scholarly journals Selective neuronal damage and blood pressure in atherosclerotic major cerebral artery disease

2019 ◽  
Vol 90 (9) ◽  
pp. 975-980 ◽  
Author(s):  
Hiroshi Yamauchi ◽  
Shinya Kagawa ◽  
Masaaki Takahashi ◽  
Kuninori Kusano ◽  
Chio Okuyama

ObjectiveIn patients with atherosclerotic major cerebral artery disease, low blood pressure might impair cerebral perfusion, thereby exacerbate the risk of selective neuronal damage. The purpose of this retrospective study was to determine whether low blood pressure at follow-up is associated with increased selective neuronal damage.MethodsWe retrospectively analysed data from 76 medically treated patients with atherosclerotic internal carotid artery or middle cerebral artery disease with no ischaemic episodes on a follow-up of 6 months or more. All patients had measurements of the distribution of central benzodiazepine receptors twice using positron emission tomography and 11C-flumazenil. Using three-dimensional stereotactic surface projections, we quantified abnormal decreases in the benzodiazepine receptors of the cerebral cortex within the middle cerebral artery distribution and correlated these changes in the benzodiazepine receptors index with blood pressure values at follow-up examinations.ResultsThe changes in the benzodiazepine receptor index during follow-up (mean 27±21 months) were negatively correlated with systolic blood pressure at follow-up. The relationship between changes in benzodiazepine receptor index and systolic blood pressure was different among patients with and without decreased cerebral blood flow at baseline (interaction, p<0.005). Larger increases in benzodiazepine receptor index (neuronal damage) were observed at lower systolic blood pressure levels in patients with decreased cerebral blood flow than in patients without such decreases.ConclusionIn patients without ischaemic stroke episodes at follow-up but with decreased cerebral blood flow due to arterial disease, low systolic blood pressure at follow-up may be associated with increased selective neuronal damage.

2017 ◽  
Vol 39 (2) ◽  
pp. 324-331 ◽  
Author(s):  
Hiroshi Yamauchi ◽  
Shinya Kagawa ◽  
Masaaki Takahashi ◽  
Tatsuya Higashi

In patients with major cerebral artery disease, lower blood pressure might reduce blood flow in the collateral pathways, thereby impairing the growth of cerebral collaterals, inhibiting hemodynamic improvement. We evaluated the hemodynamic status twice using positron emission tomography and 15O-gas, over time, in 89 medically treated patients with atherosclerotic internal carotid artery or middle cerebral artery disease that had no ischemic episodes during follow-up (mean, 28 ± 23 months). Changes in the mean hemispheric values of hemodynamic parameters in the territory of the diseased artery at follow-up were correlated with the mean blood pressure values at the baseline and follow-up examinations. There was a positive linear relationship between the degree of hemodynamic improvement and systolic blood pressure. Patients with low systolic blood pressure (<130 mmHg) ( n = 18) showed hemodynamic deterioration as indicated by significant decreases in cerebral blood flow, cerebral blood flow/cerebral blood volume ratio, and increases in oxygen extraction fraction during follow-up. In contrast, there were no significant changes in patients without low systolic blood pressure. In patients with atherosclerotic internal carotid artery or middle cerebral artery disease and no ischemic episodes of stroke during follow-up, lower systolic blood pressure was associated with lesser hemodynamic improvement.


1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


Author(s):  
Juan F. Sánchez Muñoz-Torrero ◽  
Guillermo Escudero-Sánchez ◽  
Julián F. Calderón-García ◽  
Sergio Rico-Martín ◽  
Nicolás Roberto Robles ◽  
...  

Objectives: The most appropriate targets for systolic blood pressure (SBP) levels to reduce cardiovascular morbidity and mortality in patients with symptomatic artery disease remain controversial. We compared the rate of subsequent ischemic events or death according to mean SBP levels during follow-up. Design: Prospective cohort study. FRENA is an ongoing registry of stable outpatients with symptomatic coronary (CAD), cerebrovascular (CVD) or peripheral artery disease (PAD). Setting: 24 Spanish hospitals. Participants: 4789 stable outpatients with vascular disease. Results: As of June 2017, 4789 patients had been enrolled in different Spanish centres. Of these, 1722 (36%) had CAD, 1383 (29%) CVD and 1684 (35%) PAD. Over a mean follow-up of 18 months, 136 patients suffered subsequent myocardial infarction, 125 had ischemic stroke, 74 underwent limb amputation, and 260 died. On multivariable analysis, CVD patients with mean SBP levels 130–140 mm Hg had a lower risk of mortality than those with levels <130 mm Hg (hazard ratio (HR): 0.39; 95% CI: 0.20–0.77), as did those with levels >140 mm Hg (HR: 0.46; 95% CI: 0.26–0.84). PAD patients with mean SBP levels >140 mm Hg had a lower risk for subsequent ischemic events (HR: 0.57; 95% CI: 0.39–0.83) and those with levels 130–140 mm Hg (HR: 0.47; 95% CI: 0.29–0.78) or >140 mm Hg (HR: 0.32; 95% CI: 0.21–0.50) had a lower risk of mortality. We found no differences in patients with CAD. Conclusions: In this real-world cohort of symptomatic arterial disease patients, most of whom are not eligible for clinical trials, the risk of subsequent events and death varies according to the levels of SBP and the location of previous events. Especially among patients with large artery atherosclerosis, PAD or CVD, SBP <130 mm Hg may result in increased mortality. Due to potential factors in this issue, Prospective, well designed studies are warranted to confirm these observational data.


