conscious, habituated rats. During the control period the systolic arterial pressure (BP_s), heart rate (f _c), breathing frequency (f _b), cardiac output ( _c), arterial acid-base chemistry and glucose, as well as _CBF distribution (r _CBF) were similar in the two groups of animals. During O₂ exposure, the acid-base chemistry remained unchanged. The haemoglobin decreased in group 2, but remained unchanged in group 1. The f _c decreased rapidly in both groups during the change in gas composition, after which f _c remained constant both in group 1 and in group 2, for whom pressure was increased. The _c and f _b decreased and BP_s increased similarly in the two groups. Total _CBF and r _CBF decreased to the same extent in both groups, and the r _CBF changes were equally scattered. In group 1, breathing of pure O₂ did not increase the O₂ supply to any cerebral region except to the thalamus and colliculi after 60 min, whereas the O₂ supply to the hypothalamus decreased and remained low. In group 2, the O₂ supply was unchanged compared to the control period in all regions. These findings agree with previous observations during exposures to higher O₂ pressures. In air after O₂ exposure the acid-base chemistry remained normal. The f _c and f _b increased to higher levels than during the control period. The BP_s remained high. The brain blood flows were increased, inducing elevated O₂ supply to several brain regions compared to the control period. In conclusion, O₂ supply to the central nervous system was found to be in the main unchanged during breathing of O₂ at 101 kPa and 150 kPa.     

The effect of exercise intensity and duration on the oxygen deficit and excess post-exercise oxygen consumption

Summary Nine males with mean maximal oxygen consumption ( ) =63.0 ml· kg^–1 · min^–1, SD 5.7 and mean body fat = 10.6%, SD 3.1 each completed nine counterbalanced treatments comprising 20, 50 and 80 min of treadmill exercise at 30, 50 and 70% . The OZ deficit, 8 h excess post-exercise oxygen consumption (EPOC) and EPOC:O₂ deficit ratio were calculated for all subjects relative to mean values obtained from 2 control days each lasting 9.3 h. The O₂ deficit, which was essentially independent of exercise duration, increased significantly (P<0.05) with intensity such that the overall mean values for the three 30%, 50% and 70% workloads were 0.83, 1.89 and 3.09 l, respectively. While there were no significant differences (P>0.05) between the three EPOCs after walking at 30% for 20 (1.01 l), 50 (1.43 l) and 80 min (1.041), respectively, the EPOC thereafter increased (P<0.05) with both intensity and duration such that the increments were much greater for the three 70% workloads (EPOC: 20 min=5.68 l; 50 min=10.04 l; 80 min= 14.59 l) than for the three 50% workload (EPOC: 20 min =3.14 l; 50 min=5.19 l; 80 min= 6.10 l). An analysis of variance indicated that exercise intensity was the major determinant of the EPOC since it explained five times more of the EPOC variance than either exercise duration or the intensity times duration interaction. The mean EPOC:O₂ deficit ratio ranged from 0.8 to 4.5 and generally increased with both exercise intensity and duration. These data imply that the EPOC is more than mere repayment of the O₂ deficit because metabolism is increasingly disturbed from resting levels as exercise intensity and duration increase due to other physiological factors occurring after the steady-state has been attained.     

Cerebral blood flow distribution and systemic haemodynamic changes after repeated hyperbaric oxygen exposures in rats

The effects of acute and repeated exposures to 500 kPa O₂ on the distribution of cerebral blood flow and systemic haemodynamics were assessed in awake rats. After habituation, the control rats (group 1,n=7) were restrained for 1 h daily for 8 days in air at 101 kPa, while the test rats (group 2,n=8) were exposed to 500 kPa O₂ for 1 h daily for 8 consecutive days. During a final exposure, both groups were exposed to 500 kPa O₂. Systolic (BP_s) and mean arterial blood pressure (BP _a), and heart rate (f _c) were measured continuously from implanted arterial catheters; while cardiac output and regional were measured by the microsphere method in air before the O₂ exposure, and after both 5 min and 60 min at 500 kPa O₂ in all the animals. The baseline measurements in air of BP_s andBP _a were higher andf _c was lower in group 2, while the acid-base chemistries were similar in the two groups. Total was similar in both groups. However in group 2, blood flows and calculated O₂ supplies to colliculi, hippocampus, hypothalamus, and most cerebral cortical regions were higher, but lower to pons and medulla oblongata. During O₂ exposure andf _c decreased, andBP _a, BP_s, and peripheral vascular resistance increased in all the rats. Arterial partial pressure of CO₂ and [HCO₃ ^–] decreased in group 1, but remained at baseline levels in group 2. Total and decreased in both groups, and the distribution was altered. Calculated O₂ supplies to different brain regions varied according to the changes, so that most regions sustained baseline O₂ delivery, although O₂ delivery to some regions may have been reduced. The decline of also indicated reduced removal of waste from the brain, so that CO₂ tension and temperature could have been elevated, thereby potentiating the toxic effects of O₂ on brain cells. In conclusion, repeated O₂ exposures induced heterogeneous and persistent changes in , as well as a persistent increase in arterial pressure.     

