Reduction In Cerebral Oxygenation Research Articles

Hypoxia Altitude Simulation and Reduction of Cerebral Oxygenation in COPD Patients

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is highly prevalent and often associated with chronic hypoxia. Previous studies have shown alterations of cerebral oxygenation and cardiac repolarization in COPD patients (GOLD stage II-IV). Airplane travel is common in patients with COPD; however, the clinical effects of a diminished oxygen partial pressure in aircraft cabin environments at cruising altitude remain elusive. The aim of this study was to assess changes of cerebral oxygenation as well as parameters of cardiac repolarization during a hypoxia altitude simulation combined with mild physical activity in these patients.METHODS: Patients with COPD and healthy subjects (10 per group) randomly selected from the Charité outpatient clinic conducted a hypoxia altitude simulation test which consisted of three phases. The regional cerebral oxygen saturation (rSO₂) of the frontal cortex was measured at rest using near-infrared spectroscopy (NIRS). Furthermore, oxygen saturation (SpO₂), blood pressure, and heart rate values, as well as a 12-lead-ECG, were recorded. Subsequently, a mild treadmill exercise program (25 W) was divided into 10 min of normoxia (pre-hypoxia), 30 min of mild hypoxia (FIO₂ = 0.15), followed by a second 10-min period of normoxia (post-hypoxia). Meanwhile, mentioned parameters were recorded in 2-min intervals. P, PQ, QRS, QT, QTc, QTd, T-peak-T-end interval (TpTe), and corrected TpTe (TpTec) were measured on three ECG complexes, each at baseline, at the end of the normoxic phase, and at the end of the hypoxic phase.RESULTS: A total of 10 patients with COPD and 10 control subjects were included in this study. SpO₂ was significantly lower in COPD patients throughout the whole test. Frontal cerebral rSO₂ was significantly lower in the left hemisphere during hypoxia altitude simulation in COPD patients (59.5 ± 8.5 vs. 67.5 ± 5.7).CONCLUSIONS: We show reduced left frontal cerebral oxygenation during hypoxia and mild exercise in patients with COPD, suggesting diminished altitude resilience and altitude capabilities. Preflight hypoxia assessment might be recommended to patients with severe COPD.Dehe L, Hohendanner F, Gültekin E, Werth G, Wutzler A, Bender TO. Hypoxia altitude simulation and reduction of cerebral oxygenation in COPD patients. Aerosp Med Hum Perform. 2023; 94(3):102-106.

CEREBRAL OXYGENATION DURING EXERCISE ACROSS DIFFERENT STAGES OF CHRONIC KIDNEY DISEASE

Objective: Cognitive impairment and reduced exercise tolerance are common in patients with chronic kidney disease (CKD), in part due to reduced brain function. Proper brain function relies on sufficient blood flow and oxygen supply by the cerebral vasculature. A reduction in cerebral oxygenation of more than 10% may deteriorate brain function and influence the decision to continue exercise. This study aims to examine the cerebral oxygenation and blood volume during a mild physical stress as an index of brain activation in patients at different stages of CKD and controls without CKD. Design and method: This is a preliminary analysis of an observational study enrolling patients with CKD stage 2–4 (matched for age and sex within the different stages) and controls without CKD. All participants underwent a 3-min intermittent handgrip exercise (HG) at 35% of their maximal voluntary contraction. Changes in prefrontal oxygenation (oxyhemoglobin-O2Hb) and deoxyhemoglobin-HHb) and total blood volume (total hemoglobin-tHb) were continuously recorded during HG-exercise by near-infrared spectroscopy (NIRS). Results: A total of 59 participants are included in this preliminary analyses (n = 11 controls, n = 15 stage 2 CKD, n = 18 stage 3 CKD and n = 15 stage 4 CKD patients). During HG-exercise, O2Hb significantly increased (p < 0.001) and HHb remained relatively unchanged in all groups compared to pre-exercise values. However, this O2Hb increase was progressively lower with advancing CKD Stages (controls: 2,58 ± 1,43 stage 2: 1,51 ± 1,31 stage 3: 1,29 ± 0,97 stage 4: 0,95 ± 0,92, p = 0.006) (Figure). During HG, tHb (an index of microvascular blood volume) increased significantly in controls, stage 2, and 3 CKD patients (p < 0.05) but not in stage 4 CKD patients (p = 0.100). As before this tHb increase was progressively lower with advancing CKD stages (p = 0.030). Controlling for age differences between groups did not alter the above observations. Conclusions: Brain activation/response during a mild physical task appears to decrease with advancing CKD as suggested by the smaller rise in cerebral oxygenation and blood volume. This may contribute both impaired cognitive function and reduced exercise tolerance with advancing CKD.

