Decrease In Cerebral Perfusion Research Articles

In vivo optical assessment of cerebral and skeletal muscle microvascular response to phenylephrine.

This study aimed to investigate the simultaneous response of the cerebral and skeletal muscle microvasculature to the same phenylephrine (PE) boluses. A hybrid optical system that combines hyperspectral near-infrared spectroscopy (hs-NIRS) and diffuse correlation spectroscopy (DCS) was used to monitor changes in tissue oxygenation and perfusion. Data were collected from the head and hind limb of seven male Sprague-Dawley rats while administering intravenous (IV) injections of PE or saline to all animals. The response to saline was used as a control. Skeletal muscle oxygenation decreased significantly after PE injection, while a statistically underpowered decrease in perfusion was observed, followed by an increase beyond baseline. Vascular conductance also decreased in the muscle reflecting the drug's vasoconstrictive effects. Tissue oxygenation and perfusion increased in the brain in response to PE. Initially, there was a sharp increase in cerebral perfusion but no changes in cerebral vascular conductance. Subsequently, cerebral flow and vascular conductance decreased significantly below baseline, likely reflecting autoregulatory mechanisms to manage the excess flow. Further, fitting an exponential function to the secondary decrease in cerebral perfusion and increase in muscular blood flow revealed a quicker kinetic response in the brain to adjust blood flow. In the skeletal muscle, PE caused a transient decrease in blood volume due to vasoconstriction, which resulted in an overall decrease in hemoglobin content and tissue oxygen saturation. Since PE does not directly affect cerebral vessels, this peripheral vasoconstriction shunted blood into the brain, resulting in an initial increase in oxygenated hemoglobin and oxygen saturation.

Use of combined cerebral and somatic renal near infrared spectroscopy during noncardiac surgery in children: a proposed algorithm.

Cerebral near infrared spectroscopy (NIRS) monitoring has been extensively applied in neonatology and in cardiac surgery, becoming a standard in many pediatric cardiac centers. However, compensatory physiological mechanisms favor cerebral perfusion to the detriment of peripheral tissue oxygenation. Therefore, simultaneous measurement of cerebral and somatic oxygen saturation has been advocated to ease the differential diagnosis between central and peripheral sources of hypoperfusion, which may go undetected by standard monitoring and not mirrored by cerebral NIRS alone. A clinical algorithm already exists in cardiac surgery, aimed to correct intraoperative cerebral oxygen desaturations. A similar algorithm still lacks in noncardiac pediatric surgery. The goal of this paper is to propose a clinical algorithm for the combined use of cerebral and somatic NIRS monitoring during anesthesia in the pediatric population undergoing noncardiac surgery. A panel of experienced pediatric anesthetists developed the algorithm that is based on the clinical experience and intraoperative observations. It aims to lessen the current variability in interpreting NIRS measurement. Multisite NIRS monitoring was achieved applying one pediatric sensor to the forehead for cerebral tissue perfusion reading and a second one to the decumbent lumbar region for recording somatic renal tissue perfusion. The algorithm describes a sequence of acts aimed to identify the putative cause of intraoperative organ tissue desaturation and suggests clinical interventions expected to restore adequate tissue perfusion. It is composed of two arms: the main arm includes patients with an observed decrease in cerebral perfusion (CrO2), the second one includes those with a stable CrSO2 with declining RrSO2. Described also are five clinical cases of infants and neonates in whom pathological alterations of organ perfusion were detected using intraoperative multisite NIRS monitoring, portrayed in the accompanying figures (Annex).

THE EFFECT OF RENAL DENERVATION ON CEREBRAL BLOOD FLOW IN DIABETIC PATIENTS WITH RESISTANT HYPERTENSION

Objective: Long-term and persistent increase in blood pressure (BP) leads to vascular remodeling, which deteriorates cerebral blood flow. The combination of hypertension (HTN) with diabetes mellitus (DM) accelerates the vascular damage and impairs the cerebral blood flow autoregulation, which may be accompanied by an uncompensated decrease in cerebral perfusion in response to a decrease in BP. Renal denervation (RDN) leads to a rapid and sustained decrease in BP, therefore the aim of this study was to assess of changes in cerebral blood flow in patients with resistant HTN (RHTN) and type 2 DM at 6 month after the intervention. Design and method: Evaluation of cerebral blood flow was performed in 21 patients with RHTN and type 2 DM, who were included in single-arm prospective interventional studies (protocol numbers NCT01499810 and NCT02667912 on ClinicalTrials.gov) (mean age 61.4 ± 7.6 years, mean office (systolic/diastolic) BP (SBP/DBP) 167.1 ± 19.4/85.6 ± 15.9 mmHg, HbA1c 7.1 ± 1.3%, 8 men (32%), 19 pts (91%) had atherosclerosis of internal carotid arteries (ICA) with mean values of stenosis 22.2 ± 9.7%). All patients were undergone to ambulatory 24-hour BP, Doppler high-resolution ultrasound of ICA and middle cerebral arteries (MCA) at baseline and 6 month follow-up. The patients were instructed not to change their medication regimen during the study. Results: There was a significant decrease in mean 24-hour BP (systolic/diastolic) (-12.6/-7.3 mmHg, p < 0.05). At the same time, there was no deterioration in blood flow of ICA and MCA at 6 months after RDN. Conclusions: Our data indicate that the significant decrease in BP after RDN does not lead to deterioration of cerebral blood flow and therefore indicates the safety of this procedure for the brain in patients with RHTN with type 2 DM.

