scholarly journals Cerebral Oxygenation during Postasphyxial Seizures in Near-Term Fetal Sheep

2005 ◽  
Vol 25 (7) ◽  
pp. 911-918 ◽  
Author(s):  
Hernan Gonzalez ◽  
Christian J Hunter ◽  
Laura Bennet ◽  
Gordon G Power ◽  
Alistair J Gunn
Keyword(s):  
Blood Flow ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Immature Brain ◽  
Fetal Sheep ◽  
Blood Temperature ◽  
Cerebral Tissue Oxygenation ◽  
A1 Receptor ◽  
Near Term ◽  
The Brain

After exposure to asphyxia, infants may develop both prolonged, clinically evident seizures and shorter, clinically silent seizures; however, their effect on cerebral tissue oxygenation is unclear. We therefore examined the hypothesis that the increase in oxygen delivery during postasphyxial seizures might be insufficient to meet the needs of increased metabolism, thus causing a fall in tissue oxygenation, in unanesthetized near-term fetal sheep in utero (gestational age 125 ± 1 days). Fetuses were administered an infusion of the specific adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine, followed by 10 mins of asphyxia induced by complete umbilical cord occlusion. The fetuses then recovered for 3 days. Sixty-one episodes of electrophysiologically defined seizures were identified in five fetuses. Tissue PO2 (tPO2) did not change significantly during short seizures (<3.5 mins), 5.2 ± 0.2 versus baseline 5.6 ± 0.1 mm Hg (NS), but fell to 2.2 ± 0.2 mm Hg during seizures lasting more than 3.5 mins ( P<0.001). During prolonged seizures, cortical blood flow did not begin to increase until tPO2 had begun to fall, and then rose more slowly than the increase in metabolism, with a widening of the brain to blood temperature gradient. In conclusion, in the immature brain, during prolonged, but not short seizures, there is a transient mismatch between cerebral blood flow and metabolism leading to significant cerebral deoxygenation.

Peripheral chemoreflex activation and cardiac function during hypoxemia in near term fetal sheep without placental compromise

2021 ◽  
Author(s):  
Juulia Lantto ◽  
Tiina Erkinaro ◽  
Mervi Haapsamo ◽  
Heikki Huhta ◽  
Leena Alanne ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Artery ◽  
Arterial Oxygen ◽  
Sheep Model ◽  
Fetal Sheep ◽  
Descending Aorta ◽  
Arterial Blood ◽  
Near Term ◽  
Peripheral Chemoreflex

A drop in arterial oxygen content activates fetal chemoreflex including an increase in sympathetic activity leading to peripheral vasoconstriction and redistribution of blood flow to protect the brain, myocardium, and adrenal glands. By using a chronically instrumented fetal sheep model with intact placental circulation at near-term gestation, we investigated the relationship between peripheral chemoreflex activation induced by hypoxemia and central hemodynamics. 17 Åland landrace sheep fetuses at 115-128/145 gestational days were instrumented. Carotid artery was catheterised in 10 fetuses and descending aorta in 7 fetuses. After a 4-day recovery, baseline measurements of fetal arterial blood pressures, blood gas values, and fetal cardiovascular hemodynamics by pulsed Doppler ultrasonography were obtained under isoflurane-anesthesia. Comparable data to baseline was collected 10 (acute hypoxemia) and 60 minutes (prolonged hypoxemia) after maternal hypo-oxygenation to saturation level of 70-80% was achieved. During prolonged hypoxemia, pH and base excess (BE) were lower, and lactate levels higher in the descending aorta than in the carotid artery. During hypoxemia mean arterial blood pressure (MAP) in the descending aorta increased, while in the carotid artery MAP decreased. In addition, right pulmonary artery pulsatility index values increased, and the diastolic component in the aortic isthmus blood flow velocity waveform became more retrograde. Both fetal ventricular cardiac outputs were maintained even during prolonged hypoxemia when significant fetal metabolic acidemia developed. Fetal chemoreflex activation induced by hypoxemia decreased the perfusion pressure in the cerebral circulation. Fetal weight-indexed LVCO or AoI Net Flow-ratio did not correlate with a drop in carotid artery blood pressure.

