Acute normobaric hypoxia does not increase blood or plasma viscosity

2021 ◽  
pp. 1-4
Author(s):  
Michael Buono ◽  
Kaitlyn Rostomily
Keyword(s):  
Oxygen Saturation ◽  
Blood Viscosity ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Plasma Viscosity ◽  
Normobaric Hypoxia ◽  
Hemoglobin Oxygen Saturation ◽  
Blood Samples ◽  
Hypoxic Conditions ◽  
The Mean

BACKGROUND: It has previously been reported that chronic hypoxia increases blood viscosity. The increase is usually attributed to polycythemia-induced increases in hematocrit. However, the effect of acute hypoxia in humans on blood viscosity is unknown. OBJECTIVE: Therefore, the purpose of this study was to determine the effect of acute hypoxia, independent of changes in hematocrit, on blood and plasma viscosity. METHODS: Nine healthy volunteers breathed room air for 30 min, followed by 30 min of breathing 15% oxygen. Blood samples were collected at the end of both the normoxic and hypoxic conditions. Blood viscosity, plasma viscosity, and hematocrit were measured in each sample. RESULTS: The mean±SD hemoglobin oxygen saturation significantly (P <  0.05) decreased from 98±1% during normoxia to 87±2% during hypoxia. Hematocrit was essentially identical for the two conditions (42.1% vs. 42.0%). Blood viscosity was not significantly different for the two conditions with a mean of 2.89±0.17 cP during normoxia and 2.83±0.19 cP during hypoxia. Likewise, plasma viscosity was not significantly different for the two conditions with a mean of 1.19±0.04 cP during normoxia and 1.19±0.05 cP during hypoxia. CONCLUSION: Such results suggest that acute normobaric hypoxia, independent of changes in hematocrit, does not increase blood or plasma viscosity.

Alteration of the erythrocyte ultrastructure and blood viscosity by morphine

1978 ◽  
Vol 56 (2) ◽  
pp. 245-251 ◽  
Author(s):  
E. B. Vadas ◽  
E. A. Hosein
Keyword(s):  
Cell Volume ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Plasma Viscosity ◽  
Cell Geometry ◽  
Flow Properties ◽  
Mean Cell Volume ◽  
Morphine Administration ◽  
The Mean ◽  
Volume Cell

The effects of acute morphine administration on intact erythrocytes and on their flow properties were studied by measuring the mean cell volume, cell geometry, and whole blood and plasma viscosities. Morphine caused a small (2–7%) increase in mean cell volume. Changes in cell geometry were found to be time dependent and most pronounced in concave portions of the red cells. Whole blood viscosity was found to decrease upon morphine treatment; this may be due in part to a concurrent decrease in plasma viscosity.

scholarly journals Decrease of Nibrin expression in chronic hypoxia is associated with hypoxia-induced chemoresistance in medulloblastoma cells

2017 ◽  
Author(s):  
Sophie Cowman ◽  
Yuen Ngan Fan ◽  
Barry Pizer ◽  
Violaine Sée
Keyword(s):  
Dna Damage ◽  
Cell Line ◽  
Induced Resistance ◽  
Brain Tumours ◽  
Molecular Mechanisms ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Adult Brain ◽  
Cell Type ◽  
Hypoxic Conditions

AbstractSolid tumours are less oxygenated than normal tissues. This is called tumour hypoxia and leads to resistance to radiotherapy and chemotherapy. The molecular mechanisms underlying such resistance have been investigated in a range of tumour types, including the adult brain tumours glioblastoma, yet little is known for paediatric brain tumours. Medulloblastoma (MB) is the most common malignant brain tumour in children. Here we used a common MB cell line (D283-MED), to investigate the mechanisms of chemo and radio-resistance in MB, comparing to another MB cell line (MEB-Med8A) and to a widely used glioblastoma cell line (U87MG). In D283-MED and U87MG, chronic hypoxia (5 days), but not acute hypoxia (24 h) induced resistance to etoposide and X-ray irradiation. This acquired resistance upon chronic hypoxia was much less pronounced in MEB-Med8A cells. Using a transcriptomic approach in D283-MED cells, we found a large transcriptional remodelling upon long term hypoxia, in particular the expression of a number of genes involved in detection and repair of double strand breaks (DSB) was altered. The levels of Nibrin (NBN) and MRE11, members of the MRN complex (MRE11/Rad50/NBN) responsible for DSB recognition, were significantly down-regulated. This was associated with a reduction of Ataxia Telangiectasia Mutated (ATM) activation by etoposide, indicating a profound dampening of the DNA damage signalling in hypoxic conditions. As a consequence, p53 activation by etoposide was reduced, and cell survival enhanced. Whilst U87MG shared the same dampened p53 activity, upon chemotherapeutic drug treatment in chronic hypoxic conditions, these cells used a different mechanism, independent of the DNA damage pathway. Together our results demonstrate a new mechanism explaining hypoxia-induced resistance involving the alteration of the response to DSB, but also highlight the cell type to cell type diversity and the necessity to take into account the differing tumour genetic make-up when considering re-sensitisation therapeutic protocols.