A cervical compartment syndrome impairs cerebral circulation in post-thyroidectomy hemorrhage: data from an animal model.

Post thyroidectomy hemorrhage is a potentially life-threatening complication. As the mechanism leading to hypoxemic brain damage and death is still unknown, our aim was to examine the underlaying pathophysiology in an animal model. A series of experiments was performed in our established model for post thyroidectomy hemorrhage in 6 pigs. First, post thyroidectomy hemorrhage was simulated with an artificial increase of cervical compartment pressure. Second, spontaneous bleeding into the cervical compartment was initiated. Primary outcome measure is the correlation between cerebral oxygenation and cervical compartment pressure. With an increase in cervical compartment pressure apnea could be detected in all experiments. A significant 24.2% (9.5-34.4%) decrease of cerebral oxygenation at time of apnea (47.0%; 38.0-65.0%) compared to baseline values (63.5%; 56.0-74.0%; P=0.043) occurred due increase of cervical compartment pressure concurrent with an impaired cerebral perfusion. Apnea occurred about 200 sec after a 10% decrease of cerebral oxygenation, but 35 sec before a 10% decrease of peripheral oxygenation. Spontaneous bleeding into the cervical compartment causes an increase of cervical compartment pressure reaching levels of the mean arterial blood pressure 56.0 (35.0-72.0) mmHg. Peripheral hypoxemia occurs with relevant delay in time after decrease of cerebral perfusion and cerebral hypoxemia, therefore cerebral hypoxemia seems to be causal for a central apnea. With this evidence of impaired cerebral perfusion and cerebral hypoxemia due to an increased cervical compartment pressure we can disprove the historic theory of tracheal collapse due to a compressive hematoma in post thyroidectomy hemorrhage. A cervical compartment syndrome seems to be causal, not only for brain hypoxemia but also an additional laryngo-pharyngeal mucosal edema.

Reactive oxygen species play a modulatory role in the hyperventilatory response to poikilocapnic hyperoxia in humans

The proposed mechanism for the increased ventilation in response to hyperoxia includes a reduced brain CO2 -[H+ ] washout-induced central chemoreceptor stimulation that results from a decrease in cerebral perfusion and the weakening of the CO2 affinity for haemoglobin. Nonetheless, hyperoxia also results in excessive brain reactive oxygen species (ROS) formation/accumulation, which hypothetically increases central respiratory drive and causes hyperventilation. We then quantified ventilation, cerebral perfusion/metabolism, arterial/internal jugular vein blood gases and oxidant/antioxidant biomarkers in response to hyperoxia during intravenous infusion of saline or ascorbic acid to determine whether excessive ROS production/accumulation contributes to the hyperoxia-induced hyperventilation in humans. Ascorbic acid infusion augmented the antioxidant defence levels, blunted ROS production/accumulation and minimized both the reduction in cerebral perfusion and the increase in ventilation observed during saline infusion. Hyperoxic hyperventilation seems to be mediated by central chemoreceptor stimulation provoked by the interaction between an excessive ROS production/accumulation and reduced brain CO2 -[H+ ] washout. The hypothetical mechanism for the increase in ventilation ( ) in response to hyperoxia (HX) includes central chemoreceptor stimulation via reduced CO2 -[H+ ] washout. Nonetheless, hyperoxia disturbs redox homeostasis and raises the hypothesis that excessive brain reactive oxygen species (ROS) production/accumulation may increase the sensitivity to CO2 or even solely activate the central chemoreceptors, resulting in hyperventilation. To determine the mechanism behind the HX-evoked increase in , 10 healthy men (24±4 years) underwent 10min trials of HX under saline and ascorbic acid infusion. , arterial and right internal right jugular vein (ijv) partial pressure for oxygen (PO2 ) and CO2 (PCO2 ), pH, oxidant (8-isoprostane) and antioxidant (ascorbic acid) markers, as well as cerebral blood flow (CBF) (Duplex ultrasonography), were quantified at each hyperoxic trial. HX evoked an increase in arterial partial pressure for oxygen, followed by a hyperventilatory response, a reduction in CBF, an increase in arterial 8-isoprostane, and unchanged PijvCO2 and ijv pH. Intravenous ascorbic acid infusion augmented the arterial antioxidant marker, blunted the increase in arterial 8-isoprostane and attenuated both the reduction in CBF and the HX-induced hyperventilation. Although ascorbic acid infusion resulted in a slight increase in PijvCO2 and a substantial decrease in ijv pH, when compared with the saline bout, HX evoked a similar reduction and a paired increase in the trans-cerebral exchanges for PCO2 and pH, respectively. These findings indicate that the poikilocapnic hyperoxic hyperventilation is likely mediated via the interaction of the acidic brain interstitial fluid and an increase in central chemoreceptor sensitivity to CO2 , which, in turn, seems to be evoked by the excessive ROS production/accumulation.

