scholarly journals Cortical Spreading Depression Impairs Oxygen Delivery and Metabolism in Mice

2011 ◽  
Vol 32 (2) ◽  
pp. 376-386 ◽  
Author(s):  
Izumi Yuzawa ◽  
Sava Sakadžić ◽  
Vivek J Srinivasan ◽  
Hwa Kyoung Shin ◽  
Katharina Eikermann-Haerter ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Oxygen Delivery ◽  
Cortical Spreading Depression ◽  
Oxygen Supply ◽  
Spreading Depression ◽  
Oxygen Demand ◽  
Oxygen Metabolism ◽  
Cerebral Metabolic Rate ◽  
Tissue Oxygen Delivery ◽  
Steep Decline

Cortical spreading depression (CSD) is associated with severe hypoperfusion in mice. Using minimally invasive multimodal optical imaging, we show that severe flow reductions during and after spreading depression are associated with a steep decline in cerebral metabolic rate of oxygen. Concurrent severe hemoglobin desaturation suggests that the oxygen metabolism becomes at least in part supply limited, and the decrease in cortical blood volume implicates vasoconstriction as the mechanism. In support of oxygen supply-demand mismatch, cortical nicotinamide adenine dinucleotide (NADH) fluorescence increases during spreading depression for at least 5 minutes, particularly away from parenchymal arterioles. However, modeling of tissue oxygen delivery shows that cerebral metabolic rate of oxygen drops more than predicted by a purely supply-limited model, raising the possibility of a concurrent reduction in oxygen demand during spreading depression. Importantly, a subsequent spreading depression triggered within 15 minutes evokes a monophasic flow increase superimposed on the oligemic baseline, which markedly differs from the response to the preceding spreading depression triggered in naive cortex. Altogether, these data suggest that CSD is associated with long-lasting oxygen supply-demand mismatch linked to severe vasoconstriction in mice.

scholarly journals Non-Invasive measurement of the cerebral metabolic rate of oxygen using MRI in rodents

2021 ◽  
Vol 6 ◽  
pp. 109
Author(s):  
Tobias C Wood ◽  
Diana Cash ◽  
Eilidh MacNicol ◽  
Camilla Simmons ◽  
Eugene Kim ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Imaging Techniques ◽  
Glucose Consumption ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Strongly Correlated ◽  
Non Invasive ◽  
Cerebral Metabolic Rate ◽  
Invasive Measurement

Malfunctions of oxygen metabolism are suspected to play a key role in a number of neurological and psychiatric disorders, but this hypothesis cannot be properly investigated without an in-vivo non-invasive measurement of brain oxygen consumption. We present a new way to measure the Cerebral Metabolic Rate of Oxygen (CMRO2) by combining two existing magnetic resonance imaging techniques, namely arterial spin-labelling and oxygen extraction fraction mapping. This method was validated by imaging rats under different anaesthetic regimes and was strongly correlated to glucose consumption measured by autoradiography.

Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs

1990 ◽  
Vol 258 (6) ◽  
pp. G910-G918 ◽  
Author(s):  
K. Nagano ◽  
S. Gelman ◽  
E. L. Bradley ◽  
D. Parks
Keyword(s):  
Reperfusion Injury ◽  
Oxygen Delivery ◽  
Oxygen Supply ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Venous Blood ◽  
Oxygen Demand ◽  
Base Line ◽  
Hepatic Oxygen Delivery ◽  
Normothermic Group

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.

Effect of hyperoxia on cerebral metabolic rate for oxygen measured using positron emission tomography in patients with acute severe head injury

2007 ◽  
Vol 106 (4) ◽  
pp. 526-529 ◽  
Author(s):  
Michael N. Diringer ◽  
Venkatesh Aiyagari ◽  
Allyson R. Zazulia ◽  
Tom O. Videen ◽  
William J. Powers
Keyword(s):  
Positron Emission Tomography ◽  
Metabolic Rate ◽  
Oxygen Metabolism ◽  
Emission Tomography ◽  
Arterial Oxygen ◽  
Normobaric Hyperoxia ◽  
Brain Oxygen ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Brain Oxygen Metabolism