Validation of Oxygen Saturation Monitoring in Neonates

2007 ◽  
Vol 16 (2) ◽  
pp. 168-178 ◽  
Author(s):  
Shyang-Yun Pamela K. Shiao ◽  
Ching-Nan Ou
Keyword(s):  
Oxygen Saturation ◽  
Pulse Oximetry ◽  
Venous Blood ◽  
Arterial Oxygen ◽  
Dissociation Curve ◽  
Oxyhemoglobin Dissociation Curve ◽  
Blood Samples ◽  
Arterial Blood ◽  
The Mean ◽  
Oxyhemoglobin Dissociation

•Background Pulse oximetry is commonly used to monitor oxygenation in neonates, but cannot detect variations in hemoglobin. Venous and arterial oxygen saturations are rarely monitored. Few data are available to validate measurements of oxygen saturation in neonates (venous, arterial, or pulse oximetric). •Purpose To validate oxygen saturation displayed on clinical monitors against analyses (with correction for fetal hemoglobin) of blood samples from neonates and to present the oxyhemoglobin dissociation curve for neonates. •Method Seventy-eight neonates, 25 to 38 weeks’ gestational age, had 660 arterial and 111 venous blood samples collected for analysis. •Results The mean difference between oxygen saturation and oxyhemoglobin level was 3% (SD 1.0) in arterial blood and 3% (SD 1.1) in venous blood. The mean difference between arterial oxygen saturation displayed on the monitor and oxyhemoglobin in arterial blood samples was 2% (SD 2.0); between venous oxygen saturation displayed on the monitor and oxyhemoglobin in venous blood samples it was 3% (SD 2.1) and between oxygen saturation as determined by pulse oximetry and oxyhemoglobin in arterial blood samples it was 2.5% (SD 3.1). At a Pao2 of 50 to 75 mm Hg on the oxyhemoglobin dissociation curve, oxyhemoglobin in arterial blood samples was from 92% to 95%; oxygen saturation was from 95% to 98% in arterial blood samples, from 94% to 97% on the monitor, and from 95% to 97% according to pulse oximetry. •Conclusions The safety limits for pulse oximeters are higher and narrower in neonates (95%–97%) than in adults, and clinical guidelines for neonates may require modification.

scholarly journals Left ventricular depression and pulmonary edema in rats after short-term normobaric hypoxia: effects of adrenergic blockade and reduced fluid load

2021 ◽  
Author(s):  
Peter Appelt ◽  
Philipp Gabriel ◽  
Christian Bölter ◽  
Nicole Fiedler ◽  
Katrin Schierle ◽  
...  
Keyword(s):  
Acute Hypoxia ◽  
Fluid Management ◽  
High Plasma ◽  
Left Ventricular ◽  
Normobaric Hypoxia ◽  
Plasma Catecholamine ◽  
Adrenergic Blockade ◽  
Pulmonary Injury ◽  
Hypoxic Conditions ◽  
Fluid Load

AbstractAcute normobaric hypoxia may induce pulmonary injury with edema (PE) and inflammation. Hypoxia is accompanied by sympathetic activation. As both acute hypoxia and high plasma catecholamine levels may elicit PE, we had originally expected that adrenergic blockade may attenuate the severity of hypoxic pulmonary injury. In particular, we investigated whether administration of drugs with reduced fluid load would be beneficial with respect to both cardiocirculatory and pulmonary functions in acute hypoxia. Rats were exposed to normobaric hypoxia (10% O2) over 1.5 or 6 h and received 0.9% NaCl or adrenergic blockers either as infusion (1 ml/h, increased fluid load) or injection (0.5 ml, reduced fluid load). Control animals were kept in normoxia and received infusions or injections of 0.9% NaCl. After 6 h of hypoxia, LV inotropic function was maintained with NaCl injection but decreased significantly with NaCl infusion. Adrenergic blockade induced a similar LV depression when fluid load was low, but did not further deteriorate LV depression after 6 h of infusion. Reduced fluid load also attenuated pulmonary injury after 6 h of hypoxia. This might be due to an effective fluid drainage into the pleural space. Adrenergic blockade could not prevent PE. In general, increased fluid load and impaired LV inotropic function promote the development of PE in acute hypoxia. The main physiologic conclusion from this study is that fluid reduction under hypoxic conditions has a protective effect on cardiopulmonary function. Consequently, appropriate fluid management has particular importance to subjects in hypoxic conditions.

