Changes in blood flow in the common femoral artery related to inactivity and muscle atrophy in individuals with long-standing paraplegia.
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Biomedical subjects
Publications and source records attributed to B Oeseburg.
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The purpose of this study was to examine muscle glycogen recovery with glucose feeding (GF) compared with fructose feeding (FF) during the first 8 h after partial glycogen depletion using 13C-nuclear magnetic resonance (NMR) on a clinical 1.5-TNMR system. After measurement of the glycogen concentration of the vastus lateralis (VL) muscle in seven male subjects, glycogen stores of the VL were depleted by bicycle exercise. During 8 h after completion of exercise, subjects were orally given either GF or FF while the glycogen content of the VL was monitored by 13C-NMR spectroscopy every second hour. The muscular glycogen concentration was expressed as percentage of the glycogen concentration measured before exercise. The glycogen recovery rate during GF (4.2 +/- 0.2%/h) was significantly higher (P < 0.05) compared with values during FF (2.2 +/- 0.3%/h). This study shows that 1) muscle glycogen levels are perceptible by 13 C-NMR spectroscopy at 1.5 T and 2) the glycogen restoration rate is higher after GF compared with after FF.
The objective of this study was to compare the effect of extracorporeal membrane oxygenation (ECMO) on cerebral oxygenation and hemodynamics in normoxemic and hypoxemic piglets. Six hypoxemic and six normoxemic piglets were put on venoarterial ECMO after cannulation of the right common carotid artery and external jugular vein with careful priming to avoid hemodilution. Changes in cerebral concentrations of oxyhemoglobin (cO2Hb), deoxyhemoglobin (cHHb), (oxidized-reduced) cytochrome aa3 (cCyt.aa3), and blood volume (CBV) were continuously measured by near infrared spectrophotometry. Heart rate, arterial O2 saturation (SaO2), arterial blood pressure, pulsatility ratio of systemic circulation (calculated as systolic-diastolic/mean arterial blood pressure), central venous pressure, intracranial pressure, and left common carotid artery blood flow (LCaBF) were simultaneously measured. We found that the cannulation procedure resulted in increased CBV, cHHb, and LCaBF in both groups. At 60 and 120 min after starting ECMO, the values of cO2Hb, CBV, and LCaBF in both groups were significantly higher than precannulation values, while the pulsatility ratio decreased. In the hypoxemic groups cHHb decreased and SaO2 increased as well. No significant changes of other variables were found. Between hypoxemic and normoxemic groups no significant differences in the response of CBV and LCaBF at 60 and 120 min were found. We conclude that in piglets cannulation for ECMO resulted in cerebral venous congestion and compensated increase in LCaBF. After starting ECMO, the cerebral O2 supply increased due to increased arterial O2 content. It was accompanied by similar increase of CBV in both groups, probably as a result of hyperperfusion, which seems to be related to the ECMO procedure itself.
Transmission pulse oximetry is widely used for oxygen monitoring. The use of pulse oximeters is steadily expanding toward situations with low arterial oxygen saturation (Sao2) values. Therefore, we evaluated transmission pulse oximetry in the unanesthetized fetal lamb at low Sao2 levels. In seven fetal lambs, fetal hypoxemia was induced by occlusion of the maternal common iliac artery, four days after the instrumentation of the animal. Two Nellcor prototype transmission Y-sensors (light emitting diodes: 660 and 890 nm) were applied, one around a forelimb muscle and one around a skinfold in the neck, and were connected to Nellcor pulse oximeters. The pulse oximeter was calibrated for the skin measurements. Pulse oximeter saturation readings (Spo2) were compared with sample Sao2 values, over an Sao2 range of 13 to 63%. For the neck sensor the SD of the difference was 5.0% (n = 101). For the muscle sensor the mean difference was 19.5% and the SD of the difference was 5.9% (n = 206). Regression analysis showed a different calibration line for the muscle sensor with the equation: Spo2 = 0.92 x Sao2 + 21.90. Continuous recordings were obtained both from the forelimb muscle and from the neck, but the recordings from the neck showed a substantial loss of signal during the hypoxemia period. We conclude that transmission pulse oximetry is less accurate below an Sao2 of 70% in fetal lambs than above 70% Sao2. At these low levels of Sao2, pulse oximeters may need to be constructed with different calibration lines for various application positions of the body.