Effects of a dual-filter-based cerebral embolic protection device in transcatheter aortic valve replacement on cerebral oxygen saturation: A prospective pilot study.

The Sentinel Cerebral Protection System (Sentinel-CPS) is increasingly used in transcatheter aortic valve replacement (TAVR). However, the impact of inserting the Sentinel-CPS inside the brain-supplying arteries on cerebral perfusion and oxygenation is unknown. Twenty patients undergoing transfemoral TAVR with (n = 10) and without (n = 10) cerebral embolic protection using the Sentinel-CPS were prospectively observed. All patients received conscious sedation and cerebral oxygen saturation (rSO2 ) was continuously measured with near-infrared spectroscopy (NIRS). The cumulative perioperative cerebral desaturation was calculated for each patient by multiplying rSO2 below an individualized desaturation threshold by time. In addition, rSO2 values at the time of Sentinel-CPS insertion, filter positioning, and device retraction were analyzed. There was no significant difference in cumulative cerebral desaturation in patients with Sentinel-CPS (median [IQR]) (0 [0/81] s%) and without (median [IQR]) (0 [0/23] s%), p = .762. A total of 6 patients (33.3%) experienced a perioperative decrease in rSO2 below the individualized desaturation threshold (n = 3 with Sentinel-CPS, n = 3 without Sentinel-CPS; p = 1.000). Cerebral desaturation was detected during valve deployment (n = 5) and after postdilatation (n = 1). No desaturation events occurred during Sentinel-CPS insertion, filter positioning, or retraction. Our pilot study revealed no difference in cumulative perioperative cerebral desaturation between TAVR with and without Sentinel-CPS. Catheter- and filter-based manipulations in the brain-supplying arteries for Sentinel-CPS application were not associated with a decrease of cerebral perfusion and oxygenation.

Neuroimaging patterns of chronic cerebrovascular insufficiency with evaluation of cerebral perfusion depending on the level of cognitive disorders

Aim. To evaluate the neuroimaging patterns of chronic cerebrovascular insufficiency with cerebral perfusion assessment depending on the level of cognitive impairment.Materials and methods. The 58 patients aged 50–79 years were examined: 45 patients with a diagnosis of сhronic cerebrovascular insufficiency and 13 conditionally healthy volunteers. Patients with Chronic cerebrovascular insufficiency were ranked into three subgroups depending on the severity of cognitive impartment (CI). T1-, T2, T2*- VI, DWI, FLAIR and non-contrast MR perfusion (ASL) were included in the MR-protocol (Toshiba Vantage Titan, 1.5 T). The analysis of MRM patterns of Chronic cerebrovascular insufficiency was carried out according to STRIVE criteria. The total cerebral blood flow and regional in the frontal and parietal lobes were evaluated by the ASLperfusion.Results. A relationship was found between the degree of leukoaraiosis, the type of expansion of the perivascular spaces of Virchow-Robin and the level of CI. According to ASL, total cerebral blood flow is higher in groups without CI and in patients with severe CI. There is a diffuse decrease of cerebral perfusion in patients with mild CI. This phenomenon is explained by initial impairment of the blood-brain barrier permeability, damage to the microvasculature. Relative hyperperfusion in the cortex of the frontal and parietal lobes of patients with dementia indicates the ineffectiveness of increased cortical blood flow and the resulting shunt blood flow due to the high resistance of the altered small cerebral vessels under high pulsating properties of the main arteries.Conclusion. ASL perfusion is a complementary link to the STRIVE criteria in the diagnosis of chronic cerebrovascular insufficiency. The absence of changes in cerebral perfusion in patients with subjective manifestations of chronic cerebrovascular insufficiency makes it advisable to search for new methods for the diagnosis of preclinical stages of vascular cognitive impairment.