scholarly journals Gene expression of the liver in response to chronic hypoxia

2010 ◽  
Vol 41 (3) ◽  
pp. 275-288 ◽  
Author(s):  
Monica M. Baze ◽  
Karen Schlauch ◽  
Jack P. Hayes
Keyword(s):  
Gene Expression ◽  
Chronic Hypoxia ◽  
Inbred Mice ◽  
Acute Hypoxia ◽  
Transcript Abundance ◽  
Differentially Expressed ◽  
Severe Hypoxia ◽  
Protein Amino Acid ◽  
Hypoxic Conditions ◽  
False Discovery

Hypoxia is an important ecological, evolutionary, and biomedical stressor. While physiological acclimatization of mammals to hypoxia is well studied, the variation in gene expression that underlies acclimatization is not well studied. We acclimatized inbred mice for 32 days to hypoxic conditions that simulated altitudes of 1400, 3000, and 4500 m. We used oligonucleotide microarrays to measure changes in steady-state abundance of mRNA in the livers of these mice. Mice exposed to more severe hypoxia (simulated altitude of 4500 m) were smaller in mass and had higher hematocrit than mice exposed to less severe hypoxia. ANOVA and false discovery rate tests indicated that 580 genes were significantly differentially expressed in response to chronic hypoxia. Few of these 580 genes have previously been reported to respond to hypoxia. In contrast, many of these 580 genes belonged to same functional groups typically respond to acute hypoxia. That is, both chronic and acute hypoxia elicit changes in transcript abundance for genes involved in angiogenesis, glycolysis, lipid metabolism, carbohydrate metabolism, and protein amino acid phosphorylation, but the particular genes affected by the two types of hypoxia were mostly different. Numerous genes affecting the immune system were differentially expressed in response to chronic hypoxia, which supports recently proposed hypotheses that link immune function and hypoxia. Furthermore, our results discovered novel elevated mRNA abundance of genes involved in hematopoiesis and oxygen transport not reported previously, but consistent with extreme hematocrits found in hypoxic mice.

Glibenclamide does not reverse attenuated vasoreactivity to acute or chronic hypoxia

1995 ◽  
Vol 79 (4) ◽  
pp. 1173-1180 ◽  
Author(s):  
M. R. Eichinger ◽  
T. C. Resta ◽  
D. S. Balderrama ◽  
G. M. Herrera ◽  
L. A. Richardson ◽  
...  
Keyword(s):  
Chronic Hypoxia ◽  
Channel Blocker ◽  
Acute Hypoxia ◽  
Peripheral Resistance ◽  
Katp Channels ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Hypoxic Conditions ◽  
Before And After

Recent studies from our laboratory have shown that acute and chronic hypoxic exposures are associated with attenuated systemic vasoreactivity in conscious rats. The present studies examined the role of adenosine triphosphate-sensitive potassium channels (KATP channels) in modulating the pressor and vasoconstrictor responses to phenylephrine (PE) in conscious instrumented rats 1) during acute hypoxia or 2) after chronic hypoxic exposure. Mean arterial pressure, mean cardiac output, and total peripheral resistance were assessed before and after graded infusions of PE in both groups of rats under normoxic or hypoxic conditions. Additionally, the role of KATP channels in attenuating vasoreactivity was determined by administration of glibenclamide (KATP channel blocker) before PE infusions. Acute hypoxia (12% O2) was associated with reduced pressor and constrictor responses to PE in control animals. Furthermore, acute return to room air did not restore the pressor and constrictor responses in the chronically hypoxic rats. Glibenclamide infusion did not influence the pressor or vasoconstrictor responses to PE in either group of animals during normoxia or acute hypoxia. Therefore, our data suggest that opening of KATP channels is not involved in the attenuated vasoreactivity associated with acute and chronic hypoxia in the conscious rat.

scholarly journals Distribution of blood viscosity values and biochemical correlates in healthy adults

1996 ◽  
Vol 42 (8) ◽  
pp. 1189-1195 ◽  
Author(s):  
R S Rosenson ◽  
A McCormick ◽  
E F Uretz
Keyword(s):  
Blood Plasma ◽  
Serum Protein ◽  
Reference Values ◽  
Blood Viscosity ◽  
Clinical Manifestations ◽  
Plasma Viscosity ◽  
Total Serum Protein ◽  
Total Serum ◽  
Viscosity Measurements ◽  
The Mean

