Some Physical Properties of the Pulmonary Arterial Bed Deduced from Pulsatile Arterial Flow and Pressure

This study aimed to quantify changes of vascular compliance and resistance of the proximal and the peripheral pulmonary arterial vessels when vascular smooth muscle was stimulated. These above vascular characteristics were derived from registrations of pulsatile pressure and flow in the pulmonary artery (PA). An in situ cat lung preparation was used, with the right heart by-passed by a pulsatile blood pump. Vascular input impedance was derived from PA pulsatile pressure and flow recordings, and impedance characteristics were used for calculation of the variables of a simple lumped analog representation of the arterial bed. PA smooth muscle was stimulated by infusions of collagen suspension, by general hypoxia and by nor-adrenaline injections. Collagen caused 40% reduction of vascular compliance (C), no changes in proximal arterial resistance (Rl) and 18076 increase in peripheral vascular resistance (R2). Hypoxia caused 5096 reduced C, 20% increased R1 and 70% increased R2. Noradrenaline caused 20:6 reduced C and 30 % increased R1 and R2. These results, together with results derived from simulation of the observed impedance changes in a computer model of the lung arterial bed, indicated that collagen infusion elicited contraction of small and medium-sized arteries, with increased arterial volume as result of increased distending pressure. Hypoxia and noradrenaline, seemed both to cause contraction of the total arterial bed. This effect being most pronounced during hypoxia.     

Influence of Moderate Vasoconstriction on the Wave Reflection Properties of the Pulmonary Arterial Bed

Increased transmural pressure in the pulmonary arterial bed may reduce vascular input impedance and reduce hydraulic power linked to pulsatile blood flow. Vascular impedance and pulsatile hydraulic power (Wp) levels of isolated perfused rabbit lungs were compared after similar rises of pulmonary arterial pressure (PAp), induced either by vasoconstriction or by left atrial pressure (LAp) elevation. Resulting Wp levels were significantly smaller after vasoconstriction than LAp elevation. Wp showed a minimum level at physiologic PAp (about 20 cm H₂O) irrespective of the cause of PAp elevation. Pressure pulse wave reflection coefficient (Γ) was calculated for control and test situations, and was found to be approximately doubled after vasoconstriction. Only minor changes in Γ were found after LAP elevation. Accordingly, moderate vasoconstriction (resulting PAp?20 cm H₂O) caused a backward traveling pressure wave of high amplitude, appearing in counter-phase to the forward pressure wave at the input site. The total pressure wave amplitude was thereby markedly lowered, resulting in a reduced Wp level. We assume that this effect of moderate vasoconstriction may be one reason for the existence of vascular smooth muscles in the pulmonary arteries.     

Use of Input Impedance to Determine Changes in the Resistance of Arterial Vessels at Different Levels in Feline Femoral Bed

In many studies, the functional state of vessels of different caliber was determined by fitting the lumped parameters of a mathematical model of the bed in order to fit the vascular input impedance (Z _in) data. However, reliability of the results obtained in such a way remains uncertain. In this study, we employed a mathematical model with seven lumped parameters and Z _in experimental data to analyze the distribution of resistance across the arterial bed of the hind limb in anesthetized cats, to test reliability of this distribution and to describe the process of ascending arterial dilation followed occlusion of iliac artery. The vascular bed was divided into three segments: large arteries, medium-sized arterial vessels and precapillary resistance vessels together with venous part of the bed. Based on the data of Z _in measured in a wide frequency range (from 0 to 150 Hz) we showed that pharmacologically induced constriction and dilation of the arterial microvessels were reflected in the model by the changes in the resistance of distal precapillary vessels only, whereas the local constriction or dilation of femoral and iliac arteries as well as artificial stenosis of the femoral artery resulted exclusively in the changes of the resistance describing the state of large arteries. Using the input impedance method we could demonstrate and quantitatively describe the process of ascending arterial dilation during the post-occlusion (reactive) hyperemia. All these results prove that the model of vascular bed with seven lumped elements used in combination with input hydraulic impedance data can be an effective tool permitted to quantitatively analyze the functional state of arterial vessels of different caliber and to describe the changes in resistance of arterial vessels during vascular reactions.     

