Reductions In Brain Blood Flow Research Articles

Hemodialysis-Related Acute Brain Injury Demonstrated by Application of Intradialytic Magnetic Resonance Imaging and Spectroscopy.

Hemodialysis (HD) results in reduced brain blood flow, and HD-related circulatory stress and regional ischemia are associated with brain injury over time. However, studies to date have not provided definitive direct evidence of acute brain injury during a HD treatment session. Using intradialytic magnetic resonance imaging (MRI) and spectroscopy to examine HD-associated changes in brain structure and neurochemistry, the authors found that multiple white (WM) tracts had diffusion imaging changes characteristic of cytotoxic edema, a consequence of ischemic insult and a precursor to fixed structural WM injury. Spectroscopy showed decreases in prefrontal N -acetyl aspartate (NAA) and choline concentrations consistent with energy deficit and perfusion anomaly. This suggests that one HD session can cause brain injury and that studies of interventions that mitigate this treatment's effects on the brain are warranted. Hemodialysis (HD) treatment-related hemodynamic stress results in recurrent ischemic injury to organs such as the heart and brain. Short-term reduction in brain blood flow and long-term white matter changes have been reported, but the basis of HD-induced brain injury is neither well-recognized nor understood, although progressive cognitive impairment is common. We used neurocognitive assessments, intradialytic anatomical magnetic resonance imaging, diffusion tensor imaging, and proton magnetic resonance spectroscopy to examine the nature of acute HD-associated brain injury and associated changes in brain structure and neurochemistry relevant to ischemia. Data acquired before HD and during the last 60 minutes of HD (during maximal circulatory stress) were analyzed to assess the acute effects of HD on the brain. We studied 17 patients (mean age 63±13 years; 58.8% were male, 76.5% were White, 17.6% were Black, and 5.9% were of Indigenous ethnicity). We found intradialytic changes, including the development of multiple regions of white matter exhibiting increased fractional anisotropy with associated decreases in mean diffusivity and radial diffusivity-characteristic features of cytotoxic edema (with increase in global brain volumes). We also observed decreases in proton magnetic resonance spectroscopy-measured N -acetyl aspartate and choline concentrations during HD, indicative of regional ischemia. This study demonstrates for the first time that significant intradialytic changes in brain tissue volume, diffusion metrics, and brain metabolite concentrations consistent with ischemic injury occur in a single dialysis session. These findings raise the possibility that HD might have long-term neurological consequences. Further study is needed to establish an association between intradialytic magnetic resonance imaging findings of brain injury and cognitive impairment and to understand the chronic effects of HD-induced brain injury. NCT03342183 .

Taking Regular Breaks From Sitting Prevents Reductions in Brain Blood Flow

Supplying the brain with enough blood flow is essential to keep us alive and maintain our brain health. Reductions in brain blood flow can negatively affect the ability to think. Decreased blood flow to the brain can also lead to brain diseases, such as dementia, which is a condition that causes permanent memory loss and confusion. Scientists are beginning to think that sitting may be bad for brain blood flow. Understanding how sitting affects the brain is therefore very important. We conducted a study in which participants either sat down without any breaks for 4 h, or sat down but took a short walking break every 30 min, or took a longer walking break every 2 h. After sitting without any breaks, brain blood flow decreased. However, when participants took a walking break every 30 min that prevented the decrease in brain blood flow. These results suggest we should encourage people to take regular breaks from sitting to help maintain brain health.

The functional and structural changes in the basilar artery due to overpressure blast injury.

Overpressure blast-wave induced brain injury (OBI) leads to progressive pathophysiologic changes resulting in a reduction in brain blood flow, blood brain barrier breakdown, edema, and cerebral ischemia. The aim of this study was to evaluate cerebral vascular function after single and repeated OBI. Male Sprague-Dawley rats were divided into three groups: Control (Naive), single OBI (30 psi peak pressure, 1 to 2 msec duration), and repeated (days 1, 4, and 7) OBI (r-OBI). Rats were killed 24 hours after injury and the basilar artery was isolated, cannulated, and pressurized (90 cm H2O). Vascular responses to potassium chloride (KCl) (30 to 100 mmol/L), endothelin-1 (10−12 to 10−7 mol/L), acetylcholine (ACh) (10−10 to 10−4 mol/L) and diethylamine-NONO-ate (DEA-NONO-ate) (10−10 to 10−4 mol/L) were evaluated. The OBI resulted in an increase in the contractile responses to endothelin and a decrease in the relaxant responses to ACh in both single and r-OBI groups. However, impaired DEA-NONO-ate-induced vasodilation and increased wall thickness to lumen ratio were observed only in the r-OBI group. The endothelin-1 type A (ETA) receptor and endothelial nitric oxide synthase (eNOS) immunoreactivity were significantly enhanced by OBI. These findings indicate that both single and r-OBI impairs cerebral vascular endothelium-dependent dilation, potentially a consequence of endothelial dysfunction and/or vascular remodelling in basilar arteries after OBI.