PTPRG is an ischemia risk locus essential for HCO3--dependent regulation of endothelial function and tissue perfusion.

Acid-base conditions modify artery tone and tissue perfusion but the involved vascular-sensing mechanisms and disease consequences remain unclear. We experimentally investigated transgenic mice and performed genetic studies in a UK-based human cohort. We show that endothelial cells express the putative HCO3--sensor receptor-type tyrosine-protein phosphatase RPTPγ, which enhances endothelial intracellular Ca2+-responses in resistance arteries and facilitates endothelium-dependent vasorelaxation only when CO2/HCO3- is present. Consistent with waning RPTPγ-dependent vasorelaxation at low [HCO3-], RPTPγ limits increases in cerebral perfusion during neuronal activity and augments decreases in cerebral perfusion during hyperventilation. RPTPγ does not influence resting blood pressure but amplifies hyperventilation-induced blood pressure elevations. Loss-of-function variants in PTPRG, encoding RPTPγ, are associated with increased risk of cerebral infarction, heart attack, and reduced cardiac ejection fraction. We conclude that PTPRG is an ischemia susceptibility locus; and RPTPγ-dependent sensing of HCO3- adjusts endothelium-mediated vasorelaxation, microvascular perfusion, and blood pressure during acid-base disturbances and altered tissue metabolism.

Female Mice Are Resistant to Inward Remodeling of Parenchymal Arterioles Observed in Male Mice During Angiotensin II‐Induced Hypertension

Hypertension increases risk of vascular cognitive impairment and dementia (VCID) by impairing the structure and function of cerebral arteries. These arterial changes result in chronic hypoperfusion of the brain parenchyma and, eventually, cognitive impairment. Epidemiological studies suggest a sex difference in development of VCID, with women being protected from its development until late in age. We have previously shown that angiotensin II (AngII)‐hypertension led to inward hypotrophic remodeling and decreased wall stress in the parenchymal arterioles (PAs) of male mice. This PA remodeling in AngII‐hypertension was associated with reduced cerebral perfusion, increased myogenic tone, and cognitive dysfunction. Female mice, however, were protected from memory impairments despite a similar increase in blood pressure and decrease in cerebral perfusion measured by scanning laser Doppler. We hypothesized that AngII‐hypertension in female mice will cause a decrease in cerebral perfusion measured by laser speckle contrast, as well as a decrease in outer diameter, lumen diameter, and wall thickness in the PAs. Sixteen to eighteen‐week‐old female C56BL/6 mice were treated with AngII (1200 ng/kg/min via osmotic mini‐pump) for four weeks. This dose was selected to produce a similar increase in blood pressure to the previously studied male mice. Sham mice served as control. Blood pressure was measured by tail‐cuff plethysmography and pial blood flow was measured. After euthanasia, brains were collected and PAs were isolated and mounted on a pressure myograph for assessment of spontaneous myogenic tone generation and structure. PA structure was assessed by increasing intralumenal pressure from 3mmHg to 120mmHg in 20mmHg increments. Results are presented as means ± SEM and PA data are reported at an intralumenal pressure of 40mmHg (n=5–12). Systolic blood pressure was increased (Sham: 141 ± 7, AngII: 179 ± 7mmHg; p<0.05) and cerebral perfusion was reduced in AngII‐hypertension (Sham: 328 ± 6, AngII: 288 ± 11 perfusion units; p<0.05). AngII infusion slightly decreased lumen (Sham: 49 ± 3, AngII: 42 ± 4μm; p=0.17) and outer (Sham: 57 ± 4, AngII: 48 ± 4μm; p=0.11) diameters, although not significantly. AngII‐hypertension reduced wall thickness (Sham: 4 ± 0.3, AngII: 3 ± 0.2μm; p<0.05) and wall area (Sham: 691 ± 83, AngII: 441 ± 52μm2; p<0.05). PAs from female mice did not show reductions in wall stress (Sham: 241.8 ± 19, AngII: 268 ± 20dynes/cm2; p>0.05) or generate more myogenic tone in response to hypertension (Sham: 27 ± 4, AngII: 22 ± 2%; p>0.05). While AngII‐hypertension resulted in reductions in lumen diameter, outer diameter, wall thickness, and wall stress in the PAs of male mice, PAs of female mice had only reduced wall thickness with modest reductions in lumen and outer diameters. Preliminary data suggest that females may be resistant to inward PA remodeling during AngII‐hypertension, despite similar reductions in cerebral blood flow as male mice. This potential protection of the cerebrovascular structure and myogenic tone generation could explain the absence of cognitive dysfunction in response to hypertension in female mice.Support or Funding Information5T32GM092715‐14

