scholarly journals Pressure Changes Within the Sac of Human Cerebral Aneurysms in Response to Artificially Induced Transient Increases in Systemic Blood Pressure

Hypertension ◽  
2015 ◽  
Vol 66 (2) ◽  
pp. 324-331 ◽  
Author(s):  
David M. Hasan ◽  
Bradley J. Hindman ◽  
Michael M. Todd
Keyword(s):  
Blood Pressure ◽  
Cerebral Aneurysms ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pressure Changes

scholarly journals Middle cerebral artery pressure changes following Pipeline flow diversion

2018 ◽  
Vol 24 (3) ◽  
pp. 297-302 ◽  
Author(s):  
Denise Brunozzi ◽  
Sophia F Shakur ◽  
Fady T Charbel ◽  
Ali Alaraj
Keyword(s):  
Blood Pressure ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Aneurysms ◽  
Systemic Blood Pressure ◽  
Mean Blood Pressure ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Before And After ◽  
Pressure Changes

Objective Pipeline embolization devices (PED) are commonly used for endovascular treatment of cerebral aneurysms but changes in intracranial hemodynamics after PED deployment are poorly understood. Here, we assess middle cerebral artery (MCA) and systemic blood pressure before and after PED treatment. Methods Records of patients with cerebral aneurysms proximal to the internal carotid artery terminus treated with PED at our institution between 2015 and 2017 were retrospectively reviewed. Patients were included if ipsilateral MCA pressure measurements were available. Ipsilateral MCA pressure was transduced via the microcatheter before and after PED deployment. Systemic arterial blood pressure was also simultaneously recorded. MCA, systemic blood pressure, and ratios of MCA to systemic blood pressure values were compared before and after treatment among the study cohort using the two-sample paired Student t test. Results Fourteen patients were included. Mean age was 54 years. Among the entire cohort, the ratio of MCA to systemic systolic and mean blood pressure were significantly higher after treatment (respectively 0.76 vs. 0.69, p = 0.01, and 0.94 vs. 0.89, p = 0.03), and the ratio of MCA to systemic diastolic pressures showed an increasing trend (1.08 vs. 1.03, p = 0.09). The percentage of ratio increase was independent of aneurysm size ( r = –0.24, p = 0.42 for systolic ratio; r = –0.09, p = 0.74 for diastolic ratio; r = –0.09; p = 0.76 for mean ratio, respectively). Conclusions Following PED deployment, the ratio of ipsilateral MCA to systemic systolic and mean blood pressure increased. These pressure changes should be further evaluated in a larger sample size.

PS 02-65 ASSOCIATION BETWEEN POSTPRANDIAL AND SLEEPING SYSTEMIC BLOOD PRESSURE CHANGES IN THE NON-DIABETIC ELDERLY

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e121
Author(s):  
Fernando Garcia ◽  
Beatriz Fidale ◽  
Sebastião Ferreira-Filho
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pressure Changes

Method for measuring brain tissue pressure

1975 ◽  
Vol 43 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Robert M. Clark ◽  
Norman F. Capra ◽  
James H. Halsey
Keyword(s):  
Blood Pressure ◽  
Brain Tissue ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Tissue Pressure ◽  
Content Type ◽  
Pressure Changes ◽  
Local Brain

✓ The authors report a method for measuring total local brain tissue pressure (BTP) using a miniature catheter transducer stereotaxically introduced into the white matter of the cat's cerebrum. Quantitative rapid phasic pressure changes were satisfactorily demonstrated. Due to some drift of baseline of the transducers and inability to perform in vivo calibration, reliable long-term quantitative pressure measurements sometimes could not be studied. The BTP from each cerebral hemisphere and the cisternal pressure (CP) were monitored during alterations of pCO2 and systemic blood pressure, and distilled H2O injection prior to and after right middle cerebral artery (MCA) ligation. The catheter transducers functioned well on chronic implantation for up to 6 weeks. Compared to the chronically implanted catheters, acutely implanted catheters responded identically except for drift. The response of intracranial pressure and CP to MCA occlusion, alterations in pCO2, and systemic blood pressure were similar. No BTP gradients appeared in response to MCA ligation, hypercapnia, hypertension, or progressive swelling of the resulting infarction.