scholarly journals Cerebral oxygenation during locomotion is modulated by respiration

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Qingguang Zhang ◽  
Morgane Roche ◽  
Kyle W. Gheres ◽  
Emmanuelle Chaigneau ◽  
Ravi T. Kedarasetti ◽  
...  
Keyword(s):  
Neural Activity ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Breathing Rate ◽  
Lifetime Measurements ◽  
Phosphorescence Lifetime ◽  
Two Photon ◽  
Animal Remains ◽  
Oxygen Dynamics ◽  
The Brain

AbstractIn the brain, increased neural activity is correlated with increases of cerebral blood flow and tissue oxygenation. However, how cerebral oxygen dynamics are controlled in the behaving animal remains unclear. We investigated to what extent cerebral oxygenation varies during locomotion. We measured oxygen levels in the cortex of awake, head-fixed mice during locomotion using polarography, spectroscopy, and two-photon phosphorescence lifetime measurements of oxygen sensors. We find that locomotion significantly and globally increases cerebral oxygenation, specifically in areas involved in locomotion, as well as in the frontal cortex and the olfactory bulb. The oxygenation increase persists when neural activity and functional hyperemia are blocked, occurred both in the tissue and in arteries feeding the brain, and is tightly correlated with respiration rate and the phase of respiration cycle. Thus, breathing rate is a key modulator of cerebral oxygenation and should be monitored during hemodynamic imaging, such as in BOLD fMRI.

scholarly journals Epinephrine’s effects on cerebrovascular and systemic hemodynamics during cardiopulmonary resuscitation

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Constantine D. Mavroudis ◽  
Tiffany S. Ko ◽  
Ryan W. Morgan ◽  
Lindsay E. Volk ◽  
William P. Landis ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Animal Studies ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Acute Effect ◽  
Correlation Spectroscopy ◽  
Neurological Injury ◽  
Swine Model ◽  
Cerebral Tissue ◽  
Cerebral Tissue Oxygenation

Abstract Background Despite controversies, epinephrine remains a mainstay of cardiopulmonary resuscitation (CPR). Recent animal studies have suggested that epinephrine may decrease cerebral blood flow (CBF) and cerebral oxygenation, possibly potentiating neurological injury during CPR. We investigated the cerebrovascular effects of intravenous epinephrine in a swine model of pediatric in-hospital cardiac arrest. The primary objectives of this study were to determine if (1) epinephrine doses have a significant acute effect on CBF and cerebral tissue oxygenation during CPR and (2) if the effect of each subsequent dose of epinephrine differs significantly from that of the first. Methods One-month-old piglets (n = 20) underwent asphyxia for 7 min, ventricular fibrillation, and CPR for 10–20 min. Epinephrine (20 mcg/kg) was administered at 2, 6, 10, 14, and 18 min of CPR. Invasive (laser Doppler, brain tissue oxygen tension [PbtO2]) and noninvasive (diffuse correlation spectroscopy and diffuse optical spectroscopy) measurements of CBF and cerebral tissue oxygenation were simultaneously recorded. Effects of subsequent epinephrine doses were compared to the first. Results With the first epinephrine dose during CPR, CBF and cerebral tissue oxygenation increased by > 10%, as measured by each of the invasive and noninvasive measures (p < 0.001). The effects of epinephrine on CBF and cerebral tissue oxygenation decreased with subsequent doses. By the fifth dose of epinephrine, there were no demonstrable increases in CBF of cerebral tissue oxygenation. Invasive and noninvasive CBF measurements were highly correlated during asphyxia (slope effect 1.3, p < 0.001) and CPR (slope effect 0.20, p < 0.001). Conclusions This model suggests that epinephrine increases CBF and cerebral tissue oxygenation, but that effects wane following the third dose. Noninvasive measurements of neurological health parameters hold promise for developing and directing resuscitation strategies.

