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Tissue PO2 (tissue + po2)
Selected AbstractsTheoretical Simulation of Oxygen Transport to Brain by Networks of Microvessels: Effects of Oxygen Supply and Demand on Tissue HypoxiaMICROCIRCULATION, Issue 4 2000T.W. SECOMB ABSTRACT Objective: Simulations of oxygen delivery by a three-dimensional network of microvessels in rat cerebral cortex were used to examine how the distribution of partial pressure of oxygen (PO2) in tissue depends on blood flow and oxygen consumption rates. Methods: Network geometry was deduced from previously published scanning electron micrographs of corrosion casts. A nonlinear least-squares method, using images obtained at three different angles, was used to estimate vessel locations. The network consisted of 50 segments in a region 140 µm × 150 µm × 160 µm. A Green's function method was used to predict the PO2 distribution. Effects of varying perfusion and consumption were examined, relative to a control state with consumption 10 cm3O2/100 g per min and perfusion 160 cm3/100 g per min. Results: In the control state, minimum tissue PO2 was 7 mm Hg. A Krogh-type model with the same density of vessels, but with uniform spacing, predicted a minimum tissue PO2 of 23 mm Hg. For perfusion below 60% of control, tissue hypoxia (PO2 <1 mm Hg) was predicted. When perfusion was reduced by 75%, the resulting hypoxia could be eliminated by a 31% reduction in oxygen consumption rate. Conclusions: The simulations suggest that tissue hypoxia resulting from a severe decrease in brain perfusion, as can occur in stroke, may be avoided by a moderate decrease in oxygen consumption rate. [source] Baseline physiological state and the fMRI-BOLD signal response to apnea in anesthetized ratsNMR IN BIOMEDICINE, Issue 5 2003Sridhar S. Kannurpatti Abstract To decipher the biophysical mechanism behind the fMRI-BOLD response to apnea and its dependence on the baseline cerebral blood flow and oxygenation, fMRI and laser Doppler flow (LDF) studies were carried out in anesthetized rats. Baseline cerebral blood flow (CBF) and PaO2 were modulated by ventilating with different gas mixtures namely, room air (21% O2), 100% O2, carbogen (95% O2+5% CO2), 2% CO2 in air or 5% CO2 in air, respectively. A decrease in BOLD signal intensity was observed after the onset of apnea with either room air, 2% CO2 or 5% CO2 ventilation. PaO2 and cerebral tissue PO2 decreased during apnea under these conditions. However, the apnea-induced BOLD signal intensity was unaffected with carbogen ventilation and increased with 100% O2 ventilation, during which PaO2 remained constant and cerebral tissue PO2 increased. When baseline CBF was high during hypercapnia, a faster decrease occurred in the apnea-induced BOLD signal. Apnea induced the largest increase in CBF of 85±25% when ventilated with 2% CO2 while a 44±8% increase was observed with room air. During the other ventilatory conditions, minimal or no significant change in CBF was observed during apnea. These results show a significant correlation between the BOLD signal change and tissue PO2 in response to apnea under different physiological conditions. Apnea-induced increase in CBF affects the magnitude of the BOLD signal response when PaO2 remains constant or changes minimally. Copyright © 2001 John Wiley & Sons, Ltd. [source] 3122: Regulation of retinal tissue oxygenationACTA OPHTHALMOLOGICA, Issue 2010CJ POURNARAS Purpose To evaluate the changes in the retinal oxygen partial pressure (PO2) following physiological stimuli. Methods Evaluation of either the preretinal and intraretina partial pressure of oxygen (PO2) distribution, using oxygen sensitive microelectrodes, in various animal models. Measurements were obtained during changes of the perfusion pressure, systemic hyperoxia, hypoxia, hypercapnia, carbogen breathing and following carbonic anydrase inhibitors use. Results The oxygen tension (PO2) in the inner half of the retina remains largely unaffected by moderate changes in perfusion pressure. The increase of the systemic PaO2 through breathing of 100% O2 (hyperoxia) induces endothelin (ET) mediated marked vasoconstriction of the inner retinal arterioles in both anesthetized animals and normal human subjects. The regulatory vasoconstriction maintains the PO2 in retinal