Capillary structures and O2 supply to tissue

2006 ◽  
pp. 149-209 ◽  
Author(s):  
W. A. Grunewald ◽  
W. Sowa
Keyword(s):  
O2 Supply

Effect of medial arterial calcification on O2 supply to exercising diabetic feet

Diabetes ◽  
1990 ◽  
Vol 39 (8) ◽  
pp. 938-941 ◽  
Author(s):  
E. Chantelau ◽  
X. Y. Ma ◽  
S. Herrnberger ◽  
C. Dohmen ◽  
P. Trappe ◽  
...  
Keyword(s):  
Arterial Calcification ◽  
O2 Supply ◽  
Medial Arterial Calcification

Metabolic and circulatory responses of normoxic skeletal muscle to whole-body hypoxia

1988 ◽  
Vol 65 (5) ◽  
pp. 2063-2068 ◽  
Author(s):  
D. L. Bredle ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Autologous Blood ◽  
Whole Body ◽  
Membrane Oxygenator ◽  
O2 Uptake ◽  
Ici 118,551 ◽  
Autoregulatory Escape ◽  
Beta 2 ◽  
O2 Supply

Whole-body hypoxia may increase peripheral O2 demand because it increases catecholamine calorigenesis, an effect attributable to beta 2-adrenoceptors. We tested these possibilities by pump-perfusing innervated hindlimbs in eight dogs with autologous blood kept normoxic by a membrane oxygenator while ventilating the animals for 40 min with 9% O2 in N2 (NOB group). Similar periods of normoxic ventilation preceded and followed the hypoxic period. A second group (n = 8, beta B) was pretreated with the specific beta 2 blocker ICI 118,551. Hindlimb O2 uptake was elevated by 25 min of hypoxia in NOB, whereas whole-body O2 uptake was reduced. Limb O2 uptake remained elevated in recovery, but all effects on limb O2 uptake were absent in beta B. Hindlimb resistance and perfusion pressure increased in hypoxia in both groups, and there was little evidence of local escape from reflex vasoconstriction. These results clearly indicated that global hypoxia increased O2 demand in muscle when the local O2 supply was not limited and that beta 2-receptors were necessary for this response. Autoregulatory escape of limb muscle blood flow from centrally mediated vasoconstriction during whole-body hypoxia was also shown to be practically nil, if normoxia was maintained in the limb.

Analysis of oxygen delivery and uptake relationships in the Krogh tissue model

1989 ◽  
Vol 67 (3) ◽  
pp. 1234-1244 ◽  
Author(s):  
P. T. Schumacker ◽  
R. W. Samsel
Keyword(s):  
Blood Flow ◽  
Critical Point ◽  
Real Data ◽  
Whole Body ◽  
O2 Uptake ◽  
Highly Sensitive ◽  
O2 Extraction ◽  
O2 Supply ◽  
Experimental Findings ◽  
O2 Delivery

Normally, tissue O2 uptake (VO2) is set by metabolic activity rather than O2 delivery (QO2 = blood flow X arterial O2 content). However, when QO2 is reduced below a critical level, VO2 becomes limited by O2 supply. Experiments have shown that a similar critical QO2 exists, regardless of whether O2 supply is reduced by progressive anemia, hypoxemia, or reduction in blood flow. This appears inconsistent with the hypothesis that O2 supply limitation must occur by diffusion limitation, since very different mixed venous PO2 values have been seen at the critical point with hypoxic vs. anemic hypoxia. The present study sought to begin clarifying this paradox by studying the theoretical relationship between tissue O2 supply and uptake in the Krogh tissue cylinder model. Steady-state O2 uptake was computed as O2 delivery to tissue representative of whole body was gradually lowered by anemic, hypoxic, or stagnant hypoxia. As diffusion began to limit uptake, the fall in VO2 was computed numerically, yielding a relationship between QO2 and VO2 in both supply-independent and O2 supply-dependent regions. This analysis predicted a similar biphasic relationship between QO2 and VO2 and a linear fall in VO2 at O2 deliveries below a critical point for all three forms of hypoxia, as long as intercapillary distances were less than or equal to 80 microns. However, the analysis also predicted that O2 extraction at the critical point should exceed 90%, whereas real tissues typically extract only 65–75% at that point. When intercapillary distances were larger than approximately 80 microns, critical O2 extraction ratios in the range of 65–75% could be predicted, but the critical point became highly sensitive to the type of hypoxia imposed, contrary to experimental findings. Predicted gas exchange in accord with real data could only be simulated when a postulated 30% functional peripheral O2 shunt (arterial admixture) was combined with a tissue composed of Krogh cylinders with intercapillary distances of less than or equal to 80 microns. The unrealistic efficacy of tissue O2 extraction predicted by the Krogh model (in the absence of postulated shunt) may be a consequence of the assumed homogeneity of tissues, because real tissues exhibit many forms of heterogeneity among capillary units. Alternatively, the failure of the original Krogh model to fully predict tissue O2 supply dependency may arise from basic limitations in the assumptions of that model.