FC085: Cerebral Oxygenation During Exercise Across Different Stages of Chronic Kidney Disease

Abstract BACKGROUND AND AIMS Cognitive impairment and reduced exercise tolerance are common in patients with chronic kidney disease (CKD), in part due to reduced brain function. Proper brain function relies on sufficient blood flow and oxygen supply by the cerebral vasculature. A reduction in cerebral oxygenation of more than 10% may deteriorate brain function and influence the decision to continue exercise. This study aims to examine the cerebral oxygenation and blood volume during a mild physical stress as an index of brain activation in patients at different stages of CKD and controls without CKD. METHOD This is a preliminary analysis of an observational study enrolling patients with CKD stage 2–4 (matched for age and sex within the different stages) and controls without CKD. All participants underwent a 3-min intermittent handgrip exercise (HG) at 35% of their maximal voluntary contraction. Changes in prefrontal oxygenation (oxyhaemoglobin—O2Hb) and deoxyhaemoglobin—HHb) and total blood volume (total hemoglobin—tHb) were continuously recorded during HG-exercise by near-infrared spectroscopy (NIRS). RESULTS A total of 59 participants are included in this preliminary analyses (n = 11 controls, n = 15 stage 2 CKD, n = 18 stage 3 CKD and n = 15 stage 4 CKD patients). During HG-exercise, O2Hb significantly increased (P < 0.001) and HHb remained relatively unchanged in all groups compared to pre-exercise values. However, this O2Hb increase was progressively lower with advancing CKD Stages (controls: 2.58 ± 1.43; stage 2: 1.51 ± 1.31; stage 3: 1.29 ± 0.97; stage 4: 0.95 ± 0.92; P = 0.006) (Figure). During HG, tHb (an index of microvascular blood volume) increased significantly in controls, stage 2 and stage 3 CKD patients (P < 0.05) but not in stage 4 CKD patients (P = 0.100). As before this tHb increase was progressively lower with advancing CKD stages (P = 0.030). Controlling for age differences between groups did not alter the above observations. CONCLUSION Brain activation/response during a mild physical task appears to decrease with advancing CKD as suggested by the smaller rise in cerebral oxygenation and blood volume. This may contribute both impaired cognitive function and reduced exercise tolerance with advancing CKD.

Cerebral oxygenation assessed by near-infrared spectroscopy in the sitting and prone positions during posterior fossa surgery: a prospective, randomized clinical study

ObjectivesSitting position (SP) or prone position (PP) are used for posterior fossa surgery. The SP induced reduction in cerebral blood flow and cerebral oxygen saturation (rSO2) has been shown in shoulder surgeries, but there is not enough data in intracranial tumor surgery. Studies showed that PP is safe in terms of cerebral oxygen saturation in patients undergoing spinal surgery. Our hypothesis is that the SP may improve cerebral oxygenation in the patients with intracranial pathologies due to reduction in intracranial pressure. Therefore, we compared the effects of the SP and PP on rSO2 in patients undergoing posterior fossa tumor surgery. MethodsData were collected patients undergoing posterior fossa surgery, 20 patients in SP compared to 21 patients in PP. The rSO2 was assessed using INVOS monitor. Heart rate (HR), mean arterial pressure (MAP), EtCO2, BIS, and bilateral rSO2 were recorded preoperatively, and at 5, 8, and 11.ßminutes after the intubation and every 3.ßminutes after patient positioning until the initial surgical incision. ResultsCerebral oxygenation slowly reduced in both the sitting and prone position patients following the positioning (p.ß<.ß0.002), without any difference between the groups. The HR and MAP were lower in the sitting SP after positioning compared to the PP. ConclusionNeurosurgery in the SP and PP is associated with slight reduction in cerebral oxygenation. We speculate that if we rise the lower limit of MAP, we might have showed the beneficial effect of the SP on rSO2.