tissue constant. A decrease in PaO2 (hypoxia) induces a vasodilation of the retinal arterioles through endothelium-derived NO release. As a result, trans-retinal PO2 profiles made during steps of systemic hypoxia have shown that the values measured in the inner retina up to half of its thickness, remain rather stable. By contrast, the PO2 values, measured close to the choroid and in the outer retina, decrease in a linear manner with the decrease of the PaO2. An increase in the PaCO2 (hypercapnia) of arteriolar blood, produces an increase in retinal blood flow and retinal tissue PO2. Intravenous injection of acetazolamide (carbonic anhydrase inhibitor) produces an increase in preretinal PO2 due to dilation of the retinal vessels Conclusion Thanks to the autoregulatory capability of the retinal circulation, the oxygen tension (PO2) in the inner half of the retina, remains largely unaffected during physiological stimuli. [source] Renal And Cardiovascular Actions Of 20-Hydroxyeicosatetraenoic Acid And Epoxyeicosatrienoic AcidsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2000Richard J Roman SUMMARY 1. Arachidonic acid (AA) is metabolized by cytochrome P450 (CYP)-dependent pathways to epoxyeicosatrienoic acids (EET) and 20-hydroxyeicosatetraenoic acid (20-HETE) in the kidney and the peripheral vasculature. 2. The present short review summarizes the renal and cardiovascular actions of these important mediators. 3. Epoxyeicosatrienoic acids are vasodilators produced by the endothelium that hyperpolarize vascular smooth muscle (VSM) cells by opening Ca2+ -activated K+ (KCa) channels. 20-Hydroxyeicosatetraenoic acid is a vasoconstrictor that inhibits the opening of KCa channels in VSM cells. Cytochrome P450 4A inhibitors block the myogenic response of small arterioles to elevations in transmural pressure and autoregulation of renal and cerebral blood flow in vivo. Cytochrome P450 4A blockers also attenuate the vasoconstrictor response to elevations in tissue PO2, suggesting that this system may serve as a vascular oxygen sensor. Nitric oxide and carbon monoxide inhibit the formation of 20-HETE and a fall in 20-HETE levels contributes to the activation of KCa channels in VSM cells and the vasodilator response to these gaseous mediators. 20-Hydroxyeicosatetraenoic acid also mediates the inhibitory actions of peptide hormones on sodium transport in the kidney and the mitogenic effects of growth factors in VSM and mesangial cells. A deficiency in the renal production of 20-HETE is associated with the development of hypertension in Dahl salt-sensitive rats. 4. In summary, the available evidence indicates that CYP metabolites of AA play a central role in the regulation of renal, pulmonary and vascular function and that abnormalities in this system may contribute to the pathogenesis of cardiovascular diseases. [source] METHODS FOR STUDYING THE PHYSIOLOGY OF KIDNEY OXYGENATIONCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2008Roger G Evans SUMMARY 1An improved understanding of the regulation of kidney oxygenation has the potential to advance preventative, diagnostic and therapeutic strategies for kidney disease. Here, we review the strengths and limitations of available and emerging methods for studying kidney oxygen status. 2To fully characterize kidney oxygen handling, we must quantify multiple parameters, including renal oxygen delivery (DO2) and consumption (VO2), as well as oxygen tension (Po2). Ideally, these parameters should be quantified both at the whole-organ level and within specific vascular, tubular and interstitial compartments. 3Much of our current knowledge of kidney oxygen physiology comes from established techniques that allow measurement of global kidney DO2 and VO2, or local tissue Po2. When used in tandem, these techniques can help us understand oxygen mass balance in the kidney. Po2 can be resolved to specific tissue compartments in the superficial cortex, but not deep below the kidney surface. We have limited ability to measure local kidney tissue DO2 and VO2. 