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There are no studies on oxygen uptake of groups of physically active subjects aged over 70. This study describes the maximal oxygen uptake (VO2max) of 153 elderly people who completed the Nijmegen annual 4-day march (at least 30 km.day-1) in 1993. A total of 97 men with a mean age of 76.7 (SD 4.6) and 56 women with a mean age of 72.8 (SD 3.6) years participated in the study. The VO2max was determined using incremental cycle ergometry; 91 men and 49 women completed a maximal exercise test. Criteria for maximal performance were respiratory exchange ratio equal to or greater than 1.00, vertilatory equivalent for oxygen equal to or greater than 30.00 and maximal heart rate equal to or greater than (beats.min-1) 210 minus age (years). Mean maximal power output was 148.2 (SD 27.2) W and 120.4 (SD 20.5) W, mean VO2max.body mass-1 was 26.8 (SD 4.9) ml.kg-1.min-1 and 24.6 (SD 4.7) ml.kg-1.min-1, mean maximal heart rate was 152 (SD 18), and 157 (SD 14) beats.min-1 in men and women respectively. The mean VO2max.body mass-1 was about 20% higher than reported in other studies on subjects over 70 years of age. Mean maximal heart rate was about 10 beats.min-1 higher than predicted from the equation 220-age. The negative effect of chronic disease on VO2max.body mass-1 was smaller than in a sedentary reference population. The mean decline in VO2max.body mass-1 with age was 0.46 and 0.38 ml.kg-1.min-1 per year in the men and women respectively, which is the same rate as found in younger subjects. It was concluded that regular exercise might substantially increase aerobic power in the physically active elderly, even when they have chronic disease, and that it is unlikely that there is an accelerated loss of aerobic power in physically active elderly people aged over 70 year.
OBJECTIVE: The objective of our study was to describe the results from human experiments during normoxia that demonstrate the effect of pulsating arteries on the measured arterial oxygen saturation (SpO2) using a reflectance pulse oximeter sensor. METHODS: In 6 healthy adults and 7 healthy neonates, a Nellcor reflection sensor (FS-10 oxisensor, Nellcor, Inc., Pleasanton, CA) was placed in three different positions: (1) on the forehead, (2) on the temporal area, with the photodiode placed over the superficial temporal artery, and (3) on the temporal area, with the light-emitting diodes (LEDs) placed over the superficial temporal artery. RESULTS: Placement of the sensor in position 2 resulted in a significantly lower SpO2 reading, compared to sensor position 1: 5.8% (p < 0.01) lower for adults and 7.5% (p < 0.01) lower for neonates. Placement of the sensor in position 3 resulted in significantly larger plethysmographic signals, compared to sensor position 1; but, the Spo2 readings were alike. CONCLUSIONS: Pulsating arteries can affect the reliability of reflection pulse oximetry. Depending on the position of the sensor, a falsely low Spo2 value can be observed.
OBJECTIVE: We studied the relationship between preductal arterial oxygen saturation and metabolic acidosis in 18 chronically instrumented fetal lambs (gestational age 119 to 133 days) in two experimental designs. In the first group the onset of metabolic acidosis was determined. In the second group the progression of metabolic acidosis was studied as was the cardiovascular and hormonal changes resulting from hypoxemia. STUDY DESIGN: In nine fetal lambs maternal fraction of inspired oxygen was lowered stepwise by increasing flows of nitrogen delivered into the trachea through a small indwelling catheter (group 1), and in nine fetal lambs maternal blood flow was reduced stepwise by means of a vascular occluder (group 2). RESULTS: Baseline arterial oxygen saturation values ranged from 26% to 67% with normal pH and extracellular fluid base excess values in both groups 1 and 2. In both groups pH and extracellular fluid base excess started to decrease below 30% arterial oxygen saturation, with a progressive decrease below 20% arterial oxygen saturation to an end value for pH of 7.14. In some fetal lambs pH and extracellular fluid base excess decreased initially at 20% to 30% arterial oxygen saturation and then stabilized at the lower level. Fetal heart rate in group 1 increased during hypoxemia from 155 to 179 beats/min. In group 2 baseline fetal heart rate was 153 beats/min and fell with every step change in arterial oxygen saturation but subsequently increased to 172 beats/min by the end of the period of hypoxemia. Baseline values for epinephrine, norepinephrine, dopamine, cortisol, and mean arterial pressure were not related to baseline arterial oxygen saturation levels, and each of these variables was increased at the end of hypoxemia in group 2. CONCLUSION: Preductal arterial oxygen saturation can reach values between 20% and 30% before anaerobic metabolism starts. During the progressive acidosis blood pressure was increased, which can be attributed to a strong rise in catecholamines.