Methylprednisolone on circulating eicosanoids and vasomotor tone after endotoxin

1986 ◽  
Vol 61 (1) ◽  
pp. 185-191 ◽  
Author(s):  
C. A. Hales ◽  
R. D. Brandstetter ◽  
C. F. Neely ◽  
M. B. Peterson ◽  
D. Kong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Physiological Effect ◽  
High Dose ◽  
Systemic Blood ◽  
Eicosanoid Production ◽  
Circulating Levels

Acute pulmonary and systemic vasomotor changes induced by endotoxin in dogs have been related, at least in part, to the production of eicosanoids such as the vasoconstrictor thromboxane and the vasodilator prostacyclin. Steroids in high doses, in vitro, inhibit activation of phospholipase A2 and prevent fatty acid release from cell membranes to enter the arachidonic acid cascade. We, therefore, administered methylprednisolone (40 mg/kg) to dogs to see if eicosanoid production and the ensuing vasomotor changes could be prevented after administration of 150 micrograms/kg of endotoxin. The stable metabolites of thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay. Methylprednisolone by itself did not alter circulating eicosanoids but when given 2.5 h before endotoxin not only failed to inhibit endotoxin-induced eicosanoid production but actually resulted in higher circulating levels of 6-keto-PGF1 alpha (P less than 0.05) compared with animals receiving endotoxin alone. Indomethacin prevented the steroid-enhanced concentrations of 6-keto-PGF1 alpha after endotoxin and prevented the greater fall (P less than 0.05) in systemic blood pressure and systemic vascular resistance with steroid plus endotoxin than occurred with endotoxin alone. Administration of methylprednisolone immediately before endotoxin resulted in enhanced levels (P less than 0.05) of both TxB2 and 6-keto-PGF1 alpha but with a fall in systemic blood pressure and vascular resistance similar to the animals pretreated by 2.5 h. In contrast to the early steroid group in which all of the hypotensive effect was due to eicosanoids, in the latter group steroids had an additional nonspecific effect. Thus, in vivo, high-dose steroids did not prevent endotoxin-induced increases in eicosanoids but actually increased circulating levels of TxB2 and 6-keto-PGF1 alpha with a physiological effect favoring vasodilation.

scholarly journals Pressure constrained mitral annular dysfunction determines severity of regurgitation in Barlow's disease – a 3D echocardiographic study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K.A Dumont ◽  
R Persson ◽  
J.P Kvitting ◽  
R Lundblad ◽  
R Haaverstad ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Aortic Valve ◽  
Mitral Regurgitation ◽  
Surface Area ◽  
Systemic Blood Pressure ◽  
Funding Source ◽  
Healthy Controls ◽  
Systemic Blood ◽  
Barlow’S Disease ◽  
3D Echo

Abstract Background Barlow's disease provides both diagnostic and therapeutic challenges. The impact of systemic blood-pressure on severity of regurgitation is still unclear. Purpose We hypothesized that mitral annulus behaves passively with enlargement during ventricular systole, and secondly, we tested the hypothesis that severity of regurgitation correlates to systemic blood-pressure (BP) of the patient. Methods Ten patients with Barlow's disease were compared with 10 healthy controls. Brachial blood-pressure was measured according to guidelines. Transthoracic 3D echo was obtained from an apical view (38.6±8.2 frames per second). Data was analyzed using a holographic display. We measured commissure width (CW), septallateral length (SL) and mitral annular surface area throughout the cardiac cycle. Aortic flow ejection time was derived from continuous Doppler across the aortic valve. Timing of aortic valve closure was visually assessed by 3D echo. Onset and end of mitral regurgitation was derived from continuous wave Doppler of transmitral flow. Results Systolic BP in controls and patients were 122±5 and 133±12 mmHg, respectively (p<0.05). Enddiastolic volume was 87±7 ml/m2 (controls) and 100±14 ml/m2 (Barlow), p<0.02. Left ventricular EF in controls and patients were 59±5 and 62±5%, respectively, p=NS. Barlow patients had moderate or severe late systolic regurgitation with mean regurgitation volume of 51±18 ml. Annular surface area, CW and SL behaved passively with enlargement during ventricular systole (Figure 1). Peak systolic surface area, CW and SL in healthy controls and Barlow patients were 8.7±0.5 vs 20.7±3.2 cm2 (p<0.001), 30.1±1.5 vs 49.5±4.9 mm (p<0.001) and 30.9±1.5 vs 44.9±3.3 mm (p<0.001). Peak annular surface area and regurgitation volume in patients showed a positive correlation with systolic BP (y = 0.156x − 0.077, r=0.60 and y = 1.136x − 99.7, r=0.80, respectively). Conclusions We have demonstrated pressure constrained mitral annular dysfunction in Barlow's disease, indicating that systemic blood pressure may modify the severity of regurgitation. The study provides novel insights into mechanisms of mitral regurgitation and potential therapeutic actions in the future. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Grieg Foundation

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