An Observational Study on the Effect of Nimodipine on Cerebral Blood Flow Velocity and Oxygenation in Patients with Subarachnoid Haemorrhage

Objective In patients with subarachnoid haemorrhage (SAH), nimodipine is administered to prevent for cerebral vasospasm. In this prospective observational study, we examined the effect of nimodipine on cerebral blood flow velocity (BFV) (transcranial Doppler, TCD) and regional oxygen saturation (rSO2) (near-infrared spectroscopy, NIRS) as well as its systemic haemodynamic effects. Methods After ethics approval, we enrolled 18 adult patients (11 females) with SAH after aneurysm rupture. After treatment of the bleeding source, patients underwent extended haemodynamic monitoring by transpulmonary thermodilution (PiCCOTM, Pulsion, Maquet Getinge Group, Feldkirchen, Germany). Measurements of systemic haemodynamics as well as cerebral oxygenation and blood flow velocity were performed 30 minutes before and after the enteral administration of nimodipine (60 mg). Data was compared by paired t-test. A p<0.05 was considered as statistically significant. Data are expressed as mean ± SD. Results Patients’ mean age was 59 ± 11 years. Enteral nimodipinincrease in heart rate (75 vs. 79/min, p<0.05) and cardiac index (3.27 vs. 3.58 l/min/m2, p<0.05). While noe administration was associated with a decrease in mean arterial pressure (93 vs. 88 mmHg, p<0.05), an radrenaline dose and BFV did not change significantly, NIRS revealed a reduction in cerebral oxygenation, but rSO2 values remained within a healthy range in all patients (right 71 vs. 69 %, p<0.05; left 74 vs. 72 %, p<0.05). Conclusions In patients with SAH, enteral nimodipine led to inconclusive changes in systemic haemodynamics. Although cerebral oxygenation as assessed by NIRS decreased after nimodipine administration, BFV remained stable. Keywords: Cerebral blood flow velocity; Cerebral oxygenation; Nimodipine; Subarachnoid haemorrhage; Systemic haemodynamics.

Effects of Acceleration-Induced Reductions in Retinal and Cerebral Oxygenation on Human Performance

BACKGROUND: Ischemic hypoxia induced by suprathreshold G-force loading can adversely affect vision, cognition, and lead to loss of consciousness (LOC). The purpose of this study was to determine whether reductions in cerebral oxygenation, caused by subthreshold G-forces (up to 4 Gz and of limited durations that do not lead to LOC), would affect visual perception and working memory performance.METHODS: Sixteen subjects performed visual perception and working memory tasks both before and during Gz exposures (1, 2.2, 3, 4 with leg pressurization, 4 with leg and abdomen pressurization) within a human-use centrifuge.RESULTS: As measured using near-infrared spectroscopy, blood oxygenation over medial prefrontal cortex was similar in the 1 and 2.2 Gz conditions, but was reduced to a similar extent in the 3 and 4 Gz conditions. In parallel, visual perception accuracy was reduced in the 3 and 4 Gz conditions, with no difference between the 3 and 4 Gz conditions. No change in reaction time was seen. Conversely, neither accuracy nor reaction time changes were observed for the visual working memory task.DISCUSSION: These results indicate that although visual working memory is not affected, the ability to visually discriminate between stimuli is reduced at G-forces as low as 3 and 4 Gz. This may have important ramifications for pilots who are routinely subjected to such forces.Croft RJ, Klegrd R, Tribukait A, Taylor NAS, Eiken O. Effects of acceleration-induced reductions in retinal and cerebral oxygenation on human performance. Aerosp Med Hum Perform. 2021; 92(2):7582.

Effects of hypothermia, hypoxia, and hypercapnia on brain oxygenation and hemodynamic parameters during simulated avalanche burial: a porcine study.

Avalanche patients who are completely buried but still able to breathe are exposed to hypothermia, hypoxia, and hypercapnia (triple H syndrome). Little is known about how these pathological changes affect brain physiology. The study aim was to investigate the effect of hypothermia, hypoxia, and hypercapnia on brain oxygenation and systemic and cerebral hemodynamics. Anesthetized pigs were surface cooled to 28°C. Fraction of inspiratory oxygen ([Formula: see text]) was reduced to 17% and hypercapnia induced. Hemodynamic parameters and blood gas values were monitored. Cerebral measurements included cerebral perfusion pressure (CPP), brain tissue oxygen tension ([Formula: see text]), cerebral venous oxygen saturation ([Formula: see text]), and regional cerebral oxygen saturation (rSo2). Tests were interrupted when hemodynamic instability occurred or 60 min after hypercapnia induction. ANOVA for repeated measures was used to compare values across phases. There was no clinically relevant reduction in cerebral oxygenation ([Formula: see text], [Formula: see text], rSo2) during hypothermia and initial [Formula: see text] reduction. Hypercapnia was associated with an increase in pulmonary resistance followed by a decrease in cardiac output and CPP, resulting in hemodynamic instability and cerebral desaturation (decrease in [Formula: see text], [Formula: see text], rSo2). Hypercapnia may be the main cause of cardiovascular instability, which seems to be the major trigger for a decrease in cerebral oxygenation in triple H syndrome despite severe hypothermia.NEW & NOTEWORTHY Avalanche patients who are completely buried but still able to breathe are exposed to hypothermia, hypoxia, and hypercapnia (triple H syndrome). In a porcine model, there was no clinically relevant reduction in cerebral oxygenation during hypothermia and initial reduction of fraction of inspiratory oxygen ([Formula: see text]), as observed during hypercapnia. Hypercapnia may be the main cause of cardiovascular instability, which seems to be the major trigger for a decrease in cerebral oxygenation in triple H syndrome despite severe hypothermia.