5‐Hydroxytryptamine‐induced microvascular pressure transients in lungs of anaesthetized rabbits

We determined lung microvascular pressure transients induced by 5‐hydroxytryptamine (5HT), by the micropuncture technique. We mechanically ventilated anaesthetized (halothane 0.8%), open‐chested rabbits, in which we recorded pulmonary artery (PA), left atrial (LA) and carotid artery pressures and cardiac output. For 4‐min periods of stopped ventilation, we constantly inflated the lung with airway pressure of 7 cmH₂O, then micropunctured the lung to determine pressures in arterioles and venules of 20–25 μm diameter. An intravenous bolus infusion of 5HT (100 μg), increased total pulmonary vascular resistance by 59%. Prior to 5HT infusion, the arterial, microvascular and venous segments comprised 30, 50 and 19% of the total pulmonary vascular pressure drop, respectively. However 14 s after 5HT infusion, the PA‐arteriole pressure difference (arterial pressure drop) increased 46%, while the venule‐LA pressure difference (venous pressure drop) increased >100%. The arteriole–venule pressure difference (microvascular pressure drop) was abolished. The increase in the arterial pressure drop was maintained for 4.8 min, whereas the increased venous pressure drop reverted to baseline in <1 min. We conclude that in the rabbit lung in situ, a 5HT bolus causes sustained arterial constriction and a strong but transient venous constriction.     

Effects of venous pressure elevation on myogenic vasoconstrictive responses to static and dynamic arterial pressures

In order to establish the nature of the stretch-evoked dynamic properties of vascular smooth muscle in arterioles, we have examined the static and dynamic effects of both arterial pulse pressure and elevated venous pressure on the resistance vessels (arteries and arterioles) in an intestinal mesenteric preparation derived from dogs. The dynamic myogenic response to stretch stimuli was directly related to both the frequency of arterial pulse pressure (1-20 c/min) and the level of venous pressure (0-45 mmHg). Under elevated venous pressure (20 mmHg), the mean arterial flow decreased with an increase in the frequency of arterial pulse pressure. The arteriolar vascular tone (namely, vascular resistance) was seen to be enhanced. We found that elevated venous pressure promotes active constriction (9-53%) of arteriolar smooth muscle (myogenic mechanism). The elevation of venous pressure also caused a rhythmic constriction (vasomotion) in the site of both vein and artery, which was completely abolished by an alpha-blocker (phentolamine). The results suggest that during venous pressure elevation a very pronounced myogenic constriction in terminal arterioles is caused by either a local neural reflex or a propagated myogenic response in the arteriolar network.     

True Arterial System Compliance Estimated From Apparent Arterial Compliance

A new method has been developed to estimate total arterial compliance from measured input pressure and flow. In contrast to other methods, this method does not rely on fitting the elements of a lumped model to measured data. Instead, it relies on measured input impedance and peripheral resistance to calculate the relationship of arterial blood volume to input pressure. Generally, this transfer function is a complex function of frequency and is called the apparent arterial compliance. At very low frequencies, the confounding effect of pulse wave reflection disappears, and apparent compliance becomes total arterial compliance. This study reveals that frequency components of pressure and flow below heart rate are generally necessary to obtain a valid estimate of compliance. Thus, the ubiquitous practice of estimating total arterial compliance from a single cardiac cycle is suspect under most circumstances, since a single cardiac cycle does not contain these frequencies. © 2000 Biomedical Engineering Society. PAC00: 8719Uv, 8719Rr     

Augmented vasoconstrictor response to changes in vascular transmural pressure in patients with essential arterial hypertension

The vasoconstrictor response to increase in venous transmural pressure in subcutaneous tissue was studied in 9 patients with essential arterial hypertension. Subcutaneous blood flow was measured on the distal part of the forearm and at the lateral malleolus by the local ¹³³Xe washout technique. Increase in venous transmural pressure was obtained by lowering the area under study 40cm below midaxillary line in the recumbent subject. Average mean arterial pressure ± 1 S.E. was 133 ± 6 mmHg. The fractional increase in vascular resistance induced by arteriolar constriction was more pronounced in the hypertensive patients than in a normotensive control group. “Minimal vascular resistance” in the papaverine relaxed vascular bed was higher in the hypertensive patients than in the controls. Distensibility of the papaverine relaxed resistance vessels was diminished in the patients. Follow-up studies after 6–18 months of anti-hypertensive treatment indicate that the vasoconstrictor response as well as “minimal vascular resistance” are normalized, whereas the distensibility of the papaverine relaxed arterioles remained unaltered in the hypertensive patients. The results indicate that the arteriolar smooth muscle cells of hypertensive patients are subjected to reversible hypertrophy whereas the reduced distensibility of the resistance vessels is due to irreversible structural changes.     

