Preserved arterial flow secures hepatic oxygenation during haemorrhage in the pig.
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1. This study examined the extent of liver perfusion and its oxygenation during progressive haemorrhage. We examined hepatic arterial flow and hepatic oxygenation following the reduced portal flow during haemorrhage in 18 pigs. The hepatic surface oxygenation was assessed by near-infrared spectroscopy and the hepatic metabolism of oxygen, lactate and catecholamines determined the adequacy of the hepatic flow. 2. Stepwise haemorrhage until circulatory collapse resulted in proportional reductions in cardiac output and in arterial, central venous and pulmonary wedge pressures. While heart rate increased, pulmonary arterial pressure remained stable. In addition, renal blood flow decreased, renal vascular resistance increased and there was elevated noradrenaline spill-over. Further, renal surface oxygenation was lowered from the onset of haemorrhage. 3. Similarly, the portal blood flow was reduced in response to haemorrhage, and, as for the renal flow, the reduced splanchnic blood flow was associated with an elevated noradrenaline spill-over. In contrast, hepatic arterial blood flow was only slightly reduced by haemorrhage, and surface oxygenation did not change. The hepatic oxygen uptake was maintained until the blood loss represented more than 30 % of the estimated blood volume. At 30 % reduced blood volume, hepatic catecholamine uptake was reduced, and the lactate uptake approached zero. 4. Subsequent reduction of cardiac output and portal blood flow elicited a selective dilatation of the hepatic arterial vascular bed. Due to this dilatation liver blood flow and hepatic cell oxygenation and metabolism were preserved prior to circulatory collapse. (+info)
Carbogen-induced changes in rat mammary tumour oxygenation reported by near infrared spectroscopy.
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We have evaluated the ability of steady-state, radially-resolved, broad-band near infrared diffuse reflectance spectroscopy to measure carbogen-induced changes in haemoglobin oxygen saturation (SO2) and total haemoglobin concentration in a rat R3230 mammary adenocarcinoma model in vivo. Detectable shifts toward higher saturations were evident in all tumours (n = 16) immediately after the onset of carbogen breathing. The SO2 reached a new equilibrium within 1 min and remained approximately constant during 200-300 s of administration. The return to baseline saturation was more gradual when carbogen delivery was stopped. The degree to which carbogen increased SO2 was variable among tumours, with a tendency for tumours with lower initial SO2 to exhibit larger changes. Tumour haemoglobin concentrations at the time of peak enhancement were also variable. In the majority of cases, haemoglobin concentration decreased in response to carbogen, indicating that increased tumour blood volume was not responsible for the observed elevation in SO2. We observed no apparent relationship between the extent of the change in tumour haemoglobin concentration and the magnitude of the change in the saturation. Near infrared diffuse reflectance spectroscopy provides a rapid, non-invasive means of monitoring spatially averaged changes in tumour haemoglobin oxygen saturation induced by oxygen modifiers. (+info)
Dynamics of tissue oxygenation in isolated rabbit heart as measured with near-infrared spectroscopy.
(3/1225)
We investigated the role of myoglobin (Mb) in supplying O2 to mitochondria during transitions in cardiac workload. Isovolumic rabbit hearts (n = 7) were perfused retrogradely with hemoglobin-free Tyrode solution at 37 degrees C. Coronary venous O2 tension was measured polarographically, and tissue oxygenation was measured with two-wavelength near-infrared spectroscopy (NIRS), both at a time resolution of approximately 2 s. During transitions to anoxia, 68 +/- 2% (SE) of the NIRS signal was due to Mb and the rest to cytochrome oxidase. For heart rate steps from 120 to 190 or 220 beats/min, the NIRS signal decreased significantly by 6.9 +/- 1.3 or 11.1 +/- 2.1% of the full scale, respectively, with response times of 11.0 +/- 0.8 or 9.1 +/- 0.5 s, respectively. The response time of end-capillary O2 concentration ([O2]), estimated from the venous [O2], was 8.6 +/- 0.8 s for 190 beats/min (P < 0.05 vs. NIRS time) or 8.5 +/- 0.9 s for 220 beats/min (P > 0.05). The mean response times of mitochondrial O2 consumption (VO2) were 3.7 +/- 0.7 and 3.6 +/- 0.6 s, respectively. The deoxygenation of oxymyoglobin (MbO2) accounted for only 12-13% of the total decrease in tissue O2, with the rest being physically dissolved O2. During 11% reductions in perfusion flow at 220 beats/min, Mb was 1.5 +/- 0.4% deoxygenated (P < 0.05), despite the high venous PO2 of 377 +/- 17 mmHg, indicating metabolism-perfusion mismatch. We conclude that the contribution of MbO2 to the increase of VO2 during heart rate steps in saline-perfused hearts was small and slow compared with that of physically dissolved O2. (+info)
Comparative analysis of NMR and NIRS measurements of intracellular PO2 in human skeletal muscle.