Effects of Single Loading Dose of Intravenous Caffeine on Cerebral Oxygenation in Preterm Infants.

The aim of this study was to evaluate the effects of caffeine on cerebral oxygenation in preterm infants. This was a prospective study of infants with a gestational age (GA) of < 34 weeks who were treated intravenously with a loading dose of 20 mg/kg caffeine citrate within the first 48 hours of life. Regional cerebral oxygen saturation (rSO2C) and cerebral fractional tissue oxygen extraction (cFTOE) were measured using near-infrared spectroscopy before administering caffeine (baseline), immediately after administering caffeine, and 1, 2, 3, 4, 6, and 12 hours after dose completion; postdose values were compared with the baseline values. A total of 48 infants with a mean GA of 29.0 ± 1.9 weeks, birth weight of 1,286 ± 301 g, and postnatal age of 32.4 ± 11.3 hours were included in the study. rSO2C significantly decreased from 81.3 to 76.7% soon after administering caffeine, to 77.1% at 1 hour, and to 77.8% at 2 hours with recovery at 3 hours postdose. rSO2C was 80.2% at 12 hours postdose. cFTOE increased correspondingly. Although rSO2C values were lower and cFTOE values were higher compared with the baseline values at 3, 4, 6, and 12 hours after caffeine administration, this was not statistically significant. A loading dose of caffeine temporarily reduces cerebral oxygenation and increases cerebral tissue oxygen extraction in preterm infants. Most probably these changes reflect a physiological phenomenon without any clinical importance to the cerebral hemodynamics, as the reduction in cerebral oxygenation and increase in cerebral tissue oxygen extraction remain well within acceptable range.

Continuous reduction in cerebral oxygenation during endurance exercise in patients with pulmonary arterial hypertension.

BackgroundPatients with pulmonary arterial hypertension (PAH) have lower cerebral blood flow (CBF) and oxygenation compared to healthy sedentary subjects, the latter negatively correlating with exercise capacity during incremental cycling exercise. We hypothesized that patients would also exhibit altered CBF and oxygenation during endurance exercise, which would correlate with endurance time.MethodsResting and exercise cardiorespiratory parameters, blood velocity in the middle cerebral artery (MCAv; transcranial doppler) and cerebral oxygenation (relative changes in cerebral tissue oxygenation index (ΔcTOI) and cerebral deoxyhemoglobin (ΔcHHb); near‐infrared spectroscopy) were continuously monitored in nine PAH patients and 10 healthy‐matched controls throughout endurance exercise. Cardiac output (CO), systemic blood pressure (BP) and oxygen saturation (SpO2), ventilatory metrics and end‐tidal CO2 pressure (PETCO2) were also assessed noninvasively.ResultsDespite a lower workload and endurance oxygen consumption, similar CO and systemic BP, ΔcTOI was lower in PAH patients compared to controls (p < .01 for interaction). As expected during exercise, patients were characterized by an altered MCAv response to exercise, a lower PETCO2 and SpO2, as wells as a higher minute‐ventilation/CO2 production ratio (V˙E/V˙CO2 ratio). An uncoupling between changes in MCAv and PETCO2 during the cycling endurance exercise was also progressively apparent in PAH patients, but absent in healthy controls. Both cHHb and ΔcTOI correlated with V˙E/V˙CO2 ratio (r = 0.50 and r = −0.52; both p < .05 respectively), but not with endurance time.ConclusionPAH patients present an abnormal cerebrovascular profile during endurance exercise with a lower cerebral oxygenation that correlate with hyperventilation but not endurance exercise time. These findings complement the physiological characterization of the cerebral vascular responses to exercise in PAH patients.

Responses of cerebral blood velocity and tissue oxygenation to low-frequency oscillations during simulated haemorrhagic stress in humans.