Cortical microinfarcts in memory clinic patients are associated with reduced cerebral perfusion

Cerebral cortical microinfarcts (CMIs) are small ischemic lesions associated with cognitive impairment and dementia. CMIs are frequently observed in cortical watershed areas suggesting that hypoperfusion contributes to their development. We investigated if presence of CMIs was related to a decrease in cerebral perfusion, globally or specifically in cortex surrounding CMIs. In 181 memory clinic patients (mean age 72 ± 9 years, 51% male), CMI presence was rated on 3-T magnetic resonance imaging (MRI). Cerebral perfusion was assessed from cortical gray matter of the anterior circulation using pseudo-continuous arterial spin labeling parameters cerebral blood flow (CBF) (perfusion in mL blood/100 g tissue/min) and spatial coefficient of variation (CoV) (reflecting arterial transit time (ATT)). Patients with CMIs had a 12% lower CBF (beta = −.20) and 22% higher spatial CoV (beta = .20) (both p < .05) without a specific regional pattern on voxel-based CBF analysis. CBF in a 2 cm region-of-interest around the CMIs did not differ from CBF in a reference zone in the contralateral hemisphere. These findings show that CMIs in memory clinic patients are primarily related to global reductions in cerebral perfusion, thus shedding new light on the etiology of vascular brain injury in dementia.

Evaluation of cerebral oxygen perfusion during shoulder arthroplasty performed in the semi–beach chair position

The beach chair position is commonly used when performing shoulder arthroplasty. However, this position has been associated with hypotension, potentially leading to cerebral hypoperfusion, which may cause neurologic injury. In addition, shoulder arthroplasty cases are associated with longer operative times, posing a potentially greater risk of cerebral hypoperfusion. We aim to evaluate the risk of cerebral desaturation events (CDEs) during the course of total shoulder arthroplasty. Twenty-six patients undergoing shoulder arthroplasties were monitored for changes in cerebral perfusion. Seven specific time-points during the procedure were labeled for comparison of events: baseline, beach chair, incision, humeral broaching, glenoid reaming, glenoid component implantation, and humeral component implantation. Cerebral oxygen perfusion was measured using near-infrared spectroscopy. A CDEwas described as a decrease of oxygen saturation greater than 20%. Nineteeen of 25 subjects experienced a CDE. 42% of these patients experienced CDEs during semi-beach chair positioning. Patients experienced the largest oxygen saturation drop during semi-beach chair positioning. Transition from baseline to semi-beach chair was the only event to have a statistically significant decrease in cerebral perfusion (8%, P < .05). There was a statistically significant percentage change in mean oxygen saturation in the semi-beach chair interval (10%, P < .01) and the semi-beach chair to incision interval (7%, P < .01). Most patients experienced an intraoperative CDE, with greatest incidence during semi-beach chair positioning. The largest decline in cerebral oxygen saturation occurred during semi-beach chair positioning. Implant implantation was not associated with decrease in cerebral oximetry.

Aggressive blood pressure reduction is not associated with decreased perfusion in leukoaraiosis regions in acute intracerebral hemorrhage patients.

Leukoaraiosis regions may be more vulnerable to decreases in cerebral perfusion. We aimed to assess perfusion in leukoaraiosis regions in acute intracerebral hemorrhage (ICH) patients. We tested the hypothesis that aggressive acute BP reduction in ICH patients is associated with hypoperfusion in areas of leukoaraiosis. In the ICH Acutely Decreasing Arterial Pressure Trial (ICH ADAPT), patients with ICH <24 hours duration were randomized to two systolic BP (SBP) target groups (<150 mmHg vs. <180 mmHg). Computed tomography perfusion (CTP) imaging was performed 2h post-randomization. Leukoaraiosis tissue volumes were planimetrically measured using semi-automated threshold techniques on the acute non-contrast CT. CTP source leukoaraiosis region-of-interest object maps were co-registered with CTP post-processed maps to assess cerebral perfusion in these areas. Seventy-one patients were included with a mean age of 69±11.4 years, 52 of whom had leukoaraiosis. The mean relative Tmax (rTmax) of leukoaraiotic tissue (2.3±2s) was prolonged compared to that of normal appearing white matter in patients without leukoaraiosis (1.1±1.2s, p = 0.04). In the 52 patients with leukoaraiosis, SBP in the aggressive treatment group (145±20.4 mmHg, n = 27) was significantly lower than that in the conservative group (159.9±13.1 mmHg, n = 25, p = 0.001) at the time of CTP. Despite this SBP difference, mean leukoaraiosis rTmax was similar in the two treatment groups (2.6±2.3 vs. 1.8±1.6 seconds, p = 0.3). Cerebral perfusion in tissue affected by leukoaraiosis is hypoperfused in acute ICH patients. Aggressive BP reduction does not appear to acutely aggravate cerebral hypoperfusion.