Object Recent observations indicate that traumatic brain injury (TBI) may be associated with mitochondrial dysfunction. This, along with growing use of brain tissue PO2 monitors, has led to considerable interest in the potential use of ventilation with 100% oxygen to treat patients who have suffered a TBI. To date, the impact of normobaric hyperoxia has only been evaluated using indirect measures of its impact on brain metabolism. To determine if normobaric hyperoxia improves brain oxygen metabolism following acute TBI, the authors directly measured the cerebral metabolic rate for oxygen (CMRO2) with positron emission tomography before and after ventilation with 100% oxygen. Methods Baseline measurements of arterial and jugular venous blood gases, mean arterial blood pressure, intracranial pressure, cerebral blood flow (CBF), cerebral blood volume, oxygen extraction fraction, and CMRO2 were made at baseline while the patients underwent ventilation with a fraction of inspired oxygen (FiO2) of 0.3 to 0.5. The FiO2 was then increased to 1.0, and 1 hour later all measurements were repeated. Five patients were studied a mean of 17.9 ±5.8 hours (range 12–23 hours) after trauma. The median admission Glasgow Coma Scale score was 7 (range 3–9). During ventilation with 100% oxygen, there was a marked rise in PaO2 (from 117 ± 31 to 371 ± 99 mm Hg, p < 0.0001) and a small rise in arterial oxygen content (12.7 ± 4.0 to 13.3 ± 4.6 vol %, p = 0.03). There were no significant changes in systemic hemodynamic or other blood gas measurements. At the baseline evaluation, bihemispheric CBF was 39 ± 12 ml/100 g/min and bihemispheric CMRO2 was 1.9 ± 0.6 ml/100 g/min. During hyperoxia there was no significant change in either of these measurements. (Values are given as the mean ± standard deviation throughout.) Conclusions Normobaric hyperoxia did not improve brain oxygen metabolism. In the absence of outcome data from clinical trials, these preliminary data do not support the use of 100% oxygen in patients with acute TBI, although larger confirmatory studies are needed.

Systems analysis of intestinal hemodynamics and oxygenation

1983 ◽  
Vol 245 (6) ◽  
pp. G786-G796 ◽  
Author(s):  
D. N. Granger ◽  
H. J. Granger
Keyword(s):  
Blood Flow ◽  
Systems Analysis ◽  
Oxygen Delivery ◽  
Oxygen Demand ◽  
Capillary Density ◽  
Capillary Recruitment ◽  
Tissue Oxygen Delivery ◽  
Cellular Hypoxia ◽  
Margin Of Safety ◽  
Intrinsic Regulation

A systems analysis of intrinsic regulation of intestinal blood flow and oxygenation is presented. The model is based on current concepts of metabolic control of tissue oxygen delivery and incorporates recent data from the literature regarding the influence of oxygen availability-to-demand ratio on intestinal vascular resistance and perfused capillary density. The model was used to evaluate the relative importance of resistance and exchange vessels in preventing cellular hypoxia during reductions in oxygen delivery or increments in oxygen demand. The model predicted that capillary recruitment is of greater quantitative significance than blood flow autoregulation in preventing cellular hypoxia when intestinal perfusion pressure is reduced. However, the combination of capillary recruitment and blood flow autoregulation provides a large margin of safety against tissue hypoxia in the intestine. Simulation results also predict that oxygen extraction plays a greater role than blood flow in providing additional oxygen to the hypermetabolic intestine irrespective of which control system (resistance or exchange vessel) is operating.

Partitioning of locomotor and feeding metabolism in sablefish (Anoplopoma fimbria)

1987 ◽  
Vol 65 (3) ◽  
pp. 486-489 ◽  
Author(s):  
Donald J. Furnell
Keyword(s):  
Blood Flow ◽  
Metabolic Rate ◽  
Oxygen Supply ◽  
Physiological Mechanism ◽  
Oxygen Demand ◽  
Metabolic Rates ◽  
Power Performance ◽  
Anoplopoma Fimbria ◽  
Performance Curves ◽  
Locomotor Muscles