The functional changes in the basilar artery due to overpressure blast injury (685.1)

Overpressure blast‐wave induced brain injury (OBI) leads to progressive pathophysiological changes resulting in a reduction in brain blood flow, blood brain barrier breakdown, edema and ischemia. The aim was to evaluate cerebral vascular function after single and repeated OBI. Male Sprague Dawley rats (250‐300 g) were divided into 3 groups: Control (Naive), single OBI [30 psi peak pressure, 1‐2 msec duration], and repeated (every three days) OBI (r‐OBI). Rats were sacrificed 24 h post injury (8th day) and the basilar artery was cannulised in the pressurized system (90cm H2O). Vascular responses to KCl (30‐50‐100 mM) endothelin (10‐11‐10‐7 M), acetylcholine (ACh) (10‐9‐10‐4 M) and diethylamine (DEA)‐NONO‐ate (10‐9‐10‐4 M) were evaluated.OBI resulted in an increase in the contractile responses to endothelin and a decrease in the relaxant responses to ACh in both single and repeated injury groups. However, impaired DEA‐induced dilation and increased wall thickness to lumen ratio were observed only in the r‐OBI group.These findings indicate that single OBI causes endothelium‐dependent and ‐independent alterations in cerebral vascular function and repeated injury results in increased arterial wall thickness.Grant Funding Source: This work was supported by the Medical Research Service of the Department of Veterans Affairs, McKni

Brain blood flow and cardiovascular responses to hot flashes in postmenopausal women

This study tested two related hypotheses: (1) brain blood flow is reduced during postmenopausal hot flashes, and (2) the magnitude of this reduction in brain blood flow is greater during hot flashes when blood pressure is reduced. Eleven healthy, normotensive postmenopausal women rested in a temperature-controlled laboratory (∼ 25°C) for approximately 120 minutes while waiting for a hot flash to occur. The onset of a hot flash was objectively identified by an abrupt increase in sternal sweat rate (capacitance hygrometry). Middle cerebral artery blood velocity (MCAv; transcranial Doppler) and mean arterial pressure (Finometer) were measured continuously. Each hot flash was divided into eight equal segments, and the segment with the largest reduction in MCAv and mean arterial pressure was identified for each hot flash. During experimental sessions, 25 hot flashes occurred (lasting a mean [SD] of 6.2 [2.8] min, with a mean frequency of 3 [1] hot flashes per participant). Seventy-six percent of hot flashes were accompanied by a clear reduction (>5%) in brain blood flow. For all hot flashes, the mean maximal decrease in MCAv was 12% (9%) (7 [6] cm s). This value did not correlate with corresponding changes in mean arterial pressure (R = 0.36). These findings demonstrate that hot flashes are often accompanied by clear reductions in brain blood flow that do not correspond with short-term reductions in mean arterial blood pressure.

Experimental Physiology -Viewpoints: Parasympathetic control of blood flow to the activated human brain

Experimental Physiology -<i>Viewpoints</i>: Parasympathetic control of blood flow to the activated human brain

Nucleus tractus solitarii (NTS) blood flow and oxygenation are compromised in spontaneously hypertensive rats (SHR)

A reduction in brain blood flow, and thus oxygen delivery, may contribute to the development and maintenance of hypertension. We tested the novel hypothesis that blood flow to the NTS, a brainstem region critical to blood pressure regulation, is reduced in the SHR. The hydrogen (H2) clearance method, where H2 clearance is proportional to regional blood flow (RBF), was employed in adult Wistar‐Kyoto rats (WKY, n=5) and SHR (n=4). MAP was elevated in SHR compared to WKY (114±3 vs 88±5 mmHg, P&lt;0.05). Although basal RBF was not different in NTS between rat strains (SHR 37±5 vs WKY 44±7 ml/100g/min, P=0.06), its ability to increase in response to neuronal activation following vagal nerve stimulation was blunted severely in the SHR (ΔRBF: SHR 8±1 vs WKY 32±7 ml/100g/min, P&lt;0.05). Further, calculation of the relative increase in regional vascular conductance (RVC=ΔRBF/ΔMAP) was also substantially blunted in SHR (18±3 vs 99±22%, P&lt;0.05). Whilst the oxygen tension of NTS was similar between rat strains (18 vs 18 mmHg), lowering MAP in SHR to levels seen in WKY rats produced severe hypoxia (6 mmHg). These findings support the hypothesis that vascular resistance in NTS of SHR is higher than WKY rats and that neuro‐vascular coupling which mediates the increase in blood flow in response to neuronal activation is severely impaired in the NTS of SHR. Supported by NIH HL059167 (JTP), NS054651 &amp; 054687 (SY), British Heart Foundation (JFRP)

Cerebral blood volume and blood flow at varying arterial carbon dioxide tension levels in rabbits during propofol anesthesia.