Direct determination of local oxygen consumption of the brain cortex in vivo

Summary A method is described to determine local oxygen consumption quantitatively in the brain cortex under in vivo conditions. Local oxygen consumption is calculated from the slope of local tissue P_{O 2} decrease during a few seconds of total ischemia of the brain for each second after the stop of circulation. The decrease of tissue P_{O 2} is recorded simultaneously at several measuring sites. To be independent of oxygen chemically bound to hemoglobin, tissue P_{O 2} values are raised above 100 Torr. The calculation of local oxygen consumption for each second during the short period of ischemia showed that the O₂ consumption remains constant only for a few seconds ranging from 5 to maximally 15 s at different locations. Then O₂ consumption decreases continuously although the tissue P_{O 2} values are still above the full saturation of hemoglobin. The rate of local oxygen consumption varies considerably at different measuring sites of the superficial layers of the brain cortex (cat). The mean value amounts to 3±1.5 ml O₂/100 g tissue and minute.     

Determinants of maximal oxygen uptake in moderate acute hypoxia in endurance athletes

The factors determining maximal oxygen consumption were explored in eight endurance trained subjects (TS) and eight untrained subjects (US) exposed to moderate acute normobaric hypoxia. Subjects performed maximal incremental tests at sea level and simulated altitudes (1,000, 2,500, 4,500 m). Heart rate (HR), stroke volume (SV), cardiac output arterialized oxygen saturation oxygen uptake ventilation ( expressed in normobaric conditions) were measured. At maximal exercise, ventilatory equivalent transport and O₂ extraction (O₂ER_max) were calculated. In TS, remained unchanged despite a significant reduction in at 4,500 m. SV_max remained unchanged. decreased in TS at 4,500 m, was lower in TS and greater at 4,500 m vs. sea level in both groups. Sa′O_2max decreased at and above 1,000 m in TS and 2,500 m in US, O₂ER_max increased at 4,500 m in both groups. decreased with altitude and was greater in TS than US up to 2,500 m but not at 4,500 m. decreased with altitude but the decrement was larger in TS at 4,500 m. In both groups in moderate hypoxia was correlated with Several differences between the two groups are probably responsible for the greater in TS at 4,500 m : (1) the relative hypoventilation in TS as shown by the decrement in at 4,500 m (2) the greater decrement in TS due to a lower Sa′O_2max and unchanged 3) the smaller increase in O₂ER_max in TS, insufficient to compensate the decrease in      

Model experiments on the effect of bifurcations on capillary blood flow and oxygen transport

O₂-delivery by a single capillary is a function of the flow rate and thefraction of flow made up of red blood cells. Capillary flow rate in turn depends upon flow resistance which is determined by thefraction of capillary volume occupied by red blood cells. Experiments were carried out to study the relationship between these parameters in an in vitro model consisting of glass capillaries (I.D. 3.3–11.0 m) branching from a large bore feeding channel which was perfused at variable flow rates with suspensions of human red cells with different hematocrits. Capillary flow rates ranged from 0–10^–4 mm³ s^–1. The results indicate that the red cell flow fraction increases with increasing capillary flow rate and with decreasing feeding vessel flow rate. Capillary volume fraction occupied by red cells similarly depends on these two parameters, but is consistently lower than the red cell flow fraction. Capillary flow resistance increases with flow rate due to increasing volume fraction of cells. If the results obtained with the model system are applicable to in vivo capillaries it must be concluded that O₂-delivery by a single capillary is not linearly related to flow rate but increases more than proportionately with flow rate. Due to alteration of resistance with flow rate another type of autoregulation of capillary flow is proposed which tends to keep flow rate constant despite changes of driving pressure.Supported by the Deutsche Forschungsgemeinschaft     

