Differences in the Behavior of Afferent Vessels in Autoregulation to Increased Intracranial Pressure and to Diminished Systemic Blood Pressure

1976 ◽  
pp. 45-49 ◽  
Author(s):  
L. Symon ◽  
N. M. Branston ◽  
A. J. Strong
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Increased Intracranial Pressure ◽  
Systemic Blood

Influences of Phasic Changes in Systemic Blood Pressure on Intracranial Pressure

1978 ◽  
Vol 17 (4) ◽  
pp. 216-225 ◽  
Author(s):  
V.E. Pettorossi ◽  
C. Di Rocco ◽  
M. Caldarelli ◽  
R. Mancinelli ◽  
F. Velardi
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Systemic Blood

Site and mechanism for compression of the venous system during experimental intracranial hypertension

1974 ◽  
Vol 41 (4) ◽  
pp. 427-434 ◽  
Author(s):  
Yoku Nakagawa ◽  
Mitsuo Tsuru ◽  
Kenzoh Yada
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Pressure Gradient ◽  
Superior Sagittal Sinus ◽  
Venous Pressure ◽  
Systemic Blood Pressure ◽  
Intraluminal Pressure ◽  
Systemic Blood ◽  
Sagittal Sinus ◽  
Bridging Vein

✓ The pressure gradient of the venous pathway between the cortical vein and superior sagittal sinus was measured in adult mongrel dogs by recording the pressures of the bridging vein, lateral lacuna (proximal portion), and superior sagittal sinus, together with the systemic blood pressure while gradually increasing the intracranial pressure up to the level of mean systemic blood pressure. The pressure gradient between the lateral lacuna and the superior sagittal sinus was also measured under increased intracranial pressure. Pressures of the bridging vein and lateral lacuna were constantly 50 to 250 mm H2O higher than the intracranial pressure, regardless of the level of intracranial pressure. An abrupt drop in the intraluminal pressure was observed at a point 1 to 2 mm proximal to the junction of the lateral lacuna and the superior sagittal sinus, regardless of the level of intracranial pressure. It is concluded that gradual stenosis of the parasagittal venous pathways took place 1 to 2 mm proximal to the junction between the lacuna and the superior sagittal sinus, and thus cortical venous pressure was maintained 50 to 250 mm H2O higher than intracranial pressure. The authors believe that an “intracranial venous pressure regulation mechanism” exists at the junction of the lateral lacuna and the superior sagittal sinus.

scholarly journals Current understanding of the effects of inspiratory resistance on the interactions between systemic blood pressure, cerebral perfusion, intracranial pressure, and cerebrospinal fluid dynamics

2019 ◽  
Vol 127 (5) ◽  
pp. 1206-1214 ◽  
Author(s):  
Pawel J. Winklewski ◽  
Jacek Wolf ◽  
Marcin Gruszecki ◽  
Magdalena Wszedybyl-Winklewska ◽  
Krzysztof Narkiewicz
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Clinical Medicine ◽  
Respiratory Muscles ◽  
Intrathoracic Pressure ◽  
Brain Perfusion ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Obstructive Sleep ◽  
Inspiratory Resistance

Negative intrathoracic pressure (nITP) is generated by the respiratory muscles during inspiration to overcome inspiratory resistance, thus enabling lung ventilation. Recently developed noninvasive techniques have made it possible to assess the effects of nITP in real time in several physiological aspects such as systemic blood pressure (BP), intracranial pressure (ICP), and cerebral blood flow (CBF). It has been shown that nITP from 0 to −20 cmH2O elevates BP and diminishes ICP, which facilitates brain perfusion. The effects of nITP from −20 to −40 cmH2O on BP, ICP, and CBF remain largely unrecognized, yet even nITP at −40 cmH2O may facilitate CBF by diminishing ICP. Importantly, nITP from −20 to −40 cmH2O has been documented in adults in commonly encountered obstructive sleep apnea, which justifies research in this area. Recent revelations about interactions between ICP and BP have opened up new fields of research in physiological regulation and the pathophysiology of common diseases, such as hypertension, brain injury, and respiratory disorders. A better understanding of these interactions may translate directly into new therapies in various fields of clinical medicine.

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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