Cerebrovascular reactivity and cerebral perfusion of rats with acute liver failure: role of L-glutamine and asymmetric dimethylarginine in L-arginine-induced response.

Cerebral blood flow (CBF) is impaired in acute liver failure (ALF), however, the complexity of the underlying mechanisms has often led to inconclusive interpretations. Regulation of CBF depends at least partially on variations in the local brain L-arginine concentration and/or its metabolic rate. In ALF, other factors, like an increased concentration of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor and elevated level of L-glutamine, may contribute to CBF alteration. This study demonstrated strong differences in the reactivity of the middle cerebral arteries and their response to extravascular L-arginine application between vessels isolated from rats with thioacetamide (TAA)-induced ALF and control animals. Our results also showed the decrease in the cerebral perfusion in TAA rats measured by arterial spin labeling perfusion magnetic resonance. Subsequently, we aimed to investigate the importance of balance between the concentration of ADMA and L-arginine in the CBF regulation. In vivo, intraperitoneal L-arginine administration in TAA rats corrected: (i) decrease in cerebral perfusion, (ii) decrease in brain extracellular L-arginine/ADMA ratio and (iii) increase in brain L-glutamine concentration. Our study implicates that impaired vascular tone of cerebral arteries is most likely associated with exposure to high ADMA and L-glutamine levels resulting in limited availability of L-arginine and might be responsible for reduced cerebral perfusion observed in ALF.

Overview of Neurovascular Physiology.

Neurophysiology is a complex network of cellular, electrical, and vascular systems which function to maximize neuronal functioning and brain performance. The brain exists in a closed system made up of parenchyma, cerebrospinal fluid, and blood with any increase in volume leading to a corresponding decrease in one of the components. Once these compensatory mechanisms are exhausted, there is a precipitous increase in the intracranial pressure leading to decreases in cerebral perfusion and resulting ischemia. The cerebral vasculature has significant control over the total volume of blood and regional flow throughout the brain via autoregulation. Through this process, blood flow is tightly regulated to prevent fluctuations and is coupled precisely with metabolic demand. Moreover, oxygen delivery and aerobic respiration are essential for proper brain functioning and can become deranged in various disease states leading to cellular injury and death. Ongoing trials have provided evidence that in addition to targeted therapy for intracranial pressure monitoring, optimizing brain tissue oxygenation and cerebral autoregulation may lead to improved clinical outcomes. An understanding of neurophysiology is not only essential for treating patients suffering from intracranial injury but also for the development of novel monitoring and therapeutic techniques.

Limb Skin Temperature as a Tool to Predict Orthostatic Instability.

Orthostatic instability is one of the main consequences of weightlessness or gravity challenge and plays as well a crucial role in public health, being one of the most frequent disease of aging. Therefore, the assessment of effective countermeasures, or even the possibility to predict, and thus prevent orthostatic instability is of great importance. Heat stress affects orthostatic stability and may lead to impaired consciousness and decrease in cerebral perfusion, specifically during the exposure to G-forces. Conversely, peripheral cooling can prevent orthostatic intolerance – even in normothermic healthy subjects. Indicators of peripheral vasodilation, as elevated skin surface temperatures, may mirror blood decentralization and an increased risk of orthostatic instability. Therefore, the aim of this study was to quantify orthostatic instability risk, by assessing in 20 fighter jet pilot candidates’ cutaneous limb temperatures, with respect to the occurrence of G-force-induced almost loss of consciousness (ALOC), before and during exposure to a push-pull maneuver, i.e., head-down tilt, combined with lower body negative pressure. Peripheral skin temperatures from the upper and lower (both proximal and distal) extremities and core body temperature via heat-flux approach (i.e., the Double Sensor), were continuously measured before and during the maneuver. The 55% of subjects that suffered an ALOC during the procedure had higher upper arm and thigh temperatures at baseline compared to the 45% that remained stable. No difference in baseline core body temperature and distal limbs (both upper and lower) skin temperatures were found between the two groups. Therefore, peripheral skin temperature data could be considered a predicting factor for ALOC, prior to rapid onset acceleration. Moreover, these findings could also find applications in patient care settings such as in intensive care units.

Cerebral Blood Flow Measurements in Adults: A Review on the Effects of Dietary Factors and Exercise.