Comparison of different oxygen exchange models

A functional distribution of coronary volume can be estimated from the response of arterio-venous O₂ content difference (AVO₂) to a flow step. However, the results depend on the assumed O₂ exchange model. The previously used model consisted of a single mixed compartment with O₂ exchange in series with an unmixed compartment without O₂ exchange (reference model). The purpose of this study is to provide an estimate of the errors made in the volume estimations by not taking into account factors as flow heterogeneity, different mixing sites or Krogh-like O₂ exchange. The approach is indirect: the response of the AVO₂ to a flow step has been calculated with alternative O₂ exchange models in which the factors mentioned are incorporated. These transients are fitted with the reference model. The resulting estimated volumes are different from the volumes assumed in the alternative models. Large differences are obtained with some of the alternative models, e.g. the model with Krogh characteristics. However, these models seem unrealistic because capillary pO₂ is higher than venous pO₂. Only small differences in volume are obtained with the more realistic models. Therefore, these results indicate that the coronary volumes are approximated well by the estimations obtained with the reference model. These volume estimations were 9.9 and 3.8 ml 100 g⁻¹ for the O₂ exchange vessels and the distal venous volume, respectively.     

Acute EPOC response in women to circuit training and treadmill exercise of matched oxygen consumption

The purpose of the study was to evaluate the effects of circuit training (CT) and treadmill exercise performed at matched rates of oxygen consumption and exercise duration on elevated post-exercise oxygen consumption (EPOC) in untrained women, while controlling for the menstrual cycle. Eight, untrained females (31.3±9.1 years; 2.04±0.26 l min^–1 estimated VO_2max; BMI=24.6±3.9 kg/m²) volunteered to participate in the study. Testing was performed during the early follicular phase for each subject to minimize hormonal variability between tests. Subjects performed two exercise sessions approximately 28 days apart. Resting, supine energy expenditure was measured for 30 min preceding exercise and for 1 h after completion of exercise. Respiratory gas exchange data were collected continuously during rest and exercise periods via indirect calorimetry. CT consisted of three sets of eight common resistance exercises. Pre-exercise and exercise oxygen consumption was not different between testing days (P>0.05). Thus, exercise conditions were appropriately matched. Analysis of EPOC data revealed that CT resulted in a significantly higher (p<0.05) oxygen uptake during the first 30 min of recovery (0.27±0.01 l min^–1 vs 0.23±0.01 l min^–1); though, at 60 min, treatment differences were not present. Mean VO₂ remained significantly higher (0.231±0.01 l min^–1) than pre-exercise measures (0.193±0.01 l min^–1) throughout the 60-min EPOC period (p<0.05). Heart rate, RPE, V_E and RER were all significantly greater during CT (p<0.05). When exercise VO₂ and exercise duration were matched, CT was associated with a greater metabolic disturbance and cost during the early phases of EPOC.     

Electrostimulation improves muscle perfusion but does not affect either muscle deoxygenation or pulmonary oxygen consumption kinetics during a heavy constant-load exercise

Electromyostimulation (EMS) is commonly used as part of training programs. However, the exact effects at the muscle level are largely unknown and it has been recently hypothesized that the beneficial effect of EMS could be mediated by an improved muscle perfusion. In the present study, we investigated rates of changes in pulmonary oxygen consumption and muscle deoxygenation during a standardized exercise performed after an EMS warm-up session. We aimed at determining whether EMS could modify pulmonary O₂ uptake and muscle deoxygenation as a result of improved oxygen delivery. Nine subjects performed a 6-min heavy constant load cycling exercise bout preceded either by an EMS session (EMS) or under control conditions (CONT). and heart rate (HR) were measured while deoxy-(HHb), oxy-(HbO₂) and total haemoglobin/myoglobin (Hb_tot) relative contents were measured using near infrared spectroscopy. EMS significantly increased (P < 0.05) the Hb_tot resting level illustrating a residual hyperaemia. The EMS priming exercise did not affect either the HHb time constant (17.7 ± 14.2 s vs. 13.1 ± 2.3 s under control conditions) or the kinetics (time-constant = 18.2 ± 5.2 s vs. 15.4 ± 4.6 s under control conditions). Likewise, the other parameters were unchanged. Our results further indicated that EMS warm-up improved muscle perfusion through a residual hyperaemia. However, neither nor [HHb] kinetics were modified accordingly. These results suggest that improved O₂ delivery by residual hyperaemia induced by EMS does not accelerate the rate of aerobic metabolism during heavy exercise at least in trained subjects.     