Coke-free operation of an all porous solid oxide fuel cell (AP-SOFC) used as an O2 supply device

2015 ◽  
Vol 3 (6) ◽  
pp. 2684-2689 ◽  
Author(s):  
Y. M. Guo ◽  
G. Largiller ◽  
C. Guizard ◽  
C. Tardivat ◽  
D. Farrusseng
Keyword(s):  
Fuel Cell ◽  
Solid Oxide Fuel Cell ◽  
Coke Formation ◽  
Solid Oxide ◽  
Operational Stability ◽  
Porous Solid ◽  
Cell Performance ◽  
Oxide Fuel ◽  
O2 Supply

An anode-supported AP-SOFC with long-term operational stability was developed to improve cell performance over 14 times without any coke formation.

scholarly journals Role of thromboxane A2 in the control of myocardial O2 supply/consumption balance and severity of ischemia during pacing-induced ischemia.

1989 ◽  
Vol 64 (3) ◽  
pp. 575-582 ◽  
Author(s):  
G J Grover ◽  
C S Parham
Keyword(s):  
Thromboxane A2 ◽  
O2 Supply

Abstract 10679: Tissue-to-Arterial Carbon Dioxide Partial Pressure Gradient as a Useful Measure for Monitoring Tissue Perfusion in a Pig Model of Hemorrhagic Shock and Resuscitation

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yusuke Endo ◽  
Lance B Becker ◽  
Ryosuke Takegawa ◽  
Santiago J Miyara ◽  
Ernesto P Molmenti ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Transfusion ◽  
Pulmonary Artery ◽  
Hemorrhagic Shock ◽  
Laboratory Data ◽  
Tissue Perfusion ◽  
Pig Model ◽  
Carbon Dioxide Partial Pressure ◽  
End Diastolic Volume ◽  
O2 Supply

Introduction: Transcutaneous CO 2 (tcPCO 2 ) and arterial CO 2 (artPCO 2 ) become decoupled during shock. Aim: To test the hypotheses the gradient between tcPCO 2 and artPCO 2 (tc-artPCO 2 ) can be an early, sensitive measure to detect inadequate tissue perfusion in a pig model of hemorrhage shock. Methods: Six female pigs were used. A transcutaneous monitor was attached to the ear for measuring transcutaneous O 2 (tcPO 2 ) and tcPCO 2 . Pulmonary artery catheter and the pulse index continuous cardiac output (PiCCO) were instrumented for monitoring a variety of hemodynamic parameters. To induce massive hemorrhagic shock, blood was withdrawn stepwisely. Then, animals were resuscitated in stages with transfusions of the stored blood. The parameters were measured at the timings of 10, 20, and 30 ml/kg of blood withdrawals and the completions of 10, 20, and 30 ml/kg of blood transfusion . Levels of systemic oxygen delivery (DO 2 ) were also calculated at all measurement points. Results: Hemorrhage and blood transfusion impacted hemodynamic and laboratory data, such as cardiac output (CO), stroke volume, MAP, heart rate, pulmonary artery wedge pressure, global end-diastolic volume, hemoglobin, and arterial lactate. The tc-artPCO 2 markedly increased as CO decreased ( Figure A ). The critical level of DO 2 (DO 2crit ) was defined as 11.72 ml/kg/min according to tcPO 2 (a threshold as 30 mmHg). There was significant correlation between tc-artPCO 2 and DO 2 (r = -0.83, P<.0001). ROC analyses revealed that the AUCs to predict DO 2crit for tc-artPCO 2 , shock index (SI), and lactate were 0.94 (95% CI, 0.87-1.00), 0.78 (0.63-0.93), and 0.65 (0.47-0.82), respectively. The AUC for tc-artPCO 2 was greater with respect to the prediction of DO 2crit than for SI (P<.05) ( Figure B ). Conclusions: The tc-artPCO 2 strongly correlated with CO and DO 2 during hemorrhage shock and resuscitation. The less-invasive tc-artPCO 2 monitoring can sensitively detect systemic inadequate O2 supply in hemorrhagic shock.

