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The effect of hyperoxia on central blood pressure in healthy subjects

View Article: PubMed Central - PubMed

ABSTRACT

Introduction: Hyperoxia increases total peripheral resistance by acting locally but also inhibits the activity of carotid body chemoreceptors. We studied the effect of hyperoxia on central pressure in normotensive subjects.

Material and methods: Medical air followed by 100% oxygen was provided to 19 subjects (12/7 female/male, age 28.2 ±1.1 years) for 15 min through a non-rebreather mask. Central blood pressure was then measured using applanation tonometry.

Results: After the first 2 min of hyperoxia, heart rate decreased significantly (65 ±2.6 beats/min vs. 61 ±2.1 beats/min, p = 0.0002). Peripheral and central blood pressure remained unchanged, while hemoglobin oxygen saturation and subendocardial viability ratio index increased (97 ±0.4% vs. 99 ±0.2%, p = 0.03; 168 ±8.4% vs. 180 ±8.2%, p = 0.009). After 15 min of 100% oxygen ventilation, heart rate and peripheral and central blood pressures remained unchanged from the first 2 min. The augmentation index, augmentation pressure and ejection duration increased as compared to baseline values and those obtained at 2 min (–5.1 ±2.9% vs. –1.2 ±2.6%, p = 0.005 and –4.6 ±2.7% vs. –1.2 ±2.6%, p = 0.0015; –1.3 ±0.7 mm Hg vs. –0.2 ±1.2 mm Hg, p = 0.003 and –1.1 ±0.7 mm Hg vs. –0.2 ±1.2 mm Hg, p = 0.012; 323 ±3.6 ms vs. 330 ±3.5 ms, p = 0.0002 and 326 ±3.5 ms vs. 330 ±3.5 ms, p = 0.021, respectively).

Conclusions: The present study shows that hyperoxia does not affect central blood pressure in young healthy subjects and may improve myocardial blood supply estimated indirectly from applanation tonometry.

No MeSH data available.


Experimental protocol
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Figure 0002: Experimental protocol

Mentions: During the session the subjects’ central blood pressure was recorded at the end of the 21% oxygen respiration period (P0), after 2 min of hyperoxia (P1) and once the 15 min hyperoxia period (P2) had ended. These time periods for recording peripheral and central blood pressure were selected so as to evaluate early responses to hyperoxia-induced carotid body deactivation [27, 28] and to determine the results of prolonged hyperoxia. Recording was performed at P1 due to the fact that early hemodynamic effects of carotid body deactivation in previous observations had started within the 1st min of exposure to hyperoxia [12] plus the time needed to perform the recording. A timeline representing the period of analyses is presented in Figure 2.


The effect of hyperoxia on central blood pressure in healthy subjects
Experimental protocol
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5016570&req=5

Figure 0002: Experimental protocol
Mentions: During the session the subjects’ central blood pressure was recorded at the end of the 21% oxygen respiration period (P0), after 2 min of hyperoxia (P1) and once the 15 min hyperoxia period (P2) had ended. These time periods for recording peripheral and central blood pressure were selected so as to evaluate early responses to hyperoxia-induced carotid body deactivation [27, 28] and to determine the results of prolonged hyperoxia. Recording was performed at P1 due to the fact that early hemodynamic effects of carotid body deactivation in previous observations had started within the 1st min of exposure to hyperoxia [12] plus the time needed to perform the recording. A timeline representing the period of analyses is presented in Figure 2.

View Article: PubMed Central - PubMed

ABSTRACT

Introduction: Hyperoxia increases total peripheral resistance by acting locally but also inhibits the activity of carotid body chemoreceptors. We studied the effect of hyperoxia on central pressure in normotensive subjects.

Material and methods: Medical air followed by 100% oxygen was provided to 19 subjects (12/7 female/male, age 28.2 ±1.1 years) for 15 min through a non-rebreather mask. Central blood pressure was then measured using applanation tonometry.

Results: After the first 2 min of hyperoxia, heart rate decreased significantly (65 ±2.6 beats/min vs. 61 ±2.1 beats/min, p = 0.0002). Peripheral and central blood pressure remained unchanged, while hemoglobin oxygen saturation and subendocardial viability ratio index increased (97 ±0.4% vs. 99 ±0.2%, p = 0.03; 168 ±8.4% vs. 180 ±8.2%, p = 0.009). After 15 min of 100% oxygen ventilation, heart rate and peripheral and central blood pressures remained unchanged from the first 2 min. The augmentation index, augmentation pressure and ejection duration increased as compared to baseline values and those obtained at 2 min (–5.1 ±2.9% vs. –1.2 ±2.6%, p = 0.005 and –4.6 ±2.7% vs. –1.2 ±2.6%, p = 0.0015; –1.3 ±0.7 mm Hg vs. –0.2 ±1.2 mm Hg, p = 0.003 and –1.1 ±0.7 mm Hg vs. –0.2 ±1.2 mm Hg, p = 0.012; 323 ±3.6 ms vs. 330 ±3.5 ms, p = 0.0002 and 326 ±3.5 ms vs. 330 ±3.5 ms, p = 0.021, respectively).

Conclusions: The present study shows that hyperoxia does not affect central blood pressure in young healthy subjects and may improve myocardial blood supply estimated indirectly from applanation tonometry.

No MeSH data available.