Author(s):  
Akikazu Nakamura ◽  
Akitsugu Kawashima ◽  
Hugo Andrade-Barazarte ◽  
Takayuki Funatsu ◽  
Juha Hernesniemi ◽  
...  

OBJECTIVEPatients with pediatric moyamoya disease (PMMD) showing recurrent symptoms or decreased cerebral blood flow after initial revascularization therapy may require additional revascularization to improve their clinical condition. The authors evaluated the clinical and hemodynamic benefits of an occipital artery (OA)–middle cerebral artery (MCA) bypass for patients with PMMD who have undergone an initial revascularization procedure.METHODSThe authors retrospectively identified 9 patients with PMMD who had undergone OA-MCA bypass between March 2013 and December 2017, and who had received a previous superficial temporal artery–MCA bypass. The following clinical data were collected: initial revascularization procedure, symptoms (presence or recurrence), pre- and postoperative cerebral blood flow and cerebrovascular reactivity (CVR) changes, posterior cerebral artery (PCA) stenosis, PCA-related and nonrelated symptoms, and latest follow-up.RESULTSPreoperatively, all patients (n = 9) suffered non–PCA-related recurrent symptoms, and 4 had PCA-related symptoms. At 1-year follow-up, all patients with PCA-related symptoms showed complete recovery. Additionally, 8 (89%) patients with non-PCA symptoms experienced improvement. Only 1 (11%) patient showed no improvement after the surgical procedure. The mean pre- and postoperative CVR values of the MCA territory were 14.8% and 31.3%, respectively, whereas the respective mean CVR values of the PCA territory were 22.8% and 40.0%.CONCLUSIONSThe OA-MCA bypass is an effective rescue therapy to improve the clinical condition and hemodynamic changes caused by PMMD in patients who experience recurrent symptoms after initial revascularization.


2014 ◽  
Vol 116 (12) ◽  
pp. 1614-1622 ◽  
Author(s):  
J. D. Smirl ◽  
Y. C. Tzeng ◽  
B. J. Monteleone ◽  
P. N. Ainslie

We examined the hypothesis that changes in the cerebrovascular resistance index (CVRi), independent of blood pressure (BP), will influence the dynamic relationship between BP and cerebral blood flow in humans. We altered CVRi with (via controlled hyperventilation) and without [via indomethacin (INDO, 1.2 mg/kg)] changes in PaCO2. Sixteen subjects (12 men, 27 ± 7 yr) were tested on two occasions (INDO and hypocapnia) separated by >48 h. Each test incorporated seated rest (5 min), followed by squat-stand maneuvers to increase BP variability and improve assessment of the pressure-flow dynamics using linear transfer function analysis (TFA). Beat-to-beat BP, middle cerebral artery velocity (MCAv), posterior cerebral artery velocity (PCAv), and end-tidal Pco2 were monitored. Dynamic pressure-flow relations were quantified using TFA between BP and MCAv/PCAv in the very low and low frequencies through the driven squat-stand maneuvers at 0.05 and 0.10 Hz. MCAv and PCAv reductions by INDO and hypocapnia were well matched, and CVRi was comparably elevated ( P < 0.001). During the squat-stand maneuvers (0.05 and 0.10 Hz), the point estimates of absolute gain were universally reduced, and phase was increased under both conditions. In addition to an absence of regional differences, our findings indicate that alterations in CVRi independent of PaCO2 can alter cerebral pressure-flow dynamics. These findings are consistent with the concept of CVRi being a key factor that should be considered in the correct interpretation of cerebral pressure-flow dynamics as indexed using TFA metrics.