What is the central question of this study? Do low-frequency oscillations in arterial pressure and cerebral blood velocity protect cerebral blood velocity and oxygenation during central hypovolaemia? What is the main finding and its importance? Low-frequency oscillations in arterial pressure and cerebral blood velocity attenuate reductions in cerebral oxygen saturation but do not protect absolute cerebral blood velocity during central hypovolaemia. This finding indicates the potential importance of haemodynamic oscillations in maintaining cerebral oxygenation and therefore viability of tissues during challenges to cerebral blood flow and oxygen delivery. Tolerance to both real and simulated haemorrhage varies between individuals. Exaggerated low-frequency (∼0.1Hz) oscillations in mean arterial pressure and brain blood flow [indexed via middle cerebral artery velocity (MCAv)] have been associated with improved tolerance to reduced central blood volume. The mechanism for this association has not been explored. We hypothesized that inducing low-frequency oscillations in arterial pressure and cerebral blood velocity would attenuate reductions in cerebral blood velocity and oxygenation during simulated haemorrhage. Fourteen subjects (11men and three women) were exposed to oscillatory (0.1 and 0.05Hz) and non-oscillatory (0Hz) lower-body negative pressure profiles with an average chamber pressure of -60mmHg (randomized and counterbalanced order). Measurements included arterial pressure and stroke volume via finger photoplethysmography, MCAv via transcranial Doppler ultrasound, and cerebral oxygenation of the frontal lobe via near-infrared spectroscopy. Tolerance was higher during the two oscillatory profiles compared with the 0Hz profile (0.05Hz, P=0.04; 0.1Hz, P=0.09), accompanied by attenuated reductions in stroke volume (P<0.001) and cerebral oxygenation of the frontal lobe (P≤0.02). No differences were observed between profiles for reductions in mean arterial pressure (P=0.17) and MCAv (P=0.30). In partial support of our hypothesis, cerebral oxygenation, but not cerebral blood velocity, was protected during the oscillatory profiles. Interestingly, more subjects tolerated the oscillatory profiles compared with the static 0Hz profile, despite similar arterial pressure responses. These findings emphasize the potential importance of haemodynamic oscillations in maintaining perfusion and oxygenation of cerebral tissues during haemorrhagic stress.

Sleep apnea syndrome caused lowering of cerebral oxygenation in a hemodialysis patient: a case report and literature review

BackgroundSleep apnea syndrome (SAS) is a sleep disturbance, which is frequently comorbid in dialysis patients. SAS induces hypoxia, and therefore, systemic and cerebral oxygenation would be low. Near-infrared spectroscopy (NIRS) has recently been used to measure regional saturation of oxygen (rSO2), as a marker of tissue oxygenation. Although cerebral rSO2 was measured in patients in various clinical settings, few reports have previously shown the associations of changes in cerebral rSO2 and systemic oxygenation using measurement of peripheral arterial oxygen saturation (SpO2) in patients undergoing hemodialysis (HD) with SAS. We herein report a first HD case with SAS-induced reduction in cerebral oxygenation during sleep.Case presentationA 74-year-old woman underwent HD therapy for 1 month, because of advanced CKD caused by hypertension and obesity. In addition, she was diagnosed with obstructive sleep apnea with polysomnography about 4 years prior. Her apnea-hypopnea index (AHI) was 77.5 per hour, and therefore, continuous positive airway pressure (CPAP) was started. Thereafter, her AHI was improved to 3 to 6 per hour. However, she discontinued CPAP therapy at HD initiation. Since her oxygenation without CPAP would deteriorate, we evaluated her SpO2 and cerebral rSO2 by NIRS monitoring during sleep. We confirmed the deterioration in cerebral rSO2 according to the SpO2 decrease, and furthermore, the improvement in cerebral rSO2 was apparently delayed even after the improvement in her SpO2. The patient’s cerebral oxygenation under CPAP therapy could not be evaluated because she refused to receive CPAP therapy after HD initiation. Therefore, as a comparison, we evaluated a 69-year-old male HD patient without SAS and found that in contrast to a patient with SAS, his SpO2 and cerebral rSO2 were maintained throughout sleep.ConclusionWe observed deterioration in cerebral oxygenation during sleep in addition to a decrease in systemic oxygenation in a patient with SAS undergoing HD. Real-time cerebral NIRS monitoring during sleep might be a useful method for detection of SAS.

Reviewing the relationship between OSA and cognition: Where do we go from here?

