Continuous Intra-Arterial PO2 Registrations with Conventional and Surface Heparinized Catheter Electrodes

2015 ◽  
pp. 48-52
Author(s):  
E. Nilsson ◽  
B. Alm� ◽  
G. Edwall ◽  
R. Larsson ◽  
P. Olsson
Keyword(s):  
Arterial Po2

Systemic Effects of ADP-induced Platelet Aggregation and Their Modification by Aspirin and by Pyridinolcarbamate

1973 ◽  
Vol 30 (01) ◽  
pp. 178-190 ◽  
Author(s):  
Itsuro Kobayashi ◽  
Paul Didisheim
Keyword(s):  
Platelet Aggregation ◽  
Venous Pressure ◽  
Systemic Effects ◽  
Central Venous ◽  
Platelet Aggregates ◽  
Induced Changes ◽  
Second Wave ◽  
Carotid Arterial ◽  
Arterial Po2

SummaryADP, AMP, or ATP was injected rapidly intravenously in rats. ADP injection resulted in the f olio wing transient changes: a drop in platelet count, a rise in central venous pressure, a fall in carotid arterial PO2, bradycardia, arrhythmia, flutter-fibrillation, and arterial hypotension. AMP and ATP produced some of these same effects; but except for hypotension, their frequency and severity Avere much less than those following ADP.Prior intravenous administration of acetylsalicylic acid or pyridinolcarbamate, two inhibitors of the second wave of ADP-induced platelet aggregation in vitro, significantly reduced the frequency and severity of all the above ADP-induced changes except hypotension. These observations suggest that many of the changes (except hypotension) observed to follow ADP injection are produced by platelet aggregates which lodge transiently in various microcirculatory beds then rapidly disaggregate and recirculate.

Platelet Function in Surgical Stress

1985 ◽  
Vol 54 (04) ◽  
pp. 849-852 ◽  
Author(s):  
O Naesh ◽  
J T Friis ◽  
I Hindberg ◽  
K Winther
Keyword(s):  
Stress Response ◽  
Negative Correlation ◽  
Surgical Stress ◽  
Plasma Concentrations ◽  
Serum Cortisol ◽  
Cortisol Concentration ◽  
Pulmonary Dysfunction ◽  
Arterial Po2 ◽  
Elective Cholecystectomy ◽  
Serum Cortisol Concentration

SummaryTen patients for elective cholecystectomy were studied pre-, per- and postoperatively. All had neurolept anesthesia. Plasma concentrations of β-TG, TXB2 and 5-HT and intraplatelet 5-HT were measured. Aggregation to ADP was recorded.Serum cortisol concentration was used as index of the stress response, showing peroperative increase and postoperative decrease. Closely related to this we observed a significant increase in P-β-TG and P-TXB2 with postoperative normalization in 6 patients without complications. P-5-HT had a peak peropera-tively and remained elevated postoperatively. A negative correlation between P--5-HT and decreasing intraplatelet 5-HT postoperatively was observed.High postoperative levels of P--5-HT seem to be related to low arterial Po2 and pulmonary dysfunction. In 3 patients with complications a second increase in P-β-TG, P-TXB2 and partly in P--5-HT was found. Platelets were temporarily refractory to ADP immediately following surgery and showed increased aggregabil-ity postoperatively. We conclude that platelets are activated in surgical stress.

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Target arterial PO2 according to the underlying pathology: a mini-review of the available data in mechanically ventilated patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Julien Demiselle ◽  
Enrico Calzia ◽  
Clair Hartmann ◽  
David Alexander Christian Messerer ◽  
Pierre Asfar ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Large Scale ◽  
Retrospective Studies ◽  
Prolonged Exposure ◽  
Oxygen Toxicity ◽  
Circulatory Shock ◽  
Mechanically Ventilated ◽  
Ischaemia Reperfusion ◽  
Arterial Po2 ◽  
Underlying Pathology

