Biomedical subjects

Dag Linnarsson

Publications and source records attributed to Dag Linnarsson.

5 recordsLinked to original sources

PubMed2003

Relationship between breath-synchronous arterial pressure and heart rate variations during orthostatic stress.

It has recently been shown that the phase relationship between respiration-induced changes in arterial pressure (AP) and heart rate (HR) are different in supine and upright postures. We wanted to further analyse the coupling between respiration, arterial blood pressure and HR in the time domain, and how this coupling was altered during orthostatic stress. Nine healthy subjects were studied. Respiration-induced changes in AP and HR were recorded during frequency- and volume-controlled breathing. This was done during supine rest with and without lower body negative pressure (-50 mmHg) (LBNP). All experiments were performed after beta1-blockade. Responses were averaged breath-by-breath to enhance the time resolution and to eliminate noise. The respiration-induced changes in arterial pulse pressure (PP) were different between control and LBNP: The peak in PP during the respiratory cycle occurred 0.9 +/- 0.8 (mean +/- SD) s before the onset of inspiration during supine control and 0.8 +/- 2.1 s after the onset of inspiration during LBNP (P = 0.03). These changes in the timing of peak PP significantly distorted the cyclic systolic AP and mean AP fluctuations during LBNP. Despite the altered AP response with LBNP, HR fluctuations closely correlated in time with respiration in all conditions, albeit with a significantly reduced amplitude during LBNP (-49%, P = 0.01). The results points to a lack of coupling between AP and HR during paced breathing and thus suggest that respiratory sinus dysrhythmia at least, to a large extent, is independent of the arterial baroreflex.

Adult↗

PubMed2002

Pulmonary gas exchange during apnoea in exercising men.

There is indirect evidence that cardiovascular responses to apnoea result in a temporary slowing of the O(2) uptake in the lungs in exercising humans. The present study was undertaken in an attempt to determine directly to what extent this occurs, and whether the magnitude of this slowing is such that it must be the result of concomitant cardiovascular readjustments and not merely a result of an isolated apnoea-induced fall in the arterial O(2) saturation ( S(a)O(2)). Eight men performed 120 W leg exercise and performed repeated apnoeas of 10-40 s duration. Heart rate, S(a)O(2), and breath-by-breath gas exchange were determined. Pulmonary O(2) uptake fell gradually as breath-holds proceeded by [mean (SEM)] 74 (3)% of the pre-apnoea O(2) uptake. This decrease was significantly larger than could be accounted for by the fall in S(a)O(2) alone [ S(a)O(2) fall -30 (3)%], which it is estimated would have resulted in a fall of pulmonary O(2) uptake of -54 (5)%. We conclude that cardiovascular responses to apnoea contribute significantly to reducing pulmonary O(2) uptake during apnoea in exercising men.

Adolescent↗

PubMed2002

Role of hypoxemia for the cardiovascular responses to apnea during exercise.

We sought to define the role of hypoxemia in eliciting the cardiovascular responses to apnea during exercise. Eleven men performed repeated apneas during 100-W steady-state exercise, either with normoxic gas (air) or 95% oxygen (oxygen). Beat-by-beat arterial blood pressure, arterial oxygen saturation, and heart rate (HR) were determined, and stroke volume (SV) was estimated from impedance cardiography calibrated with soluble gas rebreathing. There were large interindividual variabilities of HR, mean arterial pressure (MAP), and total peripheral resistance (TPR) at end-apnea (ea). However, for each individual, HR(ea), MAP(ea), and TPR(ea) were highly correlated between air and oxygen (R = 0.94, 0.78, and 0.93). HR decreased and MAP increased faster during apnea with air than with oxygen (ANOVA, P < 0.05), but MAP(ea) was not different between conditions. Cardiac output was reduced by 33% with air and by 11% with oxygen (P < 0.001 for air vs. oxygen). We conclude that the hypoxemia component cannot account for the wide interindividual differences of HR and TPR responses to apnea. However, hypoxemia augments the HR and TPR responses and may limit the MAP response to apnea by preventing a bradycardia-associated increase of SV.

Adolescent↗

PubMed2002

Lung function during and after prolonged head-down bed rest.

We determined the effects of prolonged head-down tilt bed rest (HDT) on lung mechanics and gas exchange. Six subjects were studied in supine and upright postures before (control), during [day 113 (D113)], and after (R + number of days of recovery) 120 days of HDT. Peak expiratory flow (PF) never differed between positions at any time and never differed from controls. Maximal midexpiratory flow (FEF(25-75%)) was lower in the supine than in the upright posture before HDT and was reduced in the supine posture by about 20% between baseline and D113, R + 0, and R + 3. The diffusing capacity for carbon monoxide corrected to a standardized alveolar volume (volume-corrected DL(CO)) was lower in the upright than in the supine posture and decreased in both postures by 20% between baseline and R + 0 and by 15% between baseline and R + 15. Pulmonary blood flow (Q(C)) increased from R + 0 to R + 3 by 20 (supine) and 35% (upright). As PF is mostly effort dependent, our data speak against major respiratory muscle deconditioning after 120 days of HDT. The decrease in FEF(25-75%) suggests a reduction in elastic recoil. Time courses of volume-corrected DL(CO) and Q(C) could be explained by a decrease in central blood volume during and immediately after HDT.

Adult↗

PubMed2002

Differential changes of lung diffusing capacity and tissue volume in hypergravity.

In normal gravity, lung diffusing capacity (DL(CO)) and lung tissue volume (LTV; including pulmonary capillary blood volume) change in concert, for example, during shifts between upright and supine. Accordingly, DL(CO) and LTV might be expected to decrease together in sitting subjects in hypergravity due to peripheral pooling of blood and reduced central blood volume. Nine sitting subjects in a human centrifuge were exposed to one, two, and three times increased gravity in the head-to-feet direction (G(z+)) and rebreathed a gas containing trace amounts of acetylene and carbon monoxide. DL(CO) was 25.2 +/- 2.6, 20.0 +/- 2.1, and 16.7 +/- 1.7 ml. min(-1). mbar(-1) (means +/- SE) at 1, 2, and 3 G(z+), respectively (ANOVA P < 0.001). Corresponding values for LTV increased from 541 +/- 34 to 677 +/- 43, and 756 +/- 71 ml (P < 0.001) at 2 and 3 G(z+). Results are compatible with sequestration of blood in the dependent part of the pulmonary circulation just as in the systemic counterpart. DL(CO,) which under normoxic conditions is mainly determined by its membrane component, decreased despite an increased pulmonary capillary blood volume, most likely as a consequence of a less homogenous distribution of alveolar volume with respect to pulmonary capillary blood volume.

Adult↗