There are little data on the effects of propofol on cerebral blood volume (CBV). We studied the effects of changes in PaCO(2) on CBV and cerebral blood flow (CBF) during propofol anesthesia in eight New Zealand white rabbits. We also investigated the effects of propofol over time on CBV and CBF during normocapnia (control group). At normocapnia, the mean (+/- SD) CBV and CBF values were 2.41 +/- 0.68 mL/100 g and 56 +/- 28 mL/100 g/min, respectively,. When PaCO(2) was reduced from 41 to 27 mm Hg, no significant change in either CBV or CBF was observed (P > 0.10). However, increasing PaCO(2) from 41 to 58 mm Hg resulted in a 30% increase in CBV (3.08 +/- 0.86 mL/100 g, P < 0.05) and a 91% increase in CBF (97 +/- 39 mL/100 g/min, P < 0.01). In the control group, there were no significant changes in CBV and CBF (P > 0.10) during 2 h of propofol anesthesia. These results indicate that, during propofol anesthesia, cerebrovascular reactivity of blood flow and blood volume is maintained during hypercapnia but is markedly diminished during hypocapnia. During propofol anesthesia in rabbits with normal brains, a reduction in the arterial carbon dioxide level may not always be accompanied by a reduction in brain blood flow and blood volume.

Blood Flow of the Middle Cerebral Artery With Sleep-Disordered Breathing: Correlation With Obstructive Hypopneas

To the Editor: Netzer et al1 recently reported that obstructive sleep hypopnea and apnea are associated with reductions in middle cerebral artery (MCA) blood flow compared with central sleep apnea. This study may explain the increased incidence of ischemic stroke in obstructive sleep disorders,2 3 4 although it is important to remember that other mechanisms independent of cerebral hemodynamics have also been proposed.5 6 Transcranial Doppler blood flow measurements of the MCA are assumed to reflect total brain flow, but it should be noted that this technique does not evaluate regional cerebral blood flow (CBF). Several lines of evidence suggest that localized disturbances in CBF may be important in patients who sustain cerebrovascular events in association with sleep disorders. Non-REM sleep in normal subjects is associated with a global reduction in brain blood flow (measured by stable xenon computed tomography) and global glucose hypometabolism (measured by positron emission tomography). Against this global fall in CBF are important regional variations, with some brain regions (frontal cortex, basal ganglia, thalamus, pons, cerebellum) affected to a greater degree while others (temporal cortex) are relatively unaffected.7 8 During REM sleep there is increased CBF to the associated visual area, presumably reflecting the activation involved in processing visual dream experiences, with a reduction in inferior frontal cortical flow.9 Preliminary observations in sleep apnea syndromes indicate the presence of focal cortical perfusion abnormalities in the awake or apneic state that are …

Induction of Eclampticlike Changes by Stimulation of the Celiac Ganglion in Rats

Objective: To examine the relation between the stimulation of the abdominal sympathetic nervous system and vasospasm of the brain in eclamptic seizures, we analyzed brain blood flow after stimulation of the celiac ganglion by lipopolysaccharide (LPS, 5, 50, or 500 mg/mL) or normal saline before and after denovation of sympathetic trunk in pregnant and nonpregnant rats.Methods: The brain blood flow was measured after stimulation of the celiac ganglion with 50 μL (5 mg/mL) LPS in group 1,50 μL (50 mg/mL) LPS in group II, 50 μL saline in group III, and 50 μL (500 mg/mL) LPS (after denovation of the sympathetic trunk) in group IV. A sham control experiment was also done by stimulation of the abdominal peritoneum with 50 μL (500 mg/mL) LPS in group V. Changes in water content and histological findings in the brain were also studied in this protocol.Results: A significant reduction in brain blood flow was observed in pregnant rats in groups I and II on stimulation of the celiac ganglion with LPS (p<0.0001, p<0.001) compared with before stimulation. Celiac ganglion stimulation with saline (group III) and LPS (group IV, after denovation of the sympathetic trunk) did not affect brain blood flow. Stimulation of the abdominal peritoneum with LPS (group V) could not induce any changes in brain blood flow. Repeated seizures occurred in 60% of pregnant rats and a remarkable increase in water content was observed after LPS stimulation of the celiac ganglion in groups I and II (p<0.0001, p<0.001). Histologically, we found that stimulation of the celiac ganglion with LPS caused widening of perivascular spaces with compression of the vessels leading to ischemic changes in brain tissues. There were no such findings observed in other groups. However, a lesser extent effect was noticed in nonpregnant than seen in pregnant rats.Conclusion: Stimulation of the abdominal sympathetic ganglions could induce vasoconstriction of the brain vessels, thus decreasing brain blood flow, which results in eclampsialike changes in rats.