Multi-wavelength photometers, blood gas analysers and pulse oximeters are widely used to measure various oxygen-related quantities. The definitions of these quantities are not always correct. This paper gives insight in the various definitions for oxygen quantities. Furthermore, the possible influences of dyshaemoglobins and fetal haemoglobin on the accuracy of pulse oximetry are discussed. As pulse oximeters are constructed for the determination of arterial oxygen saturation, they should be validated with sample oxygen saturation values and not with the oxyhaemoglobin fraction. The influence of carboxyhaemoglobin is insubstantial over an oxygen saturation range of 0% to 100%. Through the presence of methaemoglobin, pulse oximetry will give an underestimation above 70% and an overestimation below 70% oxygen saturation. The influence of fetal haemoglobin is insignificant in the neonatal use of pulse oximetry, in the range of 75% to 100% arterial oxygen saturation. However, a pulse oximeter underestimates the arterial oxygen saturation at the 25% level with 5%, if the pulse oximeter has been calibrated in human adults. Such a low level of arterial oxygen saturation can be present in the fetus during labor.
A piglet model was used to evaluate the accuracy of a fiberoptic oximeter over a wide range of arterial oxygen saturation (SaO2) values. In eight anaesthetized piglets, the inspired oxygen concentration was varied from 30% to 6% resulting in a SaO2 range from 100% to 15%. Paired data of the Opticath fiberoptic catheter, which was placed in the descending aorta, and blood sample SaO2 values assessed by a multiwavelength oximeter, were analysed. After in vitro calibration according to the manufacturer's instruction, the fiberoptic catheter started to underestimate the SaO2 below 78%, worsening towards lower SaO2 values. The overall bias was -3.4% and the precision 3.8%. An off-line fit with a non-linear model resulted in a standard deviation of residuals of 2.6%. After several in vivo calibration adjustments when the fiberoptic oximeter deviated more than 4% from the blood sample value, the bias was eliminated over the total SaO2 range and the precision was 3.7%. The Opticath fiberoptic oximeter could have an accuracy for the whole SaO2 range between 15-100% close to the accuracy of the multiwavelength oximeter, when the fiberoptic oximeter is adapted for the underestimation below 78% SaO2.
Conventional near infrared spectroscopy (NIRS), introduced by Jöbsis in 1977, can be considered as a reliable trend monitor for cerebral oxygenation. Quantisation, however, is complex and cumbersome. Recently a relatively simple system for cerebral oximetry (INVOS 3100, Somanetics Corporation, USA) was developed, measuring the regional oxygen saturation (rSO2) in the capillary bed of the cerebrum, presented as a numerical figure for easy interpretation. In this study a comparison was made between a conventional NIRS instrument and the new INVOS instrument, in order to obtain information about sensitivity and usefulness of the INVOS system. Changes in cerebral haemodynamics were induced by a moderate decrease of the arterial oxygen saturation (SaO2) and by varying the arterial carbon dioxide level (PaCO2). This will result in a higher (hypercapnia) or lower (hypocapnia) cerebral blood flow and subsequent change of both NIRS signals and INVOS signal. Healthy volunteers were used for this study. It was found that the steady state value for rSO2 was 70 +/- 6% (mean +/- SD). During the lowering of arterial saturation a poor correlation was found between rSO2 and SaO2 (r = 0.47). Increased cerebral blood flow induced by hypercapnia was detected by both conventional NIRS and the INVOS. Decreased cerebral blood flow induced by hypocapnia could only be detected by conventional NIRS. It was concluded that due to the variation in displayed rSO2 and the high amount of averaging in the algorithm the INVOS instrument does not yet provide more information than conventional NIRS.