Effects of aldosterone on lipid metabolism and renal oxygen consumption in the rat

Summary The plasma level of free fatty acids (FFA) in adrenalectomized rats increases by 50% after treatment with aldosterone (2 g/100 g rat).Lipolytic activity in peripheral fat tissue is lowered after adrenalectomy and doubles after in vivo administration of aldosterone to adrenalectomized rats (measured as free fatty acid release in vitro from epididymal fat tissue).Lypolysis of adipose tissue stimulated by the in vitro presence of ACTH also increases after in vivo administration of aldosterone.Incorporation of intravenously administered label from U¹⁴C-palmitate into total extractable lipid of renal tissue is augmented 3 h after aldosterone administration to adrenalectomized rats, while no increase of the radioactivity is observed in total lipid from liver tissue. Treatment with aldosterone does not affect the total lipid content of kidney or liver in adrenalectomized rats.The oxygen consumption rate of kidney cortex slices with lactate, -hydroxybuterate or acetoacetate as substrates is lowered after in vivo administration of aldosterone to adrenalectomized rats. With succinate, however, the respiratory rate of kidney slices increases after aldosterone treatment of adrenalectomized rats, the ouabain-sensitive respiration being more affected than the ouabain-insensitive respiration. An interpretation of the O₂ consumption data implicating competition of lipid metabolism for CoA-SH is discussed.     

Exercise induced augmentation of myocardial oxygen extraction in spite of normal coronary dilatory capacity in dogs

Summary Myocardial O₂-extraction rate was studied during exercise induced augmentation of cardiac work in dogs.The O₂-extraction rate at rest was 75% of arterial content. Progressive levels of exercise increased the animals' O₂-consumption from 7 ml/min · kg up to 91 ml/min · kg. Cardiac output rose from 108 ml/min · kg at rest to 484 ml/min · kg at the highest exercise level. The increase in myocardial O₂-consumption from 9 ml/min·100 g at rest up to 57 ml/min·100 g at the highest exercise level was met by an increase in coronary flow from 59 to 256 ml/min·100 g and a rise of myocardial AVDO₂ from 15 to 22 Vol%. Thus the latter contributed 40% to the augmented myocardial O₂-requirements.Coronary venous O₂-saturation decreased to 9% saturation during highest levels of exercise. This low value was not the result of a limited coronary dilatory capacity, of inadequate state of exercise training, or of a relative underperfusion of the inner layers of the left ventricle.Thus, augmentation of myocardial O₂-extraction rate seems to be a mechanism of physiological relevance during exercise induced elevation of myocardial O₂-requirements in dogs and may be explained by capillary recruitment in the myocardium.Supported by Deutsche Forschungsgemeinschaft     

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.     

Recovery dynamics of skeletal muscle oxygen uptake during the exercise off-transient

The time course of muscle recovery from contractions (i.e., muscle off-kinetics), measured directly at the site of O₂ exchange, i.e., in the microcirculation, is unknown. Whereas biochemical models based upon creatine kinase flux rates predict slower off- than on-transients [Kushmerick, M.J., 1998. Comp. Biochem. Physiol. B: Biochem. Mol. Biol.] whole muscle data [Krustrup, et al. J. Physiol.] suggest on–off symmetry.

Purpose

We tested the hypothesis that the slowed recovery blood flow (Qm) kinetics profile in the spinotrapezius muscle [Ferreira et al., 2006. J. Physiol.] was associated with a slowed muscle recovery compared with that seen at the onset of contractions (time constant, τ  23 s, Behnke et al., 2002. Resp. Physiol.), i.e., on–off asymmetry.

Methods

Measurements of capillary red blood cell flux and microvascular pressure of O₂ (P_O2mv) were combined to resolve the temporal profile of muscle across the moderate intensity contractions-to-rest transition.

Results

Muscle decreased from an end-contracting value of 7.7 ± 0.2 ml/100 g/min to 1.7 ± 0.1 ml/100 g/min at the end of the 3 min recovery period, which was not different from pre-stimulation . Contrary to our hypothesis, muscle in recovery began to decrease immediately (i.e., time delay <2 s) and demonstrated rapid first-order kinetics (τ, 25.5 ± 2.6 s) not different (i.e., symmetrical to) to those during the on-transient. This resulted in a systematic increase in microvascular P_O2 during the recovery from contractions.

Conclusions

The slowed Qm kinetics in recovery serves to elevate the ratio and thus microvascular P_O2. Whether this Qm response is obligatory to the rapid muscle kinetics and hence speeds the repletion of high-energy phosphates by maximizing conductive and diffusive O₂ flux is an important question that awaits resolution.     