The Influence of Pulmonary Blood Flow Rate on Vascular Input Impedance and Hydraulic Power in the Sympathetically and Noradrenaline Stimulated Cat Lung

This study was designed to evaluate the influence of sympathetic nerve stimulation (NS) and α-adrenergic receptor stimulation (αS) on the pulmonary vascular input impedance and hydraulic power output of the right heart during variations of cardiac output (CO). An open chest cat preparation was used and pulsatile pressure and flow in the pulmonary artery were measured by high frequency response transducers. Calculations showed that vascular resistance (VR) was inversely dependent on CO, hut input impedance of the unstimulated lung was not influenced by CO variations. NS or αS increased VR and input impedance significantly, and the relation pulsatile hydraulic power/total hydraulic power (W_p/W_t) increased 40%, indicating that such stimulation has larger relative influence on impedance than on resistance. The reduction of arterial compliance during NS (maximal stimulus) was calculated to be 60%, independent of CO. Input impedance during NS or αS was reduced by CO elevations, probably because the concomitant distension of the arterial bed reduced arterial resistance and inertance. The ratio W_p/CO, which expresses the fraction of pulsatile hydraulic power lost per ml mean arterial flow, was found to be flow dependent both in control and stimulated conditions: W_p/CO was positively correlated to CO in control condition and weakly negatively correlated to CO during stimulation. At high CO the arterial vessels could he stimulated and stiffened without much extra load on the right heart.     

Metabolic control of large-bore arterial resistance vessels,arterioles, and veins in cat skeletal muscle during exercise

The metabolic control of the vascular bed in cat gastrocnemius muscle during exercise was studied with a new technique (Björnberg et al. 1988) permitting continuous and simultaneous recordings of arteriolar and capillary pressures, and of resistances in the following consecutive vascular section: proximal arterial resistance vessels > 25 μm, arterioles < 25 μm, and on the venous side. The study thereby provided quantitative data for resistance and active intrinsic tone in these vascular segments at rest, during graded exercise vasodilatation, and in the post-exercise period. Slight activation of the metabolic control system by low-frequency somatomotor nerve stimulation (light exercise') caused inhibition of intrinsic tone and decreased vascular resistance selectively in the arteriolar section. At increasing workloads, arteriolar resistance was further decreased, but resistance and tone in the proximal arterial resistance vessels and the veins then became clearly reduced as well. This difference in effectiveness of the metabolic control system on the different segments of the vascular bed was expressed quantitatively in terms of a ‘metabolic vasodilator index’. Graded activation of the metabolic control system led to a marked segmental redistribution of intrinsic vascular tone, in turn resulting in an increased pressure drop across the proximal arterial vessels and the veins and a decreased pressure drop over the arterioles. The observed decrease in the pre- to post-capillary resistance ratio caused, at a constant arterial pressure of 100 mmHg, a graded increase in capillary pressure with increasing workloads, at maximum vasodilatation by an average value of 14 mmHg above the resting control value of 15.4 ± 0.6 mmHg. In the post-exercise period, recovery of vascular tone to control was more rapid in the proximal arterial resistance vessels and the veins than in the arteriolar segment.     

Rate and Extent of Adaptive Cardiovascular Changes in Rats during Experimental Renal Hypertension

To study the extent and exact time course of cardiovascular structural adaptation to increases in pressure load, renal hypertension was induced in normotensive male Wistar rats by renal artery constriction. At different intervals after operation the hemodynamic characteristics of the hypertensive rats and normotensive control rats were explored in paired hindquarter perfusions, from maximal dilatation up to maximal constriction (cf, Folkow et al, 1970 b). At the same time intervals the extent of left ventricular hypertrophy and of water content of the aortic wall were examined. The results reveal the presence of left ventricular hypertrophy in the hypertensive rats already after one week, soon followed by adaptive structural changes of the resistance vessels, in the form mainly of media hypertrophy, these processes being largely completed 2–3 weeks after operation. In these animals, lacking genetic predisposition for hypertension, the extent of the structural vascular changes seems large enough to explain a considerable part, but not all, of the pressure rise. An increased water content of the hypertensive aortic wall is found first 4.5 months after operation, indicating that some water logging of arterial and maybe also arteriolar walls might occur in late phases of chronic renal hypertension.     

