Oxygen tension gradients and heterogeneity in venous microcirculation: a phosphorescence quenching study

1997 ◽  
Vol 272 (5) ◽  
pp. H2233-H2240 ◽  
Author(s):  
R. D. Shonat ◽  
P. C. Johnson
Keyword(s):  
Blood Pressure ◽  
Oxygen Tension ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Microvascular Network ◽  
Waste Products ◽  
Phosphorescence Quenching ◽  
Oxygen Gradients ◽  
Weakly Dependent ◽  
Made In

Localized measurements of intravascular oxygen tension (PO2) at multiple locations in the microvascular network of the rat spinotrapezius muscle were used to study the spatial distribution of PO2 in venular structures. By use of a newly developed phosphorescence system to rapidly and repeatedly measure PO2, 538 individual measurements were made in 18 different networks during rest. Average intravascular PO2 was (in mmHg +/- SD) 33 +/- 9, 21 +/- 9, 26 +/- 10, and 33 +/- 8 in small arcade arterioles, postcapillary venules (PV), 3 degrees venules (3V), and arcade venules, respectively. The coefficient of variation (CV), a descriptive indicator of spatial heterogeneity, was correspondingly 0.28, 0.45, 0.37, and 0.23 for the different vessel groups. PO2 was found to increase significantly (P < 0.001) from PV to 3V, rising 0.009 +/- 0.002 mmHg/microns along the vessel. By linear regression, the slope of PO2 for the vessel difference group, PV-3V as a function of mean systemic blood pressure (BPm; in mmHg) was -0.09 +/- 0.04 (P < 0.05), indicating that the measured longitudinal oxygen gradients and CV are only weakly dependent on BPm. The results support the hypothesis that oxygen can diffuse across the walls of postcapillary vessels and suggest that the venular structures are not merely passive conduits for removing oxygen and waste products but may play an important role in regulating oxygen delivery.

EFFECTS OF HYDRAZINOPHTHALAZINE (APRESOLINE®) ON BLOOD PRESSURE AND RENAL FUNCTION IN CHILDREN WITH ACUTE NEPHRITIS

PEDIATRICS ◽  
1953 ◽  
Vol 12 (1) ◽  
pp. 29-37
Author(s):  
W. W. MCCRORY ◽  
M. RAPOPORT
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Flow ◽  
Chronic Renal Disease ◽  
Renal Plasma Flow ◽  
Systemic Blood Pressure ◽  
Urine Flow ◽  
Systemic Blood ◽  
Excretory Function ◽  
Made In

The response of hypertension occurring in acute nephritis in children to apresoline® has been studied. Significant temporary reductions in elevated blood pressure were produced by parenteral and oral apresoline® in 5 of 7 children with acute nephritis. The effect of this agent in two patients with hypertension and chronic renal disease was less impressive. Studies of changes in renal function following parenteral administration of apresoline® were made in seven children with acute nephritis. Significant temporary depressions of the glomerular filtration rate and urine flow were observed in every instance in which apresoline® induced a fall in systemic blood pressure. Apresoline® did not regularly induce an increase in renal plasma flow in these subjects. Changes in renal plasma flow were variable, and even decreases were observed. Even though apresoline® can induce a fall in blood pressure in children with hypertension and acute nephritis, this response may be associated with a temporary depression in renal excretory function.

Management of sudden deafness

1983 ◽  
Vol 91 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Ugo Fisch
Keyword(s):  
Blood Pressure ◽  
Oxygen Tension ◽  
Intravenous Infusion ◽  
Oxygen Supply ◽  
Randomized Study ◽  
Systemic Blood Pressure ◽  
Sudden Deafness ◽  
Systemic Blood ◽  
Noninvasive Treatment ◽  
Factors Influencing

Measurements according to the polarographic principle in cats have shown that the factors influencing the perilymphatic oxygen tension are the arterial Pco2, the arterial Po2, and the systemic blood pressure. In patients with sudden deafness, the oxygen supply to the vestibular tissues is significantly reduced but the response to carbogen is still possible. The vasodilation induced by carbogen in sudden deafness is not accompanied by a reduction (stealing effect) but by an increase of perilymphatic oxygenation. Therefore carbogen inhalation was used for the treatment of sudden deafness. In a prospective randomized study, carbogen inhalation yielded significantly better results than the intravenous infusion of papaverine and low-molecular dextran. Carbogen inhalation is recommended for the effective, noninvasive treatment of sudden deafness.