AbstractThere is an ongoing discussion whether hyperoxia, i.e. ventilation with high inspiratory O2 concentrations (FIO2), and the consecutive hyperoxaemia, i.e. supraphysiological arterial O2 tensions (PaO2), have a place during the acute management of circulatory shock. This concept is based on experimental evidence that hyperoxaemia may contribute to the compensation of the imbalance between O2 supply and requirements. However, despite still being common practice, its use is limited due to possible oxygen toxicity resulting from the increased formation of reactive oxygen species (ROS) limits, especially under conditions of ischaemia/reperfusion. Several studies have reported that there is a U-shaped relation between PaO2 and mortality/morbidity in ICU patients. Interestingly, these mostly retrospective studies found that the lowest mortality coincided with PaO2 ~ 150 mmHg during the first 24 h of ICU stay, i.e. supraphysiological PaO2 levels. Most of the recent large-scale retrospective analyses studied general ICU populations, but there are major differences according to the underlying pathology studied as well as whether medical or surgical patients are concerned. Therefore, as far as possible from the data reported, we focus on the need of mechanical ventilation as well as the distinction between the absence or presence of circulatory shock. There seems to be no ideal target PaO2 except for avoiding prolonged exposure (> 24 h) to either hypoxaemia (PaO2 < 55–60 mmHg) or supraphysiological (PaO2 > 100 mmHg). Moreover, the need for mechanical ventilation, absence or presence of circulatory shock and/or the aetiology of tissue dysoxia, i.e. whether it is mainly due to impaired macro- and/or microcirculatory O2 transport and/or disturbed cellular O2 utilization, may determine whether any degree of hyperoxaemia causes deleterious side effects.

Abstract 5858: Role of Oxygen Tension and Oxidative Stress in Human Saphenous Vein Remodeling

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Binata Joddar ◽  
Rashmeet K Reen ◽  
Michael Firstenberg ◽  
Keith J Gooch
Keyword(s):  
Oxidative Stress ◽  
Oxygen Tension ◽  
Ex Vivo ◽  
Neointimal Hyperplasia ◽  
Fold Increase ◽  
List Type ◽  
Saphenous Veins ◽  
Arterial Po2 ◽  
And Oxidative Stress

Vessels cultured ex vivo maintain viability and vasoactivity for weeks and can remodel in response to mechanical cues. When cultured in the presence of 5% CO2/balance air veins develop neointimal hyperplasia (IH) while arteries do not suggesting that exposure to significant increases in pO2 levels might stimulate IH. Neointimal hyperplasia (IH) is a known mechanism by which saphenous veins have a decreased patency compared to arterial conduits when used for coronary artery bypass. We sought to explore the role of oxygen tension and oxidative stress in IH. Test the hypothesis that exposure of human saphenous veins (HSV) to arterial pO2 stimulates IH via ROS-mediated pathways. Almost 40 HSV remnants acquired following CABG were cultured ex vivo with arterial (~95mmHg) pO2 or venous (~40mmHg) pO2 for 14 days. All differences reported have a p<0.05 via Student’s t-test. Results: HSV cultured at arterial pO2 exhibited significant IH as evidenced by disruption of the IEL, invasion of cells from the media, and a 2.8-fold greater intimal area than fresh HSV, a 5.8-fold increase in cell proliferation compared to fresh HSV, increased ROS levels and oxidative stress as evidenced by 4-fold increase in 4-HNE level (a marker of oxidative stress), increased DHE staining (indicative of superoxide generation), and a progressive increase in total ROS levels with time as assessed by DCF fluorescence, and a 3-fold increase in phosphorylated p38-MAPK, which is implicated in SMC proliferation. In stark contrast vessels culture at arterial pO2, HSV cultured with venous pO2 did not develop increased IH and were indistinguishable from fresh vessels with respect to proliferation, markers of oxidative stress, and MAPK expression levels. Supplementing culture medium with antioxidants including Tiron or NAC blocked the pO2-induced changes. These data indicate that exposure to arterial pO2 increases cellular proliferation and stimulates IH, potentially via oxidative stress or ROS signaling and also suggest that exposure to elevated arterial pO2 might stimulate pathological remodeling of veins grafted into the arterial circulation. This research has received full or partial funding support from the American Heart Association, AHA Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania & West Virginia).