Low Cerebral Oxygenation Levels during Resuscitation in Out-of-hospital Cardiac Arrest Are Associated with Hyperfibrinolysis

2015 ◽  
Vol 123 (4) ◽  
pp. 820-829 ◽  
Author(s):  
Anne Duvekot ◽  
Victor A. Viersen ◽  
Simone E. Dekker ◽  
Leo M. G. Geeraedts ◽  
Lothar A. Schwarte ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Plasminogen Activator ◽  
Protein C ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Fibrinolytic System ◽  
Cerebral Tissue ◽  
Cerebral Tissue Oxygenation ◽  
Hospital Cardiac Arrest

Abstract Background: The authors investigated whether patients with out-of-hospital cardiac arrest with an initial low cerebral oxygen level during cardiopulmonary resuscitation are more prone to develop hyperfibrinolysis than patients with normal cerebral oxygenation levels and which part of the fibrinolytic system is involved in this response. Methods: In 46 patients, hyperfibrinolysis was diagnosed immediately upon emergency department admission using rotational thromboelastometry and defined as a lysis more than 15%. Simultaneously, initial cerebral tissue oxygenation was measured using near-infrared spectroscopy, and oxygen desaturation was defined as a tissue oxygenation index (TOI) of 50% or less. Blood sample analysis included markers for hypoperfusion and fibrinolysis. Results: There was no difference in prehospital cardiopulmonary resuscitation duration between patients with or without hyperfibrinolysis. An initial TOI of 50% or less was associated with more clot lysis (91% [17 to 100%; n = 16]) compared with patients with a normal TOI (6% [4 to 11%]; n = 30; P &lt; 0.001), with lower levels of plasminogen (151.6 ± 61.0 vs. 225.3 ± 47.0 μg/ml; P &lt; 0.001) and higher levels of tissue plasminogen activator (t-PA; 18.3 ± 7.4 vs. 7.9 ± 4.7 ng/ml; P &lt; 0.001) and plasminogen activator inhibitor-1 (19.3 ± 8.9 vs. 12.1 ± 6.1 ng/ml; P = 0.013). There were no differences in (activated) protein C levels among groups. The initial TOI was negatively correlated with t-PA (r = −0.69; P &lt; 0001). Mortality rates were highest in patients with hyperfibrinolysis. Conclusion: Activation of the fibrinolytic system is more common in out-of-hospital cardiac arrest patients with an initial cerebral tissue oxygenation value of 50% or less during resuscitation and is linked to increased levels of t-PA rather than involvement of protein C.

Cerebral blood flow and metabolism during exercise: implications for fatigue

2008 ◽  
Vol 104 (1) ◽  
pp. 306-314 ◽  
Author(s):  
Neils H. Secher ◽  
Thomas Seifert ◽  
Johannes J. Van Lieshout
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Perceived Exertion ◽  
Cerebral Oxygenation ◽  
Metabolic Response ◽  
Work Of Breathing ◽  
Whole Body ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
The Brain

During exercise: the Kety-Schmidt-determined cerebral blood flow (CBF) does not change because the jugular vein is collapsed in the upright position. In contrast, when CBF is evaluated by 133Xe clearance, by flow in the internal carotid artery, or by flow velocity in basal cerebral arteries, a ∼25% increase is detected with a parallel increase in metabolism. During activation, an increase in cerebral O2 supply is required because there is no capillary recruitment within the brain and increased metabolism becomes dependent on an enhanced gradient for oxygen diffusion. During maximal whole body exercise, however, cerebral oxygenation decreases because of eventual arterial desaturation and marked hyperventilation-related hypocapnia of consequence for CBF. Reduced cerebral oxygenation affects recruitment of motor units, and supplemental O2 enhances cerebral oxygenation and work capacity without effects on muscle oxygenation. Also, the work of breathing and the increasing temperature of the brain during exercise are of importance for the development of so-called central fatigue. During prolonged exercise, the perceived exertion is related to accumulation of ammonia in the brain, and data support the theory that glycogen depletion in astrocytes limits the ability of the brain to accelerate its metabolism during activation. The release of interleukin-6 from the brain when exercise is prolonged may represent a signaling pathway in matching the metabolic response of the brain. Preliminary data suggest a coupling between the circulatory and metabolic perturbations in the brain during strenuous exercise and the ability of the brain to access slow-twitch muscle fiber populations.

