4 research outputs found
Sensitivities to Hypoxia for Individual Participants
<p>Results are shown in terms of the number of (normal control group) standard deviations by which each participant's response differed from the mean response of the normal control participants. The patients with CP were significantly different from the normal control group in their ventilatory and pulmonary vascular responses to both mild and moderate hypoxia, and in their heart rate responses to mild hypoxia. BP, blood pressure.</p
Aldolase C and <i>VEGF</i> mRNA Expression at Different Oxygen Tensions
<p>Lymphocytes were isolated from venous blood taken from CP patients and normal control participants, and incubated at eight different levels of oxygen tension prior to RNA isolation. Gene expression is shown relative to a standard calibrator sample. Basal gene expression at 20% oxygen was significantly higher in CP patients for both
<i>Aldolase C</i> (A) and
<i>VEGF</i> (B) (
<i>p</i> < 0.05). Both genes were induced by hypoxia, and at the lowest oxygen tension (0.1%) expression was no longer significantly different for either gene. Values are mean ± standard error of the mean. Asterisks indicate
<i>p</i> < 0.05 (unpaired
<i>t</i>-test).
</p
Systemic Vascular Responses to Mild and Moderate Hypoxia
<div><p>(A and B) Heart rate. Mild hypoxia provoked a rise of 11.7 beats/min in the CP patient group, compared with 3.6 beats/min in normal control participants (
<i>p</i> < 0.05). No other statistically significant differences in systemic vascular responses were detected between these two groups.
</p>
<p>(C and D) Blood pressure, showing systolic pressure (upper plot) and diastolic pressure (lower plot).</p>
<p>(E and F) Cardiac output, assessed non-invasively using Doppler echocardiography.</p>
<p>All responses are shown during mild (A, C, and E) and moderate (B, D, and F) hypoxia. Values are mean ± standard error of the mean.</p></div
End-Tidal Gas Control, Ventilatory, and Pulmonary Vascular Responses to Mild and Moderate Hypoxia
<div><p>(A and B) End-tidal gas control.
</p><p>Pet<sub>O<sub>2</sub></sub></p> and
Pet<sub>CO<sub>2</sub></sub> were well controlled.
<p>Pet<sub>O<sub>2</sub></sub></p> was well matched between all groups.
Pet<sub>CO<sub>2</sub></sub> was lower in the CP patient group, reflecting this group's lower baseline air-breathing
Pet<sub>CO<sub>2</sub></sub>.
<p></p>
<p>(C and D) Ventilation, given at body temperature and pressure, saturated with water vapour. Mild hypoxia provoked an increase in ventilation of 4.4 l/min in the CP patients versus 1.6 l/min in normal controls (
<i>p</i> < 0.05), while moderate hypoxia induced increases of 24.5 versus 10.0 l/min in these two groups, respectively (
<i>p</i> < 0.05).
</p>
<p>(E and F) Pulmonary vascular tone. This was assessed using Doppler echocardiography to determine ΔP<sub>max</sub>, a standard non-invasive index of pulmonary vascular tone. With mild hypoxia, ΔP<sub>max</sub> increased by 11.5 mm Hg in the CP patient group compared with only 1.1 mm Hg in the normal control group (
<i>p</i> < 0.05). Moderate hypoxia stimulated a rise in ΔP<sub>max</sub> of 35.3 mm Hg compared with 6.1 mm Hg in these two groups, respectively (
<i>p</i> < 0.001).
</p>
<p>All responses are shown during mild (A, C, and E) and moderate (B, D, and F) hypoxia. Values are mean ± standard error of the mean.</p></div