(4/1225)
1H NMR has detected both the deoxygenated proximal histidyl NdeltaH signals of myoglobin (deoxyMb) and deoxygenated Hb (deoxyHb) from human gastrocnemius muscle. Exercising the muscle or pressure cuffing the leg to reduce blood flow elicits the appearance of the deoxyMb signal, which increases in intensity as cellular PO2 decreases. The deoxyMb signal is detected with a 45-s time resolution and reaches a steady-state level within 5 min of pressure cuffing. Its desaturation kinetics match those observed in the near-infrared spectroscopy (NIRS) experiments, implying that the NIRS signals are actually monitoring Mb desaturation. That interpretation is consistent with the signal intensity and desaturation of the deoxyHb proximal histidyl NdeltaH signal from the beta-subunit at 73 parts per million. The experimental results establish the feasibility and methodology to observe the deoxyMb and Hb signals in skeletal muscle, help clarify the origin of the NIRS signal, and set a stage for continuing study of O2 regulation in skeletal muscle. (+info)
Noninvasive assessment of changes in cytochrome-c oxidase oxidation in human subjects during visual stimulation.
(5/1225)
In this study the authors used a whole-spectrum near-infrared spectroscopy approach to noninvasively assess changes in hemoglobin oxygenation and cytochrome-c oxidase redox state (Cyt-Ox) in the occipital cortex during visual stimulation. The system uses a white light source (halogen lamp). The light reflected from the subject's head is spectrally resolved by a spectrograph and dispersed on a cooled charge-coupled device camera. The authors showed the following using this approach: (1) Changes in cerebral hemoglobin oxygenation (increase in concentration of oxygenated hemoglobin, decrease in concentration of deoxygenated hemoglobin) in the human occipital cortex during visual stimulation can be assessed quantitatively. (2) The spectral changes during functional activation cannot be completely explained by changes in hemoglobin oxygenation solely; Cyt-Ox has to be included in the analysis. Only if Cyt-Ox is considered can the spectral changes in response to increased brain activity be explained. (3) Cytochrome-c oxidase in the occipital cortex of human subjects is transiently oxidized during visual stimulation. This allows us to measure vascular and intracellular energy status simultaneously. (+info)
Low cerebral blood flow is a risk factor for severe intraventricular haemorrhage.
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AIMS: To investigate the relation between cerebral blood flow on the first day of postnatal life and the severity of any subsequent germinal matrix haemorrhage-intraventricular haemorrhage (GMH-IVH). METHODS: Cerebral blood flow was measured in 24 babies during the first 24 hours of life using near infrared spectroscopy. Repeated cerebral ultrasound examination was performed to define the maximum extent of GMH-IVH. Infants were classified as: normal scan, minor periventricular haemorrhage (haemorrhage that resolved), or severe GMH-IVH (haemorrhage distending the ventricles, that progressed to either post haemorrhagic dilatation or porencephalic cyst formation). RESULTS: Cerebral blood flow was significantly lower in the infants with GMH-IVH (median 7.0 ml/100 g/min) than those without haemorrhage (median 12.2 ml/100 g/min), despite no difference in carbon dioxide tension and a higher mean arterial blood pressure. On subgroup analysis, those infants with severe GMH-IVH had the lowest cerebral blood flow. CONCLUSION: A low cerebral blood flow on the first day of life is associated with the subsequent development of severe intraventricular haemorrhage. (+info)
Blood lactate accumulation and muscle deoxygenation during incremental exercise.
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Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration ([La](b)) increases at submaximal workloads (). We combined, on five well-trained subjects [mountain climbers; peak O(2) consumption (VO(2peak)), 51.0 +/- 4.2 (SD) ml. kg(-1). min(-1)] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe [La](b) with determinations of concentration changes of oxygenated Hb (Delta[O(2)Hb]) and deoxygenated Hb (Delta[HHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A "point of inflection" of [La](b) vs. was arbitrarily identified at the lowest [La](b) value which was >0.5 mM lower than that obtained at the following. Total Hb volume (Delta[O(2)Hb + HHb]) in the muscle region of interest increased as a function of up to 60-65% of VO(2 peak), after which it remained unchanged. The oxygenation index (Delta[O(2)Hb - HHb]) showed an accelerated decrease from 60- 65% of VO(2 peak). In the presence of a constant total Hb volume, the observed Delta[O(2)Hb - HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r(2) = 0.95; P < 0.01) with the point of inflection of [La](b) vs., i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous PO(2) levels at higher than approximately 60% of maximal O(2) consumption. Thus muscle deoxygenation observed in the present study from 60-65% of VO(2 peak) could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular PO(2) levels, as a consequence of a rightward shift of the O(2)Hb dissociation curve determined by the onset of lactic acidosis. (+info)
Muscle O(2) consumption by NIRS: a theoretical model.
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In the past, the measurement of O(2) consumption ((2)) by the muscle could be carried out noninvasively by near-infrared spectroscopy from oxyhemoglobin and/or deoxyhemoglobin measurements only at rest or during steady isometric contractions. In the present study, a mathematical model is developed allowing calculation, together with steady-state levels of (2), of the kinetics of (2) readjustment in the muscle from the onset of ischemic but aerobic constant-load isotonic exercises. The model, which is based on the known sequence of exoergonic metabolic pathways involved in muscle energetics, allows simultaneous fitting of batched data obtained during exercises performed at different workloads. A Monte Carlo simulation has been carried out to test the quality of the model and to define the most appropriate experimental approach to obtain the best results. The use of a series of experimental protocols obtained at different levels of mechanical power, rather than repetitions of the same load, appears to be the most suitable procedure. (+info)