Justification of Increasing the Blood Flow Velocity in the Arteries of the Thyroid Gland in Autoimmune Thyroiditis as a Reflection of Endothelial Changes Due to Inflammatory Status

2018 ◽  
Vol 15 (1) ◽  
pp. 61-65
Author(s):  
Nataliia I. Chekalina ◽  
Yurii H. Burmak ◽  
Yeuhen Ye. Petrov ◽  
Zinaiida O. Borysova ◽  
Tetiana A. Trybrat ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Flow Velocity ◽  
Autoimmune Thyroiditis ◽  
Blood Flow Velocity ◽  
Carotid Arteries ◽  
Resistance Index ◽  
Systemic Blood Pressure ◽  
Healthy Individuals ◽  
Systemic Blood

Objective: The aim of the research was to determine the dependence of the blood flow velocity in the thyroid arteries in patients with Autoimmune Thyroiditis (AIT) on the presence of atherosclerotic carotid disease and the level of systemic blood pressure. Methods: The research involved 20 patients with AIT in euthyroid state, 30 patients AIT in euthyroid state with stable Coronary Heart Disease (CHD), 30 patients with stable CHD and 30 healthy individuals. Participants of the research were examined using ultrasound of carotid arteries and inferior thyroid arteries. Parameters of blood flow velocity were compared with the level of systemic blood pressure. Results: In AIT peak systolic velocity and resistance index in the inferior thyroid arteries were significantly higher than in healthy individuals and patients with CHD (p<0.05). In patients with CHD velocity parameters in carotid arteries were high, unlike in the healthy individuals and patients with AIT (p<0.05). In patients with AIT without CHD the atherosclerotic changes of carotid arteries were not found. Increased systemic blood pressure was noticed in all patients with CHD without significant differences between groups. Conclusion: The value of peak systolic velocity and resistance index of inferior thyroid arteries in autoimmune thyroiditis are noticed even with euthyroidism and do not depend on systemic blood pressure and atherosclerosis of carotid arteries. Increasing the thyroid arterial blood flow velocity parameters should be considered as sign of an active inflammatory period AIT, where advanced fibrosis is not present.

Systemic Blood Pressure and Cerebral Blood Flow Velocity During Carotid Surgery

1999 ◽  
Vol 47 (06) ◽  
pp. 381-385 ◽  
Author(s):  
G. Grubhofer ◽  
A. Lassnigg ◽  
T. Pernerstorfer ◽  
O. Ipsiroglu ◽  
M. Czerny ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Systemic Blood Pressure ◽  
Carotid Surgery ◽  
Systemic Blood

Complexity of middle cerebral artery blood flow velocity: effects of tilt and autonomic failure

1997 ◽  
Vol 273 (5) ◽  
pp. H2209-H2216 ◽  
Author(s):  
A. P. Blaber ◽  
R. L. Bondar ◽  
F. Stein ◽  
P. T. Dunphy ◽  
P. Moradshahi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Autonomic Failure ◽  
Systemic Blood Pressure ◽  
Arterial Blood ◽  
Different Response

We examined spectral fractal characteristics of middle cerebral artery (MCA) mean blood flow velocity (MFV) and mean arterial blood pressure adjusted to the level of the brain (MAPbrain) during graded tilt (5 min supine, −10°, 10°, 30°, 60°, −10°, supine) in eight autonomic failure patients and age- and sex-matched controls. From supine to 60°, patients had a larger drop in MAPbrain (62 ± 4.7 vs. 23 ± 4.5 mmHg, P < 0.001; means ± SE) and MFV (16.4 ± 3.8 vs. 7.0 ± 2.5 cm/s, P < 0.001) than in controls. From supine to 60°, there was a trend toward a decrease in the slope of the fractal component (β) of MFV (MFV-β) in both the patients and the controls, but only the patients had a significant decrease in MFV-β (supine: patient = 2.21 ± 0.18, control = 1.99 ± 0.60; 60°: patient = 1.46 ± 0.24, control = 1.62 ± 0.19). The β value of MAPbrain(MAPbrain-β; 2.19 ± 0.05) was not significantly different between patients and controls and did not change with tilt. High and low degrees of regulatory complexity are indicated by values of β close to 1.0 and 2.0, respectively. The increase in fractal complexity of cerebral MFV in the patients with tilt suggests an increase in the degree of autoregulation in the patients. This may be related to the drop in MAPbrain. The different response of MFV-β compared with that of MAPbrain-β also indicates that MFV-β is related to the regulation of cerebral vascular resistance and not systemic blood pressure.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

Diurnal variation in time to presyncope and associated circulatory changes during a controlled orthostatic challenge

2010 ◽  
Vol 299 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
N. C. S. Lewis ◽  
G. Atkinson ◽  
S. J. E. Lucas ◽  
E. J. M. Grant ◽  
H. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diurnal Variation ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Orthostatic Challenge ◽  
Arterial Blood ◽  
Neurally Mediated Syncope

Epidemiological data indicate that the risk of neurally mediated syncope is substantially higher in the morning. Syncope is precipitated by cerebral hypoperfusion, yet no chronobiological experiment has been undertaken to examine whether the major circulatory factors, which influence perfusion, show diurnal variation during a controlled orthostatic challenge. Therefore, we examined the diurnal variation in orthostatic tolerance and circulatory function measured at baseline and at presyncope. In a repeated-measures experiment, conducted at 0600 and 1600, 17 normotensive volunteers, aged 26 ± 4 yr (mean ± SD), rested supine at baseline and then underwent a 60° head-up tilt with 5-min incremental stages of lower body negative pressure until standardized symptoms of presyncope were apparent. Pretest hydration status was similar at both times of day. Continuous beat-to-beat measurements of cerebral blood flow velocity, blood pressure, heart rate, stroke volume, cardiac output, and end-tidal Pco2 were obtained. At baseline, mean cerebral blood flow velocity was 9 ± 2 cm/s (15%) lower in the morning than the afternoon ( P < 0.0001). The mean time to presyncope was shorter in the morning than in the afternoon (27.2 ± 10.5 min vs. 33.1 ± 7.9 min; 95% CI: 0.4 to 11.4 min, P = 0.01). All measurements made at presyncope did not show diurnal variation ( P > 0.05), but the changes over time (from baseline to presyncope time) in arterial blood pressure, estimated peripheral vascular resistance, and α-index baroreflex sensitivity were greater during the morning tests ( P < 0.05). These data indicate that tolerance to an incremental orthostatic challenge is markedly reduced in the morning due to diurnal variations in the time-based decline in blood pressure and the initial cerebral blood flow velocity “reserve” rather than the circulatory status at eventual presyncope. Such information may be used to help identify individuals who are particularly prone to orthostatic intolerance in the morning.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

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.

Suctioning and Cerebral Blood Flow

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Arterial Blood Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Base Line ◽  
Arterial Blood

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.

Sign in / Sign up

Export Citation Format

Share Document