ASSESSMENT OF ALVEOLAR VENTILATION, CARDIAC OUTPUT AND TISSUE O2 SUPPLY UTILISING ESTIMATION OF MIXED VENOUS PCO2 BY A REBERATHING TECHNIQUE

1979 ◽  
Vol 7 (3) ◽  
pp. 138
Author(s):  
Alexander C. P. Powles ◽  
Kari Smedstad ◽  
John R. A. Rigg
Keyword(s):  
Cardiac Output ◽  
Alveolar Ventilation ◽  
Venous Pco2 ◽  
O2 Supply ◽  
Mixed Venous

Abstract W MP91: Supply-demand Mismatch Transients Trigger Peri-infarct Depolarizations In Ischemic Penumbra

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Daniel von Bornstädt ◽  
Jessica Seidel ◽  
Mathias Bernard Houben ◽  
Ergin Dilekoz ◽  
Tao Qin ◽  
...  
Keyword(s):  
Tactile Stimulation ◽  
Focal Cerebral Ischemia ◽  
Sensory Stimulation ◽  
Artery Occlusion ◽  
Cortical Activation ◽  
Normobaric Hyperoxia ◽  
Critical Range ◽  
O2 Supply ◽  
Cerebral Artery Occlusion ◽  
Distal Middle Cerebral Artery

Background: Peri-infarct depolarizations (PIDs) worsen the outcome of ischemic stroke. Unlike their impact on metabolism and perfusion, triggering factors are virtually unknown. We hypothesized that transient worsening of O2 supply-demand mismatch precipitates a PID in critically hypoperfused penumbra. Methods: We optically imaged cortical blood flow and oxygenation during distal middle cerebral artery occlusion in mice under full systemic physiological monitoring, and tested whether a transient (5 min) drop in O2 supply (hypotension or hypoxia) or increase in O2 demand (somatosensory cortical activation) can trigger PIDs during acute focal cerebral ischemia. Results: Transient hypotension (<70 mmHg) or hypoxia (<90 mmHg) triggered a PID 90% of the time (p<0.01). Increasing the O2 demand by functional activation (tactile stimulation) of moderately ischemic cortex (contralesional forepaw or shoulder S1) increased the 5-min incidence of PIDs by approximately five-fold (p=0.001). Cortical oxyhemoglobin levels dropped by 35-40% in the activated S1 immediately before a PID (p=0.004) confirming increased O2 demand. Cortical foci from which PIDs originated during tactile stimulation had 27-32% residual CBF, indicating the presence of a critical range of ischemia vulnerable to PID initiation upon increased demand. Consistently, activation of non-ischemic cortex (hindpaw S1) or severely ischemic cortex (whisker S1) did not significantly increase the PID rate. Both tetrodotoxin (1 μM topical) and normobaric hyperoxia prevented somatosensory triggering of PIDs. Conclusion: PIDs are triggered upon O2 supply-demand mismatch transients in metastable peri-infarct hot zones due to increased demand or reduced supply. We propose that minimizing sensory stimulation and hypoxic or hypotensive transients in the early stages of stroke and brain injury would reduce PID incidence and their adverse impact on outcome.

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