scholarly journals RheoSens; RheoPatch

2020 ◽  
Author(s):  
Tariq H. Khan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Minimally Invasive ◽  
Brain Injuries ◽  
Tissue Oxygenation ◽  
Traumatic Brain Injuries ◽  
Invasive Device ◽  
The Brain ◽  
Minimally Invasive Device

Rheo Probe is a minimally invasive device, implanted in the brain matter for patients in a coma following brain haemorrage or traumatic brain injuries to measure cerebral blood flow, intracranial pressure, temperature and oxygenation parameters. Nearinfrared sensors assess levels of tissue oxygenation as well as cerebral blood flow by measuring oxygenated and deoxygenated hemoglobin based on spectrometry.

Assessment of a noninvasive cerebral oxygenation monitor in patients with severe traumatic brain injury

2014 ◽  
Vol 120 (4) ◽  
pp. 901-907 ◽  
Author(s):  
Guy Rosenthal ◽  
Alex Furmanov ◽  
Eyal Itshayek ◽  
Yigal Shoshan ◽  
Vineeta Singh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Jugular Bulb ◽  
Tissue Oxygen ◽  
Cerebral Tissue ◽  
Brain Tissue Oxygen ◽  
Severe Tbi ◽  
Cerebral Tissue Oxygenation

Object Development of a noninvasive monitor to assess cerebral oxygenation has long been a goal in neurocritical care. The authors evaluated the feasibility and utility of a noninvasive cerebral oxygenation monitor, the CerOx 3110, which uses near-infrared spectroscopy and ultrasound to measure regional cerebral tissue oxygenation in patients with severe traumatic brain injury (TBI), and compared measurements obtained using this device to those obtained using invasive cerebral monitoring. Methods Patients with severe TBI admitted to the intensive care unit at Hadassah-Hebrew University Hospital requiring intracranial pressure (ICP) monitoring and advanced neuromonitoring were included in this study. The authors assessed 18 patients with severe TBI using the CerOx monitor and invasive advanced cerebral monitors. Results The mean age of the patients was 45.3 ± 23.7 years and the median Glasgow Coma Scale score on admission was 5 (interquartile range 3–7). Eight patients underwent unilateral decompressive hemicraniectomy and 1 patient underwent craniotomy. Sixteen patients underwent insertion of a jugular bulb venous catheter, and 18 patients underwent insertion of a Licox brain tissue oxygen monitor. The authors found a strong correlation (r = 0.60, p < 0.001) between the jugular bulb venous saturation from the venous blood gas and the CerOx measure of regional cerebral tissue saturation on the side ipsilateral to the catheter. A multivariate analysis revealed that among the physiological parameters of mean arterial blood pressure, ICP, brain tissue oxygen tension, and CerOx measurements on the ipsilateral and contralateral sides, only ipsilateral CerOx measurements were significantly correlated to jugular bulb venous saturation (p < 0.001). Conclusions Measuring regional cerebral tissue oxygenation with the CerOx monitor in a noninvasive manner is feasible in patients with severe TBI in the neurointensive care unit. The correlation between the CerOx measurements and the jugular bulb venous measurements of oxygen saturation indicate that the CerOx may be able to provide an estimation of cerebral oxygenation status in a noninvasive manner.

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