Abstract Increases in the viscosity of blood and plasma predict clinical manifestations of atherothrombotic vascular disease. The clinical utility of viscosity measurements in cardiovascular risk factor analysis requires reference values established from a healthy disease-free population. A cohort of 126 (71 men, 55 women) healthy nonsmoking adults had fasting blood analysis after a 12-14-h fast. Viscosity measurements were made on samples of whole blood, plasma, and serum at 37 degrees C with a coaxial cylinder microviscometer. The mean blood viscosity at shear rates of 100, 50, and 1 s-1 were 3.26 +/- 0.43, 4.37 +/- 0.60, and 5.46 +/- 0.84 mPa.s, respectively. Men had significantly higher blood viscosity values than women at each shear rate. The differences in blood viscosity did not remain significant after blood viscosity values were normalized to a hematocrit of 45%, except at 100 s-1. For the entire group, normalized blood viscosity values at each measured rate correlated inversely with HDL cholesterol and positively with fibrinogen. The mean plasma viscosity was 1.39 +/- 0.08 mPa.s and the mean serum viscosity was 1.27 +/- 0.06 mPa.s. Plasma viscosity correlated with fibrinogen (r = 0.51, P &lt; 0.0001), total serum protein (r = 0.33, P &lt; 0.0001), and triglyceride concentrations (r = 0.33, P &lt; 0.0015). Serum viscosity correlated with total serum protein (r = 0.50, P &lt; 0.0001) and LDL cholesterol (r = 0.24, P = 0.0065). This study provides reference values for the viscosity of blood, plasma, and serum that may assist in evaluating hemorheological profiles.

scholarly journals Evaluation of Acute Exogenous Hypoxia Impact on the Fraction of Exhaled Nitric Oxide in Healthy Males

Folia Medica ◽  
2016 ◽  
Vol 57 (3-4) ◽  
pp. 230-234
Author(s):  
Peter K. Dimov ◽  
Blagoi I. Marinov ◽  
Ilcho S. Ilchev ◽  
Zdravko Z. Taralov ◽  
Stefan S. Kostianev
Keyword(s):  
Nitric Oxide ◽  
Oxygen Saturation ◽  
Reference Range ◽  
Exhaled Breath ◽  
Pulmonary Vessels ◽  
Atmospheric Air ◽  
Hypoxic Conditions ◽  
Hypoxic Environment ◽  
Exhaled Air ◽  
The Mean

Abstract Introduction: Exogenous hypoxia increases ventilation and contracts the pulmonary vessels. Whether those factors change the values of nitric oxide in exhaled air has not yet been evaluated. Objective: To examine the effect of exogenous normobaric hypoxia on the values of the fraction of nitric oxide in exhaled breath (FeNO). Subjects аnd Methods: Twenty healthy non-smoker males at mean age of 25.4 (SD = 3.7) were tested. The basal FeNO values were compared with those at 7 min. and 15 min. after introducing into the hypoxic environment (hypoxic tent), imitating atmospheric air with oxygen concentration corresponding to 3200 m above sea level. Exhaled breath temperature was measured at baseline and at 10-12 min. of the hypoxic exposition. Heart rate and oxygen saturation were registered by pulse-oximetry. Results: All the subjects had FeNO values in the reference range. The mean baseline value was 14.0 ± 3.2 ppb, and in hypoxic conditions - 15.5 ± 3.8 ppb (7 min.) and 15.3 ± 3.6 ppb (15 min.), respectively, as the elevation is statistically significant (p = 0.011 and p = 0.008). The values of exhaled breath temperature were 33.79 ± 1.55°С and 33.87 ± 1.83°С (p = 0.70) at baseline and in hypoxic conditions, respectively. Baseline oxygen saturation in all subjects was higher than that, measured in hypoxia (96.93 ± 1.29% vs. 94.27 ± 2.53%; p < 0.001). Conclusions: Exogenous hypoxia leads to an increase of FeNO values, but does not affect the exhaled breath temperature.

NOTES ON THE APPLICATION OF THE HERSCH GALVANIC OXYGEN CELL TO MEASUREMENT OF BLOOD OXYGEN CONTENT AND TENSION

1961 ◽  
Vol 39 (6) ◽  
pp. 991-999 ◽  
Author(s):  
D. V. Bates ◽  
E. V. Harkness
Keyword(s):  
Standard Deviation ◽  
Oxygen Saturation ◽  
Oxygen Content ◽  
Oxygen Tension ◽  
Blood Oxygen ◽  
Average Volume ◽  
Blood Samples ◽  
Factors Influencing ◽  
The Mean

A number of galvanic oxygen cells have been built to the design of Hersch (1). Factors influencing the sensitivity of this type of cell to oxygen have been studied, and the potentialities of the cells in the analysis of small gas samples have been explored. With the cell used in the manner described, analysis of 105 samples of air of an average volume of 0.001 ml showed the standard deviation of the percentage of oxygen to be 0.9%. The mean oxygen percentage of these samples was correct at 20.8%. These cells were found to be suitable for the analysis of the oxygen contained in very small blood samples, and the method described probably offers the most precise technique there is for the determination of the oxygen saturation of 0.002 ml of blood. By bubble equilibration techniques, the cell may also be used to determine the oxygen tension of blood samples in the range 0–200 mm Hg.

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