Influence of central and peripheral changes on the hydraulic input impedance of the systemic arterial tree

The input impedance of the systemic arterial tree of the dog has been computed by Fourier analysis. It was shown that a distance between pressure and flow transducers of less than 2 cm results in appreciable errors which manifest themselves mainly in the phase of the input impedance. The input impedance for controls, occlusions at various locations in the aorta, and an increase and decrease of peripheral resistance were studied. For the same experiments, the total arterial compliance was calculated from the peripheral resistance of the diastolic aortic-pressure curve. The characterstic impedance of the ascending aorta was also estimated. The impedance in the control situation may be modelled by means of a 3-element Windkessel consisting of a peripheral resistance and (total) arterial compliance, together with a resistance equal to the characteristic impedance of the aorta. The occlusions of the aorta show that blockage at (and beyond) the trifurcation do not result in a detectable change in input impedance, except for a slight increase of the peripheral resistance. The more proximal an aortic occlusion, the more effect it has on the pattern of the input impedance. When the aorta is occluded at the diphragm, or higher, the single (uniform) tube appears to be a much better model than the Windkessel. Occlusion of one or both carotid arteries increases the mean pressure; consequently not only the peripheral resistance increases but also the total arterial compliance decreases. The Windkessel with increased peripheral resitance and decreased compliance is again a good model. After a sudden release of occlusion of the aorta, the arterial system has a low peripheral resistance and may also be modelled by the Windkessel.     

Sympathetic a-adrenergic control of large-bore arterial vessels,arterioles and veins,and of capillary pressure and fluid exchange in whole-organ cat skeletal muscle

The sympathetic nervous control of the vascular bed of cat gastrocnemius muscle was studied with a new whole-organ technique which permits simultaneous, continuous and quantitative measurements of capillary pressure (P_c), capillary fluid exchange and resistance reactions in the whole vascular bed and in its three consecutive sections: large-bore arterial vessels (> 25 μm), arterioles (< 25 μm) and veins. The results demonstrated a distinct neural control of all three consecutive vascular sections, graded in relation to the rate of nerve excitation up to maximum at 16 Hz. Stimulation at high rates, which in the steady state caused an average rise of overall regional resistance from 15.3 to 120 PRU (7.8-fold increase), thus raised large-bore arterial vessel resistance from 8.8 to 64 PRU (7.3-fold increase), arteriolar resistance from 4.5 to 49 PRU (10.9-fold increase) and venous resistance from 2.0 to 7 PRU (3.5-fold increase). The rate of resistance development (PRU s^-1) of the sympathetic constrictor response was much higher in the arteriolar than in the other sections, which indicates that the neural control is especially prompt and efficient in the arterioles. A passive component was shown to contribute to the described responses only on the venous side, but in no case by more than 10% of the total sympathetic venous resistance response, which thus is mainly active. Of special functional importance was that the new technique provided information about the adrenergic control of P_c, in absolute figures. From the control value of 19 mmHg, graded sympathetic stimulation caused a graded decline in P_c, at maximum constriction by about 7 mmHg. This resulted in marked net transcapillary fluid absorption, in turn increasing plasma volume.     

Renal arterial compliance and conductance measurement using on-line self-adaptive analog computation of model parameters

Dynamic renal arterial flow pattern, arterial compliance, and pre-glomerular conductance were predicted from the measured canine renal arterial pressure pulse pattern using on-line analog computer simulation of renal arterial parameters. The flow was accurately predicted not only under steady-state conditions but also in the presence of marked fluctuations in arterial pressure pattern, mean level, and heart rate. The model has five parameters: largeartery resistance, inertance, and compliance; a pre-glomerular arteriolar conductance; and a non-pulsatile glomerular pressure. The first two were set manually while the last three were automatically adjusted by the method of steepest descents to minimize the absolute error expressed as the instantaneous difference between the measured flow in the artery and the flow predicted by the computer.     

