Observations on behavior of the systemic blood pressure, pulse and spinal fluid pressure following craniocerebral injury

1936 ◽  
Vol 31 (3) ◽  
pp. 403-426 ◽  
Author(s):  
Jefferson Browder ◽  
Russel Meyers
Keyword(s):  
Blood Pressure ◽  
Pressure Pulse ◽  
Fluid Pressure ◽  
Systemic Blood Pressure ◽  
Spinal Fluid ◽  
Craniocerebral Injury ◽  
Systemic Blood

Flow in a Human Renal Artery Network With a Saccular Aneurysm

2013 ◽  
Author(s):  
Grant Armstrong ◽  
Samantha Peno ◽  
Wendy Espinoza ◽  
Eric Judd ◽  
Evan Lemley
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Fluid Pressure ◽  
Pressure Change ◽  
Systemic Blood Pressure ◽  
The Body ◽  
Saccular Aneurysm ◽  
Pressure Increase ◽  
Shear Stresses ◽  
Systemic Blood

Blood flow into the kidneys through the renal artery determines the systemic blood pressure which is regulated by the baroreceptors in the kidneys. When the baroreceptors sense decreases in local fluid pressure they stimulate the renin-angiotensin aldosterone (RAA) system, which increases systemic blood pressure by constricting blood vessels throughout the body. An aneurysm in the renal artery leads to high systemic blood pressure in most patients with this condition, but the mechanisms by which the pressure increase occurs are not well understood. One explanation of the pressure increase could be a drop in local fluid pressure near the aneurysm itself causing the RAA system to “correct” this low pressure by systemically increasing the blood pressure. The ongoing work reported here has focused on a model renal artery network with and without an aneurysm by simulating the flow with computational fluid dynamics (CFD) software. The fluid for the simulations was meant to mimic blood in terms of density and viscosity for shear stresses where Non-Newtonian flow effects should not be a concern. Flow into the renal artery was at a Reynolds number of almost 700, to mimic the flow rate in the renal artery. The simulations were performed to determine the difference in pressure between an inlet to the renal network and the exits from the network. These results indicate that the pressure difference through the network differed by less than 10 Pa comparing networks with and without saccular aneurysm. The pressure change that would trigger the RAA system is nearly 1000 Pa. So we conclude that the effect of changing the geometry with only a saccular aneurysm is not responsible for triggering the RAA system alone. Other effects that could lead to triggering of the RAA system are discussed as well as our initial construction of a system to perform validation experiments of our CFD results.

Effects of increased systemic blood pressure on the tissue fluid pressure threshold of peripheral nerve

1983 ◽  
Vol 1 (2) ◽  
pp. 172-178 ◽  
Author(s):  
Robert M. Szabo ◽  
Richard H. Gelberman ◽  
Richard V. Williamson ◽  
Alan R. Hargens
Keyword(s):  
Blood Pressure ◽  
Peripheral Nerve ◽  
Fluid Pressure ◽  
Systemic Blood Pressure ◽  
Tissue Fluid ◽  
Systemic Blood ◽  
Pressure Threshold

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

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
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