Obstructive sleep apnoea (OSA) is a disorder of breathing during sleep resulting in temporary reduction in cerebral oxygenation and sleep disruption. A growing body of research reveals a relatively consistent pattern of deficits in cognition, particularly in attention, episodic memory, and executive function, which are partially remediated by treatment. This is where the consensus ends. Despite a number of competing explanations regarding how OSA affects cognition, reliable evidence is hard to find, which may relate to the many, common conditions co-morbid with OSA or to the methodological challenges in this field. This paper reviews the evidence for cognitive impairment in OSA, the proposed models of cognitive harm, the impact of co-morbidities and the many methodological and theoretical challenges of exploring the effect of OSA on cognition. To overcome some of these challenges, we end by proposing a number of future directions for the field, including suggesting some core design elements for future studies.

Use of a Short-Acting β1 Blocker During Endotoxemia May Reduce Cerebral Tissue Oxygenation if Hemodynamics are Depressed by a Decrease in Heart Rate

A decrease in heart rate (HR) using a short-acting β blocker has potential benefits in sepsis; however, depression of hemodynamics and reduction of cerebral oxygenation may also occur in endotoxemia. Seventeen swine were allocated to landiolol or control groups. In the landiolol group, the dose was sequentially changed from 0 to 40 to 200 μg kg min, and stopped. Hemodynamics, blood variables, and the cerebral tissue oxygenation index (TOI) were recorded by near infrared spectroscopy at each dose. Lipopolysaccharide (LPS) was then administered continuously at 1 μg kg h after a 100 μg bolus administration. After 30 and 150 min, as two severity stages of endotoxemia (endotoxemia 1 and 2), landiolol was administered as above and measurements were made. In the control group, landiolol was not administered, but measurements were made. LPS increased HR and landiolol decreased HR, with similar effects in each endotoxemia stage. In endotoxemia 1, LPS decreased stroke volume (SV), but landiolol restored SV to a value similar to that before endotoxemia, and did not decrease cardiac output (CO), even at 200 μg kg min. In contrast, landiolol did not restore SV in endotoxemia 2, resulting in a decrease in CO and mean arterial pressure, accompanied with a dose-dependent decrease in TOI. A short-acting β blocker has various hemodynamic effects in endotoxemia. Use of a short-acting β blocker during endotoxemia may reduce cerebral tissue oxygenation if hemodynamics are depressed by a decrease in HR.

Reduction in Cerebral Oxygenation due to Patent Ductus Arteriosus Is Pronounced in Small-for-Gestational-Age Neonates

Background: A haemodynamically significant patent ductus arteriosus (hsPDA) reduces cerebral oxygenation in appropriate-for-gestational-age (AGA) preterm neonates. Reduced cerebral oxygenation has been associated with brain injury. Preterm small-for-gestational-age (SGA) neonates show higher cerebral oxygenation than AGA peers throughout the first postnatal days. To date, no studies have investigated the effect of hsPDA on cerebral oxygenation in preterm SGA neonates. Objective: We aimed to assess the effect of hsPDA on cerebral oxygenation in preterm SGA neonates compared to AGA peers. We hypothesised that higher baseline cerebral oxygenation would reduce the impact of hsPDA on cerebral oxygenation in preterm SGA neonates. Methods: We monitored regional cerebral oxygen saturation (rScO₂) with near-infrared spectroscopy and calculated the cerebral fractional tissue oxygen extraction (cFTOE) for 72 h after birth. Retrospective analysis compared 36 preterm SGA neonates (birth weight <10th percentile, 18 with hsPDA) to 36 preterm AGA neonates (birth weight 20th to 80th percentile, 18 with hsPDA). Results: In contrast to the other groups, SGA-hsPDA neonates demonstrated a significant fall in rScO₂ [69% (SEM 2.5) at 4-8 h to 61% (2.7) at 68-72 h, p < 0.001] with a concurrent rise in cFTOE [0.26 (0.026) at 4-8 h to 0.34 (0.030) at 68-72 h, p < 0.001]. Conclusions: Contrary to our hypothesis, hsPDA had a significant negative effect on cerebral oxygenation in preterm SGA neonates. Future studies should explore the potential benefits of early screening and treatment for hsPDA on long-term neurodevelopmental outcome in preterm SGA neonates.