Method for assessing the stroke-to-stroke biomechanical characteristics of coronary vessels

The biomechanical parameters of coronary vessels are estimated in a model of the coronary input impedance. The model includes the capacity of epicardial vessels, input resistance, limiting resistance, and some sources of electromotive force symbolizing the intramyocardial and critical pressure values. The theoretical value of coronary blood flow is calculated from computer-optimized parameters of the model and experimental curves representing arterial pressure and left-ventricular pressure. The theoretical and experimental curves of coronary blood flow are in good agreement both during the maximum vasodilatation and in intact tone. The basic parameters, such as epicardial vessel pliability, zero blood flow pressure, and resistance of the resistive portion of blood vessels corresponded to previous evaluations. The dispersion of calculated stroke-to-stroke parameters is 5–10%. Translated from Byulleten'Eksperimental'noi Biologii i Meditsiny, Vol. 122, No. 11, pp. 594–597, November, 1996     

Estimation of arterial compliance in aortic regurgitation: three methods evaluated in pigs

Three methods for measuring arterial compliance when aortic regurgitation is present are examined. The first two methods are based on a Windkessel model composed of two elements, compliance C and resistance R. Arterial compliance was estimated from diastolic pressure waveforms and diastolic regurgitant flow for one method, and from systolic aortic pressure waveforms and systolic flow for the other method. The third method was based on a three-element Windkessel model, composed of characteristic resistance r, compliance C and resistance R. In this method arterial compliance was calculated by adjusting the model to the modulus and phase of the first harmonic term of the aortic input impedance. The three methods were compared and validated in six anaesthetised pigs over a broad range of aortic pressures. The three methods were found to give quantitatively similar estimates of arterial compliance at mean aortic pressures above 60 mm Hg. Below 60 mm Hg, estimates of arterial compliance varied widely, probably because of poor validity of the Windkessel models in the low pressure range.     

Loci of Neurogenic and Metabolic Effects on Precapillary Vessels of Skeletal Muscle

Folkow , B., R. R. Sonnenschein , and D. L. Wright , Loci of neurogenic and metabolic effects on precapillary vessels of skeletal muscle. Acta physiol. scand. 1971. 81. 459–471. By cannulation of a branch of the proximally clamped sural artery of the anesthetized cat, distal arterial pressure (DAP) in the gastrocnemius muscle was recorded. Measurement of blood flow, femoral arterial pressure and DAP allowed calculation of total resistance (R_t) and its partition into a distal component (R_d) which included precapillary sphincters and the smaller arterioles, and a proximal component (R_P) which included the larger arteries. With sympathetic vasoconstriction, the initial increase in R_t was accounted for mainly by constriction of the distal vessels which then tended to relax; progressive constriction of proximal vessels accounted for most of the elevated R_t during the steady state; subsequent reactive hyperemia mainly involved distal vessels. R_t was less affected by sympathetic stimulation during exercise than when the muscle was at rest; constriction of distal vessels was more markedly reduced than that of proximal vessels. Ascending dilatation was evident during exercise. Sympathetic cholinergic vasodilatation mainly involved vessels more proximal to those which were dilated early in exercise. The findings are compatible with the concept that capillary flow distribution, as a function of terminal arterioles and precapillary sphincters, is adjusted by local factors towards an optimum for the prevailing metabolic level of the tissue.     

5-Hydroxytryptamine-induced microvascular pressure transients in lungs of anaesthetized rabbits.

We determined lung microvascular pressure transients induced by 5-hydroxytryptamine (5HT), by the micropuncture technique. We mechanically ventilated anaesthetized (halothane 0.8%), open-chested rabbits, in which we recorded pulmonary artery (PA), left atrial (LA) and carotid artery pressures and cardiac output. For 4-min periods of stopped ventilation, we constantly inflated the lung with airway pressure of 7 cmH2O, then micropunctured the lung to determine pressures in arterioles and venules of 20-25 microm diameter. An intravenous bolus infusion of 5HT (100 microg), increased total pulmonary vascular resistance by 59%. Prior to 5HT infusion, the arterial, microvascular and venous segments comprised 30, 50 and 19% of the total pulmonary vascular pressure drop, respectively. However 14 s after 5HT infusion, the PA-arteriole pressure difference (arterial pressure drop) increased 46%, while the venule-LA pressure difference (venous pressure drop) increased >100%. The arteriole-venule pressure difference (microvascular pressure drop) was abolished. The increase in the arterial pressure drop was maintained for 4.8 min, whereas the increased venous pressure drop reverted to baseline in <1 min. We conclude that in the rabbit lung in situ, a 5HT bolus causes sustained arterial constriction and a strong but transient venous constriction.     