4Mathematical modelling has the potential to provide new insights into the physiology of kidney oxygenation, but is limited by the quality of the information such models are based on. 5Various imaging techniques and other emerging technologies have the potential to allow Po2 mapping throughout the kidney and/or spatial resolution of Po2 in specific renal tissues, even in humans. All currently available methods have serious limitations, but with further refinement should provide a pathway through which data obtained from experimental animal models can be related to humans in the clinical setting. [source] New method of dynamic color doppler signal quantification in metastatic lymph nodes compared to direct polarographic measurements of tissue oxygenationINTERNATIONAL JOURNAL OF CANCER, Issue 6 2005Thomas Scholbach Abstract Tumor growth depends on sufficient blood and oxygen supply. Hypoxia stimulates neovascularization and is a known cause for radio- and chemoresistance. The objective of this study was to investigate the use of a novel ultrasound technique for the dynamic assessment of vascularization and oxygenation in metastatic lymph nodes. Twenty-four patients (age 44,78 years) with cervical lymph node metastases of squamous cell head and neck cancer were investigated by color duplex sonography and 17 (age 46,78 years) were investigated additionally with polarography. Sonography was performed after contrast enhancer infusion under defined conditions. Intranodal perfusion data (color hue, colored area) were measured automatically by a novel software technique. This allows an evaluation of blood flow dynamics by calculating perfusion intensity,velocity, perfused area, as well as the novel parameters tissue resistance index (TRI) and tissue pulsatility index (TPI),for each point of a complete heart cycle. Tumor tissue pO2 was measured by means of polarographic needle electrodes placed intranodally. The sonographic and polarographic data were correlated using Pearson's test. Sonography demonstrated a statistically significant inverse correlation between hypoxia and perfusion and significant TPI and TRI changes with different N-stages. The percentage of nodal fraction with less than 10 mmHg oxygen saturation was significantly inversely correlated with lymph node perfusion (r = ,0.551; p = 0.021). Nodes with a perfusion of less than 0.05 cm/sec flow velocity showed significantly larger hypoxic areas (p = 0.006). Significant differences of TPI and TRI existed between nodes in stage N1 and N2/N3 (p = 0.028 and 0.048, respectively). This new method of dynamic signal quantification allows a noninvasive and quantitative assessment of tumor and metastatic lymph node perfusion by means of commonly available ultrasound equipment. © 2004 Wiley-Liss, Inc. [source] EPR oximetry in the beating heart: Myocardial oxygen consumption rate as an index of postischemic recoveryMAGNETIC RESONANCE IN MEDICINE, Issue 4 2004Govindasamy Ilangovan Abstract Oxygen plays a critical role in the pathophysiology of myocardial injury during both ischemia and subsequent reperfusion (I/R). Thus, oxygen concentration is an important variable to measure during I/R. In the present work, electron paramagnetic resonance (EPR)-based oximetry was used to measure the oxygen concentration during a series of I/R episodes and oxygenation levels were correlated with the contractile and hemodynamic functions of the heart. A custom-developed electronically tunable surface coil resonator working at 1.1 GHz was used to determine tissue pO2 in the beating heart. Microcrystalline particulate of lithium phthalocyanine was used as an EPR oximetry probe. Isolated and perfused rat hearts were subjected to 1 or 3 hr durations of preischemic perfusion, followed by 15-min I/R cycles. In hearts perfused for 3 hr prior to 15-min I/R cycles, the myocardial pO2 decreased gradually on subsequent reperfusions of three successive I/R cycles. However, in hearts perfused for 1 hr there was almost 100% recovery of myocardial pO2 in all three I/R cycles. The extent of oxygenation recovered in each reperfusion cycle correlated with the recovery of hemodynamic and contractile function. The results also showed that the oxygen consumption rate of the heart at the end of each I/R episode decreased in direct proportion to the functional recovery. In summary, it was observed that the amount of myocardial oxygen consumption during I/R could provide a reliable index of functional impairment in the heart. Magn Reson Med 51:835,842, 2004. © 2004 Wiley-Liss, Inc. [source] | ||||||||||