Cognitive Function and Cerebral Oxygenation During Prolonged Exercise Under Hypoxia in Healthy Young Males

Dobashi, Shohei, Masahiro Horiuchi, Junko Endo, Masataka Kiuchi, and Katsuhiro Koyama. Cognitive function and cerebral oxygenation during prolonged exercise under hypoxia in healthy young males. High Alt Med Biol. 17:214-221, 2016.-The present study examined the effect of prolonged hypoxic exercise on cognitive function. Eight healthy male volunteers were required to complete exercise trials (four 30-minute cycling sessions with a 15-minute rest interval) at an intensity corresponding to 50% of their altitude-adjusted peak oxygen uptake under two different conditions: normoxia (room air at 400 m) and hypoxia (fraction of inspired oxygen: 0.141). Cognitive function was evaluated before, during, and 60 minutes after completion of the exercise trial. The color-word Stroop task (CWST) was used to assess cognitive function, with regard to the number of achievements, accuracy rate, and the number of correct responses made within 60 seconds. Cerebral oxygenation was monitored throughout the experimental period using near-infrared spectroscopy. The accuracy rate did not significantly differ between the two trials. A significant reduction in the number of correct responses during simple CWST tasks was detected in the hypoxic condition 60 minutes after exercise (p < 0.05), wherein a significant correlation was identified between reduced task performance on simple CWST and cerebral oxygenation (p < 0.01). These results demonstrate that prolonged exercise under hypoxic conditions induces a reduction in cerebral oxygenation partly associated with impairment of cognitive function.

Reduction in Cerebral Oxygenation After Prolonged Exercise in Hypoxia is Related to Changes in Blood Pressure.

We investigated the relation between blood pressure and cerebral oxygenation (COX) immediately after exercise in ten healthy males. Subjects completed an exercise and recovery protocol while breathing either 21% (normoxia) or 14.1% (hypoxia) O2 in a randomized order. Each exercise session included four sets of cycling (30 min/set, 15 min rest) at 50% of altitude-adjusted peak oxygen uptake, followed by 60 min of recovery. After exercise, mean arterial pressure (MAP; 87±1 vs. 84±1 mmHg, average values across the recovery period) and COX (68±1% vs. 58±1%) were lower in hypoxia compared to normoxia (P<0.001). Changes in MAP and COX were correlated during the recovery period in hypoxia (r=0.568, P<0.001) but not during normoxia (r=0.028, not significant). These results demonstrate that reductions in blood pressure following exercise in hypoxia are (1) more pronounced than in normoxia, and (2) associated with reductions in COX. Together, these results suggest an impairment in cerebral autoregulation as COX followed changes in MAP more passively in hypoxia than in normoxia. These findings could help explain the increased risk for postexercise syncope at high altitude.

Age, aerobic fitness, and cerebral perfusion during exercise: role of carbon dioxide.

Middle cerebral artery mean velocity (MCAvmean) is attenuated with increasing age both at rest and during exercise. The aim of this study was to determine the influence of the age-dependent reduction in arterial Pco2 (PaCO2) and physical fitness herein. We administered supplemental CO2 (CO2 trial) or no additional gas (control trial) to the inspired air in a blinded and randomized manner, and assessed middle cerebral artery mean flow velocity during graded exercise in 1) 21 young [Y; age 24 ± 3 yr (±SD)] volunteers of whom 11 were trained (YT) and 10 considered untrained (YUT), and 2) 17 old (O; 66 ± 4 yr) volunteers of whom 8 and 9 were considered trained (OT) and untrained (OUT), respectively. A resting hypercapnic reactivity test was also performed. MCAvmean and PaCO2 were lower in O [44.9 ± 3.1 cm/s and 30 ± 1 mmHg (±SE)] compared with Y (59.3 ± 2.3 cm/s and 34 ± 1 mmHg, P < 0.01) at rest, independent of aerobic fitness level. The age-related decreases in MCAvmean and PaCO2 persisted during exercise. Supplemental CO2 reduced the age-associated decline in MCAvmean by 50%, suggesting that PaCO2 is a major component in the decline. On the other hand, relative hypercapnic reactivity was neither influenced by age (P = 0.46) nor aerobic fitness (P = 0.36). Although supplemental CO2 attenuated exercise-induced reduction in cerebral oxygenation (near-infrared spectroscopy), this did not influence exercise performance. In conclusion, PaCO2 contributes to the age-associated decline in MCAvmean at rest and during exercise; however exercise capacity did not diminish this age effect.

Cerebrovascular responses during rowing: Do circadian rhythms explain morning and afternoon performance differences?