The effect of renal perfusion pressure on renal vascular resistance in the spontaneously hypertensive rat

Renal hemodynamics and renal vascular resistance (RVR) were measured in the spontaneously hypertensive rat (SHR) and in the normotensive Wistar-Kyoto rat (WKY). In addition, the autoregulatory response and segmental RVR in the SHR were studied after aortic constriction. Mean arterial pressure (MAP) and RVR were higher in the SHR than in the WKY, but renal blood flow (RBF) and glomerular filtration rate were similar in both groups. Measurement of mean afferent arteriolar diameter (AAD) by a microsphere method showed a significantly smaller AAD in SHR (17.7±0.35 m) than in the WKY (19.5±0.20 m). This decrease in AAD could account for a 47% increase in preglomerular resistance. Aortic constriction in the SHR, sufficient to reduce renal perfusion pressure from 152 to 115 mm Hg, did not alter the AAD. Since RBF and glomerular filtration were also well maintained following aortic constriction, these autoregulatory responses suggest that vessels proximal to the afferent arteriole rather than postglomerular vasculature are primarily involved in the changes on intrarenal vascular resistance in SHR.     

Blood pressure regulation V: in vivo mechanical properties of precapillary vessels as affected by long-term pressure loading and unloading

Recent studies are reviewed, concerning the in vivo wall stiffness of arteries and arterioles in healthy humans, and how these properties adapt to iterative increments or sustained reductions in local intravascular pressure. A novel technique was used, by which arterial and arteriolar stiffness was determined as changes in arterial diameter and flow, respectively, during graded increments in distending pressure in the blood vessels of an arm or a leg. Pressure-induced increases in diameter and flow were smaller in the lower leg than in the arm, indicating greater stiffness in the arteries/arterioles of the leg. A 5-week period of intermittent intravascular pressure elevations in one arm reduced pressure distension and pressure-induced flow in the brachial artery by about 50 %. Conversely, prolonged reduction of arterial/arteriolar pressure in the lower body by 5 weeks of sustained horizontal bedrest, induced threefold increases of the pressure-distension and pressure-flow responses in a tibial artery. Thus, the wall stiffness of arteries and arterioles are plastic properties that readily adapt to changes in the prevailing local intravascular pressure. The discussion concerns mechanisms underlying changes in local arterial/arteriolar stiffness as well as whether stiffness is altered by changes in myogenic tone and/or wall structure. As regards implications, regulation of local arterial/arteriolar stiffness may facilitate control of arterial pressure in erect posture and conditions of exaggerated intravascular pressure gradients. That increased intravascular pressure leads to increased arteriolar wall stiffness also supports the notion that local pressure loading may constitute a prime mover in the development of vascular changes in hypertension.     

Human cardiovascular dose-response to supplemental oxygen

Aim: The aim of the study was to examine the central and peripheral cardiovascular adaptation and its coupling during increasing levels of hyperoxaemia. We hypothesized a dose‐related effect of hyperoxaemia on left ventricular performance and the vascular properties of the arterial tree. Methods: Oscillometrically calibrated arterial subclavian pulse trace data were combined with echocardiographic recordings to obtain non‐invasive estimates of left ventricular volumes, aortic root pressure and flow data. For complementary vascular parameters and control purposes whole‐body impedance cardiography was applied. In nine (seven males) supine, resting healthy volunteers, aged 23–48 years, data was collected after 15 min of air breathing and at increasing transcutaneous oxygen tensions (20, 40 and 60 kPa), accomplished by a two group, random order and blinded hyperoxemic protocol. Results: Left ventricular stroke volume [86 ± 13 to 75 ± 9 mL (mean ± SD)] and end‐diastolic area (19.3 ± 4.4 to 16.8 ± 4.3 cm²) declined (P < 0.05), and showed a linear, negative dose–response relationship to increasing arterial oxygen levels in a regression model. Peripheral resistance and characteristic impedance increased in a similar manner. Heart rate, left ventricular fractional area change, end‐systolic area, mean arterial pressure, arterial compliance or carbon dioxide levels did not change. Conclusion: There is a linear dose–response relationship between arterial oxygen and cardiovascular parameters when the systemic oxygen tension increases above normal. A direct effect of supplemental oxygen on the vessels may therefore not be excluded. Proximal aortic and peripheral resistance increases from hyperoxaemia, but a decrease of venous return implies extra cardiac blood‐pooling and compensatory relaxation of the capacitance vessels.