Improving cerebrovascular function may be a key mechanism whereby a healthy lifestyle, of which a healthy diet combined with increased physical activity levels is a cornerstone, protects against cognitive impairments. In this respect, effects on cerebral blood flow (CBF)—a sensitive physiological marker of cerebrovascular function—are of major interest. This review summarizes the impact of specific dietary determinants and physical exercise on CBF in adults and discusses the relation between these effects with potential changes in cognitive function. A limited number of randomized controlled trials have already demonstrated the beneficial effects of an acute intake of nitrate and polyphenols on CBF, but evidence for a relationship between these effects as well as improvements in cognitive functioning is limited. Moreover, long-term trans-resveratrol supplementation has been shown to increase CBF in populations at increased risk of accelerated cognitive decline. Long-term supplementation of n-3 long-chain polyunsaturated fatty acids may also increase CBF, but related effects on cognitive performance have not yet been found. Significant decreases in cerebral perfusion were observed by commonly consumed amounts of caffeine, while alcohol intake was shown to increase CBF in a dose-dependent way. However, the long-term effects are not clear. Finally, long-term exercise training may be a promising approach to improve CBF, as increases in perfusion may contribute to the beneficial effects on cognitive functioning observed following increased physical activity levels.

Severe Traumatic Brain Injury.

Background: Inadvertent hyperventilation is associated with poor outcomes from traumatic brain injury (TBI). Hypocapnic cerebral vasoconstriction is well described and causes an immediate and profound decrease in cerebral perfusion. The hemodynamic effects of positive-pressure ventilation (PPV) remain incompletely understood but may be equally important, particularly in the hypovolemic patient with TBI. Objective: Preliminary report on the application of a previously described mathematical model of perfusion and ventilation to prehospital data to predict intrathoracic pressure. Methods: Ventilation data from 108 TBI patients (76 ground transported, 32 helicopter transported) were used for this analysis. Ventilation rate (VR) and end-tidal carbon dioxide (PetCO2) values were used to estimate tidal volume (VT). The values for VR and estimated VT were then applied to a previously described mathematical model of perfusion and ventilation. This model allows input of various lung parameters to define a pressure–volume relationship, then derives mean intrathoracic pressure (MITP) for various VT and VR values. For this analysis, normal lung parameters were utilized. Separate analyses were performed assuming either fixed or variable PaCO2–PetCO2 differences. Ground and air medical patients were compared with regard to VR, PetCO2, estimated VT, and predicted MITP. Results: A total of 10,647 measurements were included from the 108 TBI patients, representing Received July 11, 2014 from the Department of Emergency Medicine, University of California at San Diego, La Jolla, California (DPD, SAA, GV, JVD), School of Medicine, University of California San Diego, La Jolla, California (KS), Division of Cardiology, University of California San Diego, La Jolla, California (RDH), Division of Cardiology, The Ohio State University, Columbus, Ohio (RDH), Department of Anesthesiology (AM) and Division of Pulmonary and Critical Care (RS), University of California at San Diego, La Jolla, California, and Rural/Metro Ambulance, San Diego, California, and San Diego Department of Fire–Rescue, San Diego, California (RF, CB, JVD). Accepted for publication August 4, 2014. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. This paper was presented orally at the Resuscitation Science Symposium, 2011. Address correspondence to Steve A. Aguilar, MD, UC San Diego Emergency Medicine, 200 West Arbor Drive #8676, San Diego, CA 92103, USA. E-mail: SteveAguilarMD@gmail.com doi: 10.3109/10903127.2014.959228 about 13 minutes of ventilation per patient. Mean VR values were higher for ground patients versus air patients (21.6 vs. 19.7 breaths/min; p < 0.01). Estimated VT values were similar for ground and air patients (399 mL vs. 392 mL; p = NS) in the fixed model but not the variable (636 vs. 688 mL, respectively; p < 0.01). Mean PetCO2 values were lower for ground versus air patients (30.6 vs. 33.8 mmHg; p < 0.01). Predicted MITP values were higher for ground versus air patients, assuming either fixed (9.0 vs. 8.1 mmHg; p < 0.01) or variable (10.9 vs. 9.7 mmHg; p < 0.01) PaCO2–PetCO2 differences. Conclusions: Predicted MITP values increased with ventilation rates. Future studies to externally validate this model are warranted.

Assessment of cerebral perfusion with contrast-enhanced ultrasound during constriction of the neck mimicking malposition of the BD Odon Device™: a study in newborn piglets.