Limitations of Transcutaneous Po2 and Pco2 Monitoring in Infants with Bronchopulmonary Dysplasia

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 217-220
Author(s):  
Ellen S. Rome ◽  
Eileen K. Stork ◽  
Waldemar A. Carlo ◽  
Richard J. Martin
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Premature Infants ◽  
Neonatal Period ◽  
Postnatal Life ◽  
Pco2 Monitoring ◽  
Arterial Po2 ◽  
Transcutaneous Po2

Despite the well-documented correlation between transcutaneous and arterial Po2 and Pco2 in sick neonates, the effect of maturation on this relationship has not been well characterized. Eight premature infants with bronchopulmonary dysplasia (BPD) and indwelling arterial lines beyond the immediate neonatal period were studied. Transcutaneous Po2 always underestimated Pao2 beyond 10 weeks of postnatal life, such that transcutaneous Po2 - Pao2 was -16 ± 5 torr (P &lt; .001). Corrected transcutaneous Pco2 simultaneously overestimated PaCo2 by 9 ± 3 torr (P &lt; .001), although this occurred over a wider range of postnatal ages. Transcutaneous Po2 monitoring may be a useful tool for estimating Pao2 in this population, provided an appropriate correction is made beyond 10 weeks of age. It is suggested that caution be exercised when using transcutaneous Pco2 measurements to estimate absolute arterial values in older infants with bronchopulmonary dysplasia.

Effect of Acute Hemorrhage on Transcutaneous, Subcutaneous, Intramuscular, and Arterial Oxygen Tensions

PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 881-883
Author(s):  
Frederick A. Matsen ◽  
Craig R. Wyss ◽  
Racheal V. King ◽  
Charles W. Simmons
Keyword(s):  
Arterial Oxygen ◽  
Peripheral Blood Flow ◽  
Danger Signal ◽  
Close Approximation ◽  
Monitoring Method ◽  
Acute Hemorrhage ◽  
Tissue Po2 ◽  
Oxygen Tensions ◽  
Arterial Po2 ◽  
Transcutaneous Po2

Although transcutaneous Po2 is a close approximation of arterial Po2 in most neonates, infants in shock often show lower transcutaneous than arterial Po2 values. For a better understanding of this discrepancy, we investigated the effect of acute hemorrhage on transcutaneous, tissue, and arterial Po2 in rabbits. With progressive hemorrhage, transcutaneous and tissue Po2 values declined steeply while arterial Po2 values did not. We speculate that the progressive decrement in transcutaneous and tissue Po2 values with hemorrhage is produced by diminished peripheral blood flow. Rather than representing a failure of the transcutaneous Po2 monitoring method, we speculate that transcutaneous hypoxia with shock may be a clinically valuable danger signal.

Gas exchange in dogs in the prone and supine positions

1992 ◽  
Vol 72 (6) ◽  
pp. 2292-2297 ◽  
Author(s):  
K. C. Beck ◽  
J. Vettermann ◽  
K. Rehder
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Prone Position ◽  
Pulmonary Blood Flow ◽  
Random Order ◽  
Arterial Pco2 ◽  
Supine Posture ◽  
Pulmonary Shunting ◽  
The Difference ◽  
Arterial Po2

To determine the cause of the difference in gas exchange between the prone and supine postures in dogs, gas exchange was assessed by the multiple inert gas elimination technique (MIGET) and distribution of pulmonary blood flow was determined using radioactively labeled microspheres in seven anesthetized paralyzed dogs. Each animal was studied in the prone and supine positions in random order while tidal volume and respiratory frequency were kept constant with mechanical ventilation. Mean arterial PO2 was significantly lower (P less than 0.01) in the supine [96 +/- 10 (SD) Torr] than in the prone (107 +/- 6 Torr) position, whereas arterial PCO2 was constant (38 Torr). The distribution of blood flow (Q) vs. ventilation-to-perfusion ratio obtained from MIGET was significantly wider (P less than 0.01) in the supine [ln SD(Q) = 0.75 +/- 0.26] than in the prone position [ln SD (Q) = 0.34 +/- 0.05]. Right-to-left pulmonary shunting was not significantly altered. The distribution of microspheres was more heterogeneous in the supine than in the prone position. The larger heterogeneity was due in part to dorsal-to-ventral gradients in Q in the supine position that were not present in the prone position (P less than 0.01). The decreased efficiency of oxygenation in the supine posture is caused by an increased ventilation-to-perfusion mismatch that accompanies an increase in the heterogeneity of Q distribution.

Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

1993 ◽  
Vol 74 (6) ◽  
pp. 2795-2800 ◽  
Author(s):  
R. Behm ◽  
H. Mewes ◽  
W. H. DeMuinck Keizer ◽  
T. Unger ◽  
R. Rettig
Keyword(s):  
Carotid Body ◽  
Normobaric Hypoxia ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Excretory Function ◽  
Arterial Blood ◽  
Peripheral Arterial ◽  
Renal Responses ◽  
Arterial Po2 ◽  
Sodium And Potassium

The contribution of peripheral arterial chemoreceptors to cardiovascular and renal responses to acute hypocapnic hypoxia is currently not well understood. We compared the effects of normobaric hypoxia on mean arterial blood pressure (MABP), heart rate, glomerular filtration rate (GFR), renal blood flow (RBF), and renal volume and electrolyte excretion in conscious unilaterally nephrectomized carotid body-denervated (n = 10) and sham-operated (n = 10) control rats. Thirty minutes of normobaric hypoxia (12.5% O2) resulted in significant reductions in arterial PO2 and PCO2 as well as decreases in MABP, GFR, RBF, and renal sodium, potassium, and water excretion. These effects occurred more rapidly and/or were significantly more pronounced in carotid body-denervated than in sham-operated rats. These data indicate that moderate acute hypocapnic hypoxia has profound effects on systemic and renal hemodynamics as well as on renal excretory function in conscious rats. We conclude that stimulation of the peripheral arterial chemoreceptors can partially offset the hypoxia-induced decreases in MABP, RBF, GFR, urine flow, and urinary sodium and potassium excretion, thereby helping to maintain cardiovascular as well as fluid and electrolyte homeostasis.

Predominant role of peripheral chemoreceptors in the termination of apnea in maturing newborn lambs

1996 ◽  
Vol 80 (3) ◽  
pp. 892-898 ◽  
Author(s):  
C. Delacourt ◽  
E. Canet ◽  
M. A. Bureau
Keyword(s):  
Carotid Body ◽  
Pco2 Level ◽  
Peripheral Chemoreceptor ◽  
Arterial Pco2 ◽  
Postnatal Maturation ◽  
Body Function ◽  
Life Threatening ◽  
Prolonged Apnea ◽  
Arterial Po2

Apneas are very common and normal in newborns but may become life threatening if they are not terminated appropriately. The aim of this study in newborn lambs was to investigate the influence on apnea termination of postnatal maturation, peripheral chemoreceptor function, and hypoxia. Apneas were induced by passive hyperventilation at varying inspired O2 fraction levels. The apnea termination threshold PCO2 (PATTCO2) was defined as the arterial PCO2 value at the first breath after the apnea. Three groups of awake intubated lambs were studied: 1) intact lambs tested at both 1 and 15 days of life, 2) intact 1-day-old lambs with central tissue hypoxia induced by CO inhalation, and 3) 1-day-old lambs with carotid body denervation (CBD). In individual lambs and regardless of age and carotid body function, there was a PO2-PCO2 response curve that was a determinant for the termination of an apnea. PATTCO2 invariably increased when arterial PO2 increased, regardless of age. During hypoxia and normoxia, PATTCO2 was significantly lower in 15-day-old lambs compared with 1-day-old lambs. No difference was seen during hyperoxia. PATTCO2 values were shifted to higher levels after carotid body removal. Finally, hypoxia induced by either a low inspired O2 fraction or CO inhalation consistently failed to induce a depressive effect on the PATTCO2 even in CBD lambs. In conclusion, in awake newborn lambs, the PCO2 level for apnea termination changed with postnatal age, and carotid body function was essential in lowering PATTCO2, thus protecting the lambs against prolonged apnea. Furthermore, hypoxia consistently failed to depress the reinitiation of breathing after apnea, even in CBD lambs.

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