Cerebral blood flow changes in pseudomigraine with pleocytosis analyzed by single photon emission computed tomography. A spreading depression mechanism?

Pseudomigraine with pleocytosis is a benign and autolimited syndrome. The etiology has been related to viral infection, but its pathophysiology is not yet well identified. To investigate this point, and to see if there were changes in cerebral blood flow (as in migraine), we performed single photon emission computed tomography (SPECT) studies in four patients who fulfilled the diagnostic criteria for this syndrome. This was done during the acute phase and we repeated SPECT after resolution of the syndrome in two of them. We found a reduction in brain blood flow on the side of origin of the neurological deficits during the acute phase. This normalized after recovery of the syndrome. The finding suggests that the neurological deficits in this syndrome could be produced by a spreading depression-like mechanism similar to that proposed for migraine with aura.

Demonstration of Dose-Dependent Global and Regional Cocaine-Induced Reductions in Brain Blood Flow Using a Novel Approach to Quantitative Single Photon Emission Computerized Tomography

Ischemic stroke is a common cause of morbidity and mortality in cocaine addicts. Because the previous semiquantitative single photon emission computerized tomography (SPECT) method for measuring brain blood flow does not quantify blood flow, the magnitude and specificity of cocaine’s effects during drug taking has not been well established. Here, using a novel quantitative approach to SPECT, we established that intravenous cocaine administration to nine recently abstinent cocaine-dependent subjects was associated with significant decreases in global and regional brain blood flow to dopamine-rich areas such as the prefrontal, frontal, temporal, and subcortical gray matter. Establishing the utility of this relatively new quantitative SPECT technique provides an important tool for the management of vascular disorders of the brain. Additionally, identifying the site-specific effects of cocaine provides targets for the development of putative therapeutic medications to attenuate or minimize ischemic stroke in cocaine addicts.

Effect of angiotensin II and peptide YY on cerebral and circumventricular blood flow

Angiotensin II and peptide YY (PYY) are putative neuro/humoral agents acting at several circumventricular regions. These peptides also constrict cerebral vessels. We examined the effect of acute intravenous infusion of saline, angiotensin II and peptide YY on local cerebral blood flow ( 14C-iodoantipyrine autoradiography) in the circumventricular and non-circumventricular brain regions of 17 conscious rats. No reductions in brain blood flow (28 regions) were observed although angiotensin II and PYY infusion elevated arterial blood pressure 15–25% without influencing heart rate, suggesting an increase in peripheral resistance. However, local blood flow was dependent on the peptide infused. During PYY infusion, blood flow was rather constant in the 20 non-circumventricular regions examined whereas an increase in blood flow and a slight decrease in cerebrovascular resistance occurred in the circumventricular regions. The area postrema exhibited the most pronounced changes—an elevation in blood flow of 44±11% and a reduction in resistance of 20±5% in comparison to that in control animals. During angiotensin II infusion, local cerebral blood flow was similar to that in controls and local cerebrovascular resistance was elevated. Thus, the local cerebral circulatory response to peptide administration was dependent on the location of the region examined (circumventricular or non-circumventricular) and on the vasoactive peptide infused.

Prolonged hypercarbia in the awake newborn piglet: effect on brain blood flow and cardiac output.

In adults, exposure to prolonged hypercarbia results in a normalization of the extravascular brain pH associated with a reduction in brain blood flow (BBF). Following prolonged hypercarbia, sudden normalization of the arterial PCO2 also produces a change in the extravascular brain pH to an alkaline state, resulting in a marked decrease in BBF. We examined these physiologic phenomena in newborn subjects by exposing seven awake, spontaneously breathing newborn piglets to 4 h of sustained hypercarbia (PaCO2: 60-70 mm Hg) followed by a 45-min normocarbic period. Total and regional BBF, cardiac output (radionuclide-labeled microsphere method), arterial blood pressure, plasma catecholamine and lactate concentrations, blood gases, oxygen contents, and hematocrits were measured during a baseline period, at 1/2, 2, and 4 h of sustained hypercarbia and 1/4 and 3/4 h following an abrupt onset of normocarbia. The initial 2.5-fold increase in total BBF during hypercarbia persisted for 2 h and at 4 h decreased significantly below the level of the 30-min hypercarbic measurement, although the values still remained 2-fold above the baseline values. Brain tissue pH was reduced at the onset of hypercarbia, remaining unchanged throughout the hypercarbic period. Both total BBF and brain tissue pH returned to baseline values following the return to normocarbia. Changes in regional BBF were similar to that of total BBF with the exception of the boundary zone (periventricular area in the frontoparietal region of the cerebrum, adjacent to the caudate nucleus) and the parietal area (site of the brain tissue pH electrode), where a significant decrease from the peak hyperemia was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)