The BD Odon Device™ is a new instrument for operative vaginal birth with potential for preventing maternal, fetal and newborn morbidity/mortality during a complicated second stage of labour. The device is a plastic sleeve with an air chamber inflated around the baby's head which is gently pulled through the birth canal. The aim was to monitor changes in cerebral circulation during constriction of the neck to evaluate a risk of potential malposition of the device. Randomised prospective study. Twelve newborn piglets. The anaesthetised piglets were exposed to hypoxia until base excess was -20mmol/l and/or mean arterial blood pressure had decreased to 20mmHg. At reoxygenation, an air chamber was inflated around the neck to 300mmHg and the piglets randomised into three groups: 10 (n=5), 5 (n=5) or 2 (n=2) minutes' occlusion. Cerebral perfusion was evaluated with transcranial contrast-enhanced ultrasound at four time-points, and analysed in the carotid arteries, basal ganglia, cortex and whole brain. Statistical analysis used ANOVA, linear mixed model, Kruskal-Wallis H-test. Perfusion parameters; peak intensity, time to peak intensity, upslope, mean transit time, area under the curve. The haemodynamic response was comparable between groups. Perfusion parameters showed a slight increase at end hypoxia followed by a decrease during occlusion, especially in the cortex (P=0.00-0.2). After deflation, perfusion returned towards baseline values. Simulation of malposition of the Odon Device was performed using a newborn hypoxic piglet model. Considerable compression of the neck vessels was applied, with only a moderate decrease in perfusion and with restoration of haemodynamics/cerebral perfusion after decompression. Malposition of Odon Device™ in a piglet model revealed a reversible decrease in cerebral perfusion during neck constriction.

Changes in Cerebral Oxygenation in Preterm Infants With Progressive Posthemorrhagic Ventricular Dilatation

BackgroundOptimal timing of intervention in neonatal progressive posthemorrhagic hydrocephalus is often a difficult decision. Unchecked hydrocephalus can lead to irreversible brain injury through impaired perfusion, while placement of a shunt is not without long-term morbidity. The purpose of this study was to assess the use of near-infrared spectroscopy to measure changes in regional cerebral oxygen saturation as an indicator of cerebral perfusion in infants with progressive posthemorrhagic ventricular dilatation. MethodsNear-infrared spectroscopy was used to measure regional cerebral oxygen saturation for more than a one-hour period in infants within 24 hours of cranial ultrasound. Simultaneous pulse oximetry was recorded and oxygen extraction was calculated. Ventricular size was measured by ultrasound using the frontal-occipital horn ratio and compared with average oxygen saturation and oxygen extraction. Statistical analysis was done using the Spearman rank test and analysis of variance. ResultsVentricular measurements were made in 20 very low birth weight premature infants with periventricular-intraventricular hemorrhage and 12 infants with normal ultrasound scans. Ventricular dilatation was associated with lower cerebral oxygen saturation and higher oxygen extraction (P < 0.001). Progressive ventricular dilatation was inversely related to changes in cerebral oxygen saturation (P < 0.001). ConclusionsProgressive posthemorrhagic ventricular dilatation is associated with a significant decrease in cerebral oxygenation and increase in oxygen extraction suggesting a decrease in cerebral perfusion. Near-infrared spectroscopy could potentially provide additional clinical information to assist in determining optimal timing of surgical intervention in preterm infants with progressive ventricular enlargement.

Niedawno przebyte omdlenia u pacjentów z istotnym zwężeniem tętnic szyjnych

Introduction. Syncope is a transient loss of consciousness due to a decrease in cerebral perfusion. The aim of the study is to evaluate the incidence of syncope within 2 years before the finding of significant carotid stenosis and to seek the relationship between syncope occurrence and clinical and ECG parameters. Material and methods. The study group consisted of 78 patients (31 women and 47 men aged 65.4 ± 7.7 years) admitted to the Department of Vascular Surgery in order to perform the surgery because of significant carotid stenosis. The studied patients were interviewed for syncopal history and risk factors for cardiovascular diseases. Moreover, a 12-lead resting electrocardiogram was performed. Results. In the study group 20 (25.6%) patients reported at least one faint, 7 (9%) patients reported a faint in the past 2 years. The subgroups distinguished in the basis of syncopal history in the past 2 years did not differ significantly in terms of the assessed demographic and clinical parameters. In the group of patients with syncope in the past 2 years, there was significantly more patients with QRS ≥ 120 ms than the other patients. Logistic regression analysis showed that the only parameter associated with syncope in the past 2 years has been QRS width ≥ 120 ms odds ratio (OR): 18.9; 95% confidence interval (CI) 2.4–147.4 (p = 0.005). Conclusions. 1. Syncope during the past 2 years occurs in almost 10% of patients qualified for carotid artery surgery. 2. The parameter associated with syncope in the past two years is widened QRS complex indicating a cardiac cause of syncope. 3. Gathering information about recent loss of consciousness in patients qualified for vascular surgery on the carotid arteries can have important implications for the planning further cardiological diagnostics.