The purpose of this study was to characterize cerebrovascular responses to rowing exercise, investigating whether their diurnal variation might explain performance differences across a day. Twelve male rowers completed incremental rowing exercise and a 2000-m ergometer time trial at 07:00 h and 16:00 h, 1 week apart, while middle cerebral artery velocity (MCAv), cerebral (prefrontal), and muscular (vastus lateralis) tissue oxygenation and hemoglobin volume (via near-infrared spectroscopy), heart rate, and pressure of end-tidal CO2 (PET CO2) were recorded. MCAv was 20-25% above resting levels (68 ± 12 cm/s) during submaximal and maximal exercise intensities, despite PET CO2 being reduced during maximal efforts (down ∼ 0.5-0.8 kPa); thus revealing a different perfusion profile to the inverted-U observed in other exercise modes. The afternoon time trial was 3.4 s faster (95% confidence interval 0.9-5.8 s) and mean power output 3.2% higher (337 vs 347 W; P = 0.04), in conjunction with similar exercise-induced elevations in MCAv (P = 0.60) and reductions in cerebral oxygenation (TOI) (P = 0.12). At the muscle, afternoon trials involved similar oxygen extraction (HHb volume and TOI) albeit from a relatively lower total Hb volume (P < 0.01). In conclusion, rowing performance was better in the afternoon, but not in conjunction with differences in MCAv or exercise-induced differences in cerebral oxygenation.

O2 supplementation to secure the near-infrared spectroscopy determined brain and muscle oxygenation in vascular surgical patients: a presentation of 100 cases

This study addresses three questions for securing tissue oxygenation in brain (rScO2) and muscle (SmO2) for 100 patients (age 71 ± 6 years; mean ± SD) undergoing vascular surgery: (i) Does preoxygenation (inhaling 100% oxygen before anesthesia) increase tissue oxygenation, (ii) Does inhalation of 70% oxygen during surgery prevent a critical reduction in rScO2 (<50%), and (iii) is a decrease in rScO2 and/or SmO2 related to reduced blood pressure and/or cardiac output?Intravenous anesthesia was provided to all patients and the intraoperative inspired oxygen fraction was set to 0.70 while tissue oxygenation was determined by INVOS 5100C. Preoxygenation increased rScO2 (from 65 ± 8 to 72 ± 9%; P < 0.05) and SmO2 (from 75 ± 9 to 78 ± 9%; P < 0.05) and during surgery rScO2 and SmO2 were maintained at the baseline level in most patients. Following anesthesia and tracheal intubation an eventual change in rScO2 correlated to cardiac output and cardiac stroke volume (coefficient of contingence = 0.36; P = 0.0003) rather to a change in mean arterial pressure and for five patients rScO2 was reduced to below 50%. We conclude that (i) increased oxygen delivery enhances tissue oxygenation, (ii) oxygen supports tissue oxygenation but does not prevent a critical reduction in cerebral oxygenation sufficiently, and (iii) an eventual decrease in tissue oxygenation seems related to a reduction in cardiac output rather than to hypotension.

Influence of Norepinephrine and Phenylephrine on Frontal Lobe Oxygenation During Cardiopulmonary Bypass in Patients with Diabetes

Although utilization of vasopressors recently has been associated with reduced cerebral oxygenation, the influence of vasopressors on cerebral oxygenation during cardiopulmonary bypass in patients with diabetes is unknown. The aim of this study was to document the impact of norepinephrine and phenylephrine utilization on cerebral oxygenation in patients with and without diabetes during cardiopulmonary bypass. Prospective, clinical study. Academic medical center. Fourteen patients with diabetes and 17 patients without diabetes undergoing cardiac surgery. During cardiopulmonary bypass, norepinephrine (diabetics n = 6; non-diabetics n = 8) or phenylephrine (diabetics n = 8; non-diabetics n = 9) was administered intravenously to maintain mean arterial pressure above 60 mmHg. Mean arterial pressure, venous temperature, arterial oxygenation, and frontal lobe oxygenation (monitored by near-infrared spectroscopy) were recorded before anesthesia induction (baseline) and continuously during cardiopulmonary bypass. Frontal lobe oxygenation was lowered to a greater extent in diabetics versus non-diabetics with administration of norepinephrine (-14±13 v 3±12%; p<0.05). There was also a trend towards a greater reduction in cerebral oxygenation in diabetics versus non-diabetics with administration of phenylephrine (-12±8 v -6±7%; p = 0.1) during cardiopulmonary bypass. Administration of norepinephrine to restore mean arterial pressure during cardiopulmonary bypass is associated with a reduction in frontal lobe oxygenation in diabetics but not in patients without diabetes. Administration of phenylephrine also were associated with a trend towards a greater reduction in frontal lobe oxygenation in diabetics. The clinical implications of these findings deserve future consideration.