The swimming, feeding, and standard metabolic rates of the sablefish (Anoplopoma fimbria) were determined using tunnel and mass respirometers. Swimming metabolic rate was measured for fish in both digestive and nondigestive states. Comparison of power–performance curves for fed and starved states suggested that sablefish were able to allocate oxygen supply preferentially to locomotor muscles and suppress the oxygen demand of digestion when active. Reduced blood flow to the stomach, liver, and spleen during exercise has been observed in other species and may provide a physiological mechanism to explain the results obtained with sablefish.

scholarly journals Non-Invasive measurement of the cerebral metabolic rate of oxygen using MRI in rodents

2021 ◽  
Vol 6 ◽  
pp. 109
Author(s):  
Tobias C Wood ◽  
Diana Cash ◽  
Eilidh MacNicol ◽  
Camilla Simmons ◽  
Eugene Kim ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Imaging Techniques ◽  
Glucose Consumption ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Strongly Correlated ◽  
Non Invasive ◽  
Cerebral Metabolic Rate ◽  
Invasive Measurement

Malfunctions of oxygen metabolism are suspected to play a key role in a number of neurological and psychiatric disorders, but this hypothesis cannot be properly investigated without an in-vivo non-invasive measurement of brain oxygen consumption. We present a new way to measure the Cerebral Metabolic Rate of Oxygen (CMRO2) by combining two existing magnetic resonance imaging techniques, namely arterial spin-labelling and oxygen extraction fraction mapping. This method was validated by imaging rats under different anaesthetic regimes and was strongly correlated to glucose consumption measured by autoradiography.

scholarly journals In Vivo NADH Fluorescence Imaging Indicates Effect of Aquaporin-4 Deletion on Oxygen Microdistribution in Cortical Spreading Depression

2013 ◽  
Vol 33 (7) ◽  
pp. 996-999 ◽  
Author(s):  
Alexander S Thrane ◽  
Takahiro Takano ◽  
Vinita Rangroo Thrane ◽  
Fushun Wang ◽  
Weiguo Peng ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Fluorescence Imaging ◽  
Nicotinamide Adenine Dinucleotide ◽  
Oxygen Delivery ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Aquaporin 4 ◽  
Two Photon ◽  
Nadh Fluorescence

Using in vivo two-photon imaging, we show that mice deficient in aquaporin-4 (AQP4) display increased fluorescence of nicotinamide adenine dinucleotide (NADH) when subjected to cortical spreading depression. The increased NADH signal, a proxy of tissue hypoxia, was restricted to microwatershed areas remote from the vasculature. Aqp4 deletion had no effects on the hyperemia response, but slowed [K+]o recovery. These observations suggest that K+ uptake is suppressed in Aqp4−/- mice as a consequence of decreased oxygen delivery to tissue located furthest away from the vascular source of oxygen, although increased oxygen consumption may also contribute to our observations.

scholarly journals Metabolic Control of Resting Hemispheric Cerebral Blood Flow is Oxidative, not Glycolytic

2011 ◽  
Vol 31 (5) ◽  
pp. 1223-1228 ◽  
Author(s):  
William J Powers ◽  
Tom O Videen ◽  
Joanne Markham ◽  
Vonn Walter ◽  
Joel S Perlmutter
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Metabolic Control ◽  
Univariate Analysis ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Arterial Oxygen ◽  
Whole Brain ◽  
Cerebral Metabolic Rate

Although the close regional coupling of resting cerebral blood flow (CBF) with both cerebral metabolic rate of oxygen (CMRO2) and cerebral metabolic rate of glucose (CMRglc) within individuals is well documented, there are few data regarding the coupling between whole brain flow and metabolism among different subjects. To investigate the metabolic control of resting whole brain CBF, we performed multivariate analysis of hemispheric CMRO2, CMRglc, and other covariates as predictors of resting CBF among 23 normal humans. The univariate analysis showed that only CMRO2 was a significant predictor of CBF. The final multivariate model contained two additional terms in addition to CMRO2: arterial oxygen content and oxygen extraction fraction. Notably, arterial plasma glucose concentration and CMRglc were not included in the final model. Our data demonstrate that the metabolic factor controlling hemispheric CBF in the normal resting brain is CMRO2 and that CMRglc does not make a contribution. Our findings provide evidence for compartmentalization of brain metabolism into a basal component in which CBF is coupled to oxygen metabolism and an activation component in which CBF is controlled by another mechanism.

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