The aim of this study was to determine oxygen consumption (VO2) during isometric exercise in human muscles using near infrared spectroscopy (NIRS). The technique was used to study the relationship between VO2 in the soleus muscle and the level of isometric exercise expressed as percentages of the maximum voluntary contraction (MVC). For the study 11 healthy male volunteers were recruited. Reproducibility was studied in 6 subjects. The subjects were seated in a chair with the knee joint at an angle of 90 degrees. The optodes of the NIRS instrument were attached to the lateral aspect of the soleus muscle. A horizontal bar above the knee was connected to a dynamometer. Subjects applied isometric force to the bar by producing a torque at the ankle joint. Firstly the MVC was determined. Secondly the VO2 at rest and at 5 levels of isometric exercise, ranging from 5% to 25% of MVC and increasing by 5% each stage, was measured. In all cases the VO2 at rest or during isometric contraction was determined from the decrease of the oxyhaemoglobin (O2Hb) signal immediately after arterial occlusion of the thigh. Repeated measurements showed no significant difference between trials, indicating that the measurements were reproducible. At rest a VO2 of 6.7 +/- 1.1 microMO2Hb.min-1 (mean +/- S.E.M.) was found, a result comparable with other studies. In all subjects a linear relationship was found between the VO2 and the level of exercise. The average slope of the regression lines of all individuals was 0.85 +/- 0.22 microMO2Hb.min-1.%MVC-1 (mean +/- S.E.M.). Inter-individual variation of the slopes was high and ranged from 0.28 to 2.29 microMO.Hb.min-1.%MVC-1, which can be explained by differences in fat percentage and in the measuring volume of the NIRS instrument. NIRS appeared to be a reproducible and reliable method for the non-invasive measurement of VO2 in human muscles. The method could be used to investigate regional differences as well as changes in time between muscle groups as a function of training.
OBJECTIVE: To investigate the cerebrovascular response to changes in arterial CO2 tension during extracorporeal membrane oxygenation (ECMO) in normoxaemic and hypoxaemic piglets. METHODS: Four groups of six anaesthetized, paralysed and mechanically ventilated piglets: group 1-normoxaemia without ECMO, group 2-ECMO after normoxaemia, group 3-hypoxaemia without ECMO, and group 4-ECMO after hypoxaemia, were exposed successively to hypercapnia and hypocapnia. Changes in cerebral concentrations of oxyhaemoglobin (cO2Hb), deoxyhaemoglobin (cHHb), (oxidized-reduced) cytochrome aa3 (cCyt.aa3) and blood volume (CBV) were continuously measured using near infrared spectrophotometry. Heart rate, arterial O2 saturation, arterial blood pressure, central venous pressure, intracranial pressure (ICP) and left common carotid artery blood flow (LCaBF) were measured simultaneously. RESULTS: Hypercapnia resulted in increased CBV, cO2Hb and ICP in all groups, while cHHb was decreased. No changes in LCaBF were found. Hypocapnia resulted in decreased cO2Hb and increased cHHb except in group 3. LCaBF decreased in all groups except group 2. CBV decreased only in groups 2 and 4. No effect on ICP was observed in any of the groups. The other variables showed no important changes either during hypercapnia or hypocapnia. ECMO after hypoxaemia resulted in a greater response of cO2Hb and cO2Hb and cHHb during hypocapnia. The effect of hypercapnia on CBV while on ECMO was greater than without ECMO. CONCLUSION: Since cerebrovascular reactivity to CO2 remains intact during ECMO in piglets, it is important to keep arterial CO2 tension stable and in normal range during clinical ECMO.
Cryptorchidism is the most common male sexual disorder. In the case of an abdominal testis there is no objective criterion to choose between autotransplantation or orchiopexy after ligation of the spermatic vessels with subsequent development of collateral blood supply. By combining near infrared spectroscopy (NIRS) with pulse oximetry the active testicular blood volume (ATBV) before and after occlusion of the spermatic vessels can be calculated in an animal model. NIRS is a noninvasive continuous optical technique that measures tissue oxygenation and hemodynamics. Ten boars with one non-palpable testis each were selected. The spermatic vessels and vas deferens were separately prepared and atraumatic occluders were placed around the vessels. ATBV was measured before and after occlusion of the spermatic vessels. The calculated ATBV was 18.3 +/- 2.3 ml/100 g of testicular tissue, not corrected by division by the path length factor, accounting for light scattering in the tissue. In 5 of 10 boars no significant ATBV was found after occlusion of the spermatic vessels, suggesting subsequent atrophy. NIRS combined with pulse oximetry provides us with reproducible quantification of ATBV. The method can be used to investigate the viability of a testis after (temporary) occlusion of the spermatic vessels.