Perilymphatic Oxygen Tension and Vasoactive Drugs

1978 ◽  
Vol 87 (3) ◽  
pp. 364-369 ◽  
Author(s):  
N. Yagi ◽  
U. Fisch ◽  
K. Murata
Keyword(s):  
Blood Pressure ◽  
Oxygen Tension ◽  
Intravenous Injection ◽  
Systemic Blood Pressure ◽  
Polarographic Method ◽  
Vasoactive Drugs ◽  
Systemic Blood ◽  
Rapid Changes ◽  
Perilymphatic Space

— The oxygenation of the perilymph in response to the intravenous injection of vasoactive drugs has been measured in 67 cats using the polarographic method. Of all drugs used, only angiotensin induced a significant raise of perilymphatic PO2. Histamine, 50% glycerol and 7% Na2CO3 reduced the perilymphatic PO2. Papaverine, furosemid, pyridylcarbinol, naftidrofuryl and low molecular dextran have no significant effect upon the perilymphatic oxygen tension. Rapid changes of systemic blood pressure were found to correlate with subsequent modifications of the oxygen tension in the perilymphatic space.

scholarly journals Hypoxia-induced small extracellular vesicle proteins regulate proinflammatory cytokines and systemic blood pressure in pregnant rats

2020 ◽  
Vol 134 (6) ◽  
pp. 593-607 ◽  
Author(s):  
Suchismita Dutta ◽  
Andrew Lai ◽  
Katherin Scholz-Romero ◽  
Muhammad J. A. Shiddiky ◽  
Yusuke Yamauchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Cells ◽  
Oxygen Tension ◽  
Systemic Blood Pressure ◽  
Extravillous Trophoblast ◽  
Low Oxygen ◽  
Systemic Blood ◽  
Pregnant Rats ◽  
Differentially Abundant Proteins

Abstract Small extracellular vesicles (sEVs) released from the extravillous trophoblast (EVT) are known to regulate uterine spiral artery remodeling during early pregnancy. The bioactivity and release of these sEVs differ under differing oxygen tensions and in aberrant pregnancy conditions. Whether the placental cell-derived sEVs released from the hypoxic placenta contribute to the pathophysiology of preeclampsia is not known. We hypothesize that, in response to low oxygen tension, the EVT packages a specific set of proteins in sEVs and that these released sEVs interact with endothelial cells to induce inflammation and increase maternal systemic blood pressure. Using a quantitative MS/MS approach, we identified 507 differentially abundant proteins within sEVs isolated from HTR-8/SVneo cells (a commonly used EVT model) cultured at 1% (hypoxia) compared with 8% (normoxia) oxygen. Among these differentially abundant proteins, 206 were up-regulated and 301 were down-regulated (P &lt; 0.05), and they were mainly implicated in inflammation-related pathways. In vitro incubation of hypoxic sEVs with endothelial cells, significantly increased (P &lt; 0.05) the release of GM-CSF, IL-6, IL-8, and VEGF, when compared with control (i.e. cells without sEVs) and normoxic sEVs. In vivo injection of hypoxic sEVs into pregnant rats significantly increased (P &lt; 0.05) mean arterial pressure with increases in systolic and diastolic blood pressures. We propose that oxygen tension regulates the release and bioactivity of sEVs from EVT and that these sEVs regulate inflammation and maternal systemic blood pressure. This novel oxygen-responsive, sEVs signaling pathway, therefore, may contribute to the physiopathology of preeclampsia.

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&lt;0.05). Enddiastolic volume was 87±7 ml/m2 (controls) and 100±14 ml/m2 (Barlow), p&lt;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&lt;0.001), 30.1±1.5 vs 49.5±4.9 mm (p&lt;0.001) and 30.9±1.5 vs 44.9±3.3 mm (p&lt;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

Relation of Systemic Blood Pressure to Sudden Cardiac Death

2012 ◽  
Vol 110 (3) ◽  
pp. 378-382 ◽  
Author(s):  
Jari Antero Laukkanen ◽  
J. Richard Jennings ◽  
Jussi Kauhanen ◽  
Timo Heikki Mäkikallio ◽  
Kimmo Ronkainen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Systemic Blood Pressure ◽  
Systemic Blood
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