Kinetics of oxygen uptake and recovery for supramaximal work of short duration

In order to follow the time pattern of oxygen uptake and recovery for supramaximal work of short duration, 35 male subjects (mean age 21.4 years, mean body weight 71.9 kg) pedalled a bicycle ergometer at maximal speed for 1 min. A constant frictional resistance of 5.5 kg was used, resulting in a total work output of 2890 kpm (85 revolutions, SD = 7.5). The total percent decrement in work output from the initial rate on this test was 59.7 %. The total oxygen uptake during the work averaged 2.35 l, the net oxygen recovery was 4.891, while the net work efficiency was 19.3 %. One and two component exponential curves fit the observed oxygen uptake and recovery measures with a high degree of accuracy. Comparison of the curve parameters with published data showed large differences for the post exercise oxygen recovery and the slow component of the recovery curve. The magnitude of the fast component of recovery was similar to other data. The total oxygen uptake during the test was found to be 10% lower than the maximal oxygen uptake determined on a seperate progressive step-increment test. It was shown, by curve analysis, that the maximal oxygen uptake would have been reached in approximately 2 min.     

Pancreatic O2 consumption and CO2 output during secretin-induced,exocrine secretion from the pancreas in the anesthetized dog

Secretin stimulates pancreatic water and CO₂ excretion as well as pancreatic blood flow. It has been questioned whether the production (i.e. water and CO₂ excretion) is reflected in the input-output difference of nutrients. In pentobarbital anesthetised dogs, pancreatic exocrine secretion was stimulated by secretin, (Karolinska), 1 U/kg injected as an i.v. bolus. Secretion was maximally increased at 2 min after the secretin shot and returned to a basal value at between 16 and 32 min after secretin. Blood flow was also maximally increased at 2 min, but decreased to the basal value at between 8 and 16 min. O₂ extraction first decreased (at 2 min) and then gradually increased until it was higher than the basal value (at 16 min) and then returned to the basal level (at 32 min). O₂ consumption increased quickly, reached a plateau, lasting from 1 to 16 min, and then decreased to the basal level (32 min). CO₂ transfer from blood to tissue reached a maximum at 4 min and then decreased to the basal value (at between 16 and 32 min). The curves for CO₂ transfer from tissue to pancreatic secretion and for CO₂ in the secretion had the same shape. It is concluded that the curve of production (of water and CO₂ excretion) parallels the curve of O₂ consumption fairly well. The O₂ consumption curve did not correlate either with the blood flow curve or with the O₂ extraction curve. About one quarter of the excreted CO₂ originated from pancreatic metabolism and the remaining three quarters were transferred from blood, through the pancreatic tissue into the secretion. The increase in O₂ consumption was achieved by an increase in blood flow, followed by an increase in O₂ extraction. The release of a vasodilator metabolite by the pancreatic cells upon arrival of the secretin molecules, may explain both the increase in blood flow and the successive increase in O₂ extraction. Therefore these data can be interpreted according to the model for metabolic control of tissue oxygenation.     

Respiratory gas exchange in the rat spleen in situ and intrasplenic oxyhemoglobin saturation

Measurements of splenic respiratory gas exchange and of HbO₂ saturations in the red pulp of the rat spleen have shown that there are no indications of a reduced intrasplenic O₂ availability during normoxia. The present studies provide evidence that, in the normal spleen, the intrasplenic sequestration of red blood cells cannot be explained by an O₂ deficiency in the red pulp since the commonly accepted notion of an intrasplenic hypoxia is not true.Presented in part at the 50th Meeting of the Deutsche Physiologische Gesellschaft, Göttingen 1978     

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).     

The effect of water deprivation and hypertonic salt injection on the oxygen consumption and plasma NaCl concentration in the albino rat

Summary O₂-consumption of the whole animal was measured for rats deprived of water and food, or food only, at 27°C (for 3 days), 35°C (for 1 day), and in animals injected with NaCl solution intraperitoneally (3 ml/100 g B. W. of 3% NaCl). O₂-consumption calculated per gram body weight, decreased by about 20% compared with the control value in animals deprived of water at 27°C, but increased by about 9% in animals deprived of water at 35° C. A 15% to 40% increase in the O₂-consumption over the control value was found in the salt injected animals. Plasma NaCl concentration increased by about 5% and 10% in the animals deprived of water at 27°C and 35°C respectively; an increase of about 10% was found in the salt injected group. Rectal temperature was not affected by the experimental treatments. It is suggested that the reduction of the extracellular fluid volume for a long period might explain the observed reduction in the O₂-consumption for the animals deprived of water at 27°C.This study was partially supported by the National Council for Research and Development of Israel.