The objective of this study was to investigate changes of cerebral oxygenation and hemodynamics related to opening of the bypass bridge during veno-arterial extracorporeal membrane oxygenation (ECMO). Ten newborn infants and 12 piglets were studied during opening of the bridge for 10 and 1 s, respectively. Changes in cerebral concentration of oxyhemoglobin (cO2Hb), deoxyhemoglobin (cHHb), (oxidized-reduced) cytochrome aa3 (cCyt.aa3), and blood volume (CBV) were continuously measured by near infrared spectrophotometry. Heart rate, arterial O2 saturation (saO2), and mean arterial blood pressure (MABP) were measured simultaneously. In the piglets, central venous pressure (CVP), intracranial pressure (ICP), and left common carotid artery blood flow (CaBF) were also measured. Opening of the bridge for 10 s in the infants resulted in a significant decrease in MABP, saO2, and cO2Hb, whereas cHHb increased. CBV did not change significantly. In piglets biphasic changes were observed for MABP, CaBF, cO2Hb, and CBV, showing an initial decrease followed by a smaller increase. cHHb and CVP showed reverse biphasic changes. ICP increased but saO2 was unchanged. In all cases heart rate and cCyt.aa3 did not change significantly. Opening of the bridge for 1 s resulted in minor changes in only a few variables. In conclusion, opening of the bridge resulted in a decrease of CBV and cerebral O2 supply due to a decrease of cerebral blood flow, followed by a compensatory increase of cerebral O2 extraction and vasodilatation. The return of oxygenated blood after reclosing resulted in an increase of CBV with overcompensation of cerebral O2 supply.
OBJECTIVE: To investigate cerebral oxygenation and hemodynamics in relation to changes in some relevant physiologic variables during induction of extracorporeal membrane oxygenation (ECMO) in newborn infants. METHODS: Twenty-four newborn infants requiring ECMO were studied from cannulation until 60 minutes after starting ECMO. Concentration changes of oxyhemoglobin (cO2Hb), deoxyhemoglobin (cHHb), total hemoglobin (ctHb), and (oxidized-reduced) cytochrome aa3 (cCyt.aa3) in cerebral tissue were measured continuously by near infrared spectrophotometry. Heart rate (HR), transcutaneous partial pressures of oxygen and carbon dioxide (tcPO2 and tcPCO2), arterial O2 saturation (saO2), and mean arterial blood pressure (MABP) were measured simultaneously. Intravascular hemoglobin concentration (cHb) was measured before and after starting ECMO. In 18 of the 24 infants, mean blood flow velocity (MBFV) and pulsatility index (PI) in the internal carotid and middle cerebral arteries were also measured before and after starting ECMO using pulsed Doppler ultrasound. RESULTS: After carotid ligation, cO2Hb decreased whereas cHHb increased. After jugular ligation, no changes in cerebral oxygenation were found. At 60 minutes after starting ECMO, the values of cO2Hb, saO2, tcPO2, and MABP were significantly higher than the precannulation values, whereas the value of cHHb was lower. There were no changes in cCyt.aa3, tcPCO2, and HR, whereas cHb decreased. The MBFV was significantly increased in the major cerebral arteries except the right middle cerebral artery, whereas PI was decreased in all measured arteries. Cerebral blood volume, calculated from changes in ctHb and cHb, was increased in 20 of 24 infants after starting ECMO. Using multivariate regression models, a positive correlation of delta ctHb (representative of changes in cerebral blood volume) with delta MABP and a negative correlation with delta tcPO2 were found. CONCLUSIONS: The alterations in cerebral oxygenation after carotid artery ligation might reflect increased O2 extraction. Despite increase of the cerebral O2 supply after starting ECMO, no changes in intracellular O2 availability were found, probably because of sufficient preservation of intracellular cerebral oxygenation in the pre-ECMO period despite prolonged hypoxemia. The increase in cerebral blood volume and cerebral MBFV may result from the following: (1) reactive hyperperfusion, (2) loss of autoregulation because of prolonged hypoxemia before ECMO and/or decreased arterial pulsatility, or (3) compensation for hemodilution related to the ECMO procedure.
In the fetus, the arterial oxygen saturation (SaO2) in the ascending aorta is higher than in the descending aorta. We questioned whether this difference over the ductus arteriosus (delta SaO2) would change during hypoxaemia. Therefore, six chronically instrumented fetal lambs (119-126 days of gestation) were studied, by changing the inspired oxygen (FIO2) via a tracheal tube to the ewe. The SaO2 was measured intermittently every 15 min with blood samples obtained from the ascending and descending aorta, and continuously with 2 pulse oximeters at both sides of the ductus arteriosus. delta SaO2 was at a level of 3.4-5.3% and had a tendency to decrease at preductal SaO2 levels of 10-20% and at pH levels below 7.25. The precision of the pulse oximeters, expressed as standard deviation of the differences between sample SaO2 and pulse oximeter SaO2, was around 5.0% for the individual calibration curves. This precision was not enough to show details of the course of delta SaO2 between the blood samples. Our results show that there is no change in delta SaO2 across the ductus arteriosus.
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