1993 ◽  
Vol 13 (2) ◽  
pp. 276-284 ◽  
Author(s):  
I. Mhairi Macrae ◽  
Michael J. Robinson ◽  
David I. Graham ◽  
John L. Reid ◽  
James McCulloch

The capacity of endothelin-1 to induce severe reductions in cerebral blood flow and ischaemic neuronal damage was assessed in anaesthetised rats. Endothelin-1 (25 μl of 10−7–10−4 M) was applied to the adventitial surface of an exposed middle cerebral artery and striatal blood flow assessed by the hydrogen clearance technique. Endothelin-1 induced severe dose-dependent reductions in cerebral blood flow (e.g., minimum CBF at 10−5 M of 9 ± 11 ml 100 g−1 min−1 compared to 104 ± 22 ml 100 g−1 min−1 with vehicle, p < 0.05), which persisted for at least 60 min at each concentration of endothelin-1. Application of endothelin-1 to the middle cerebral artery produced dose-dependent ischaemic brain damage (e.g., volume of damage of 65 ± 34 mm3 at 10−5 M compared to 0.22 ± 0.57 mm3 for vehicle, p < 0.01). These data demonstrate that endothelin-1 is capable of reducing blood flow to pathologically low levels and provide a new model of controlled focal ischaemia followed by reperfusion.


2018 ◽  
Vol 31 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Meltem Akcaboy ◽  
Bijen Nazliel ◽  
Tayfun Goktas ◽  
Serdar Kula ◽  
Bülent Celik ◽  
...  

AbstractBackground:Obesity affects all major organ systems and leads to increased morbidity and mortality. Whole blood viscosity is an important independent regulator of cerebral blood flow. The aim of the present study was to evaluate the effect of whole blood viscosity on cerebral artery blood flow velocities using transcranial Doppler ultrasound in pediatric patients with obesity compared to healthy controls and analyze the effect of whole blood viscosity and blood pressure status to the cerebral artery blood flow velocities.Methods:Sixty patients with obesity diagnosed according to their body mass index (BMI) percentiles aged 13–18 years old were prospectively enrolled. They were grouped as hypertensive or normotensive according to their ambulatory blood pressure monitoring. Whole blood viscosity and middle cerebral artery velocities by transcranial Doppler ultrasound were studied and compared to 20 healthy same aged controls.Results:Whole blood viscosity values in hypertensive (0.0619±0.0077 poise) and normotensive (0.0607±0.0071 poise) groups were higher than controls (0.0616±0.0064 poise), with no significance. Middle cerebral artery blood flow velocities were higher in the obese hypertensive (73.9±15.0 cm/s) and obese normotensive groups (75.2±13.5 cm/s) than controls (66.4±11.5 cm/s), but with no statistical significance.Conclusions:Physiological changes in blood viscosity and changes in blood pressure did not seem to have any direct effect on cerebral blood flow velocities, the reason might be that the cerebral circulation is capable of adaptively modulating itself to changes to maintain a uniform cerebral blood flow.


2002 ◽  
Vol 22 (9) ◽  
pp. 1124-1131 ◽  
Author(s):  
Christina Kruuse ◽  
Lars Lykke Thomsen ◽  
Torsten Bjørn Jacobsen ◽  
Jes Olesen

Cyclic nucleotides are important hemodynamic regulators in many tissues. Glyceryl trinitrate markedly dilates large cerebral arteries and increases cGMP. Here, the authors study the effect of sildenafil, a selective inhibitor of cGMP-hydrolyzing phosphodiesterase 5 on cerebral hemodynamics and headache induction. Ten healthy subjects were included in a double-blind, placebo-controlled crossover study where placebo or sildenafil 100 mg (highest therapeutic dose) were administered on two separate days. Blood velocity in the middle cerebral artery (Vmca) was recorded by transcranial Doppler, and regional cerebral blood flow in the perfusion area of the middle cerebral artery (rCBFmca) was measured using single photon emission computed tomography and 133xenon inhalation. Radial and temporal artery diameters were studied using high-frequency ultrasound. Blood pressure and heart rate were recorded repeatedly. Headache responses and tenderness of pericranial muscles were scored verbally. Sildenafil caused no significant changes in rCBFmca, Vmca, or in temporal or radial artery diameter, but heart rate increased and diastolic blood pressure decreased significantly compared to placebo. Despite the lack of cerebral arterial dilatation, sildenafil caused significantly more headache than placebo. The present results show that sildenafil 100 mg does not dilate cerebral or extracerebral arteries but nevertheless causes headache, which may be attributed to nonvascular mechanisms.


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