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J J van Lieshout

Publications and source records attributed to J J van Lieshout.

At least 19 recordsLinked to original sources
PubMed2006

The postural reduction in middle cerebral artery blood velocity is not explained by PaCO2.

In the normocapnic range, middle cerebral artery mean velocity (MCA Vmean) changes approximately 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO2) and a decrease in PaCO2 will reduce the cerebral blood flow by vasoconstriction (the CO2 reactivity of the brain). When standing up MCA Vmean and the end-tidal carbon-dioxide tension (PETCO2) decrease, suggesting that PaCO2 contributes to the reduction in MCA Vmean. In a fixed body position, PETCO2 tracks changes in the PaCO2 but when assuming the upright position, cardiac output (Q) decreases and its distribution over the lung changes, while ventilation (VE) increases suggesting that PETCO2 decreases more than PaCO2. This study evaluated whether the postural reduction in PaCO2 accounts for the postural decline in MCA Vmean). From the supine to the upright position, VE, Q, PETCO2, PaCO2, MCA Vmean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO2Hb) were followed in seven subjects. When standing up, MCA Vmean (from 65.3+/-3.8 to 54.6+/-3.3 cm s(-1) ; mean +/- SEM; P<0.05) and cO2Hb (-7.2+/-2.2 micromol l(-1) ; P<0.05) decreased. At the same time, the VE/Q ratio increased 49+/-14% (P<0.05) with the postural reduction in PETCO2 overestimating the decline in PaCO2 (-4.8+/-0.9 mmHg vs. -3.0+/-1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA Vmean seems to be explained by the reduction in PETCO2 but the small decrease in PaCO2 makes it unlikely that the postural decrease in MCA Vmean can be accounted for by the cerebral CO2 reactivity alone.

Adult↗
PubMed2005

Orthostatic blood pressure control before and after spaceflight, determined by time-domain baroreflex method.

Reduction in plasma volume is a major contributor to orthostatic tachycardia and hypotension after spaceflight. We set out to determine time- and frequency-domain baroreflex (BRS) function during preflight baseline and venous occlusion and postflight orthostatic stress, testing the hypothesis that a reduction in central blood volume could mimic the postflight orthostatic response. In five cosmonauts, we measured finger arterial pressure noninvasively in supine and upright positions. Preflight measurements were repeated using venous occlusion thigh cuffs to impede venous return and "trap" an increased blood volume in the lower extremities; postflight sessions were between 1 and 3 days after return from 10- to 11-day spaceflight. BRS was determined by spectral analysis and by PRVXBRS, a time-domain BRS computation method. Although all completed the stand tests, two of five cosmonauts had drastically reduced pulse pressures and an increase in heart rate of approximately 30 beats/min or more during standing after spaceflight. Averaged for all five subjects in standing position, high-frequency interbeat interval spectral power or transfer gain did not decrease postflight. Low-frequency gain decreased from 8.1 (SD 4.0) preflight baseline to 6.8 (SD 3.4) postflight (P = 0.033); preflight with thigh cuffs inflated, low-frequency gain was 9.4 (SD 4.3) ms/mmHg. There was a shift in time-domain-determined pulse interval-to-pressure lag, Tau, toward higher values (P < 0.001). None of the postflight results were mimicked during preflight venous occlusion. In conclusion, two of five cosmonauts showed abnormal orthostatic response 1 and 2 days after spaceflight. Overall, there were indications of increased sympathetic response to standing, even though we can expect (partial) restoration of plasma volume to have taken place. Preflight venous occlusion did not mimic the postflight orthostatic response.

Adult↗
PubMed2005

Stroke volume of the heart and thoracic fluid content during head-up and head-down tilt in humans.

BACKGROUND: The stroke volume (SV) of the heart depends on the diastolic volume but, for the intact organism, central pressures are applied widely to express the filling of the heart. METHODS: This study evaluates the interdependence of SV and thoracic electrical admittance of thoracic fluid content (TA) vs. the central venous (CVP), mean pulmonary artery (MPAP) and pulmonary artery wedge (PAWP) pressures during head-up (HUT) and head-down (HDT) tilt in nine healthy humans. RESULTS: From the supine position to 20 degrees HDT, SV [112 +/- 18 ml; mean +/- standard deviation (SD)], TA (30.8 +/- 7.1 mS) and CVP (3.6 +/- 0.9 mmHg) did not change significantly, whereas MPAP (from 13.9 +/- 2.7 to 16.1 +/- 2.5 mmHg) and PAWP (from 8.8 +/- 3.4 to 11.3 +/- 2.5 mmHg; P < 0.05) increased. Conversely, during 70 degrees HUT, SV (to 65 +/- 24 ml) decreased, together with CVP (to 0.9 +/- 1.4 mmHg; P < 0.001), MPAP (to 9.3 +/- 3.8 mmHg; P < 0.01), PAWP (to 0.7 +/- 3.3 mmHg; P < 0.001) and TA (to 26.7 +/- 6.8 mS; P < 0.01). However, from 20 to 50 min of HUT, SV decreased further (to 48 +/- 21 ml; P < 0.001), whereas the central pressures did not change significantly. CONCLUSIONS: During both HUT and HDT, SV of the heart changed with the thoracic fluid content rather than with the central vascular pressures. These findings confirm that the function of the heart relates to its volume rather than to its so-called filling pressures.

Adult↗
PubMed2004

Human cerebral venous outflow pathway depends on posture and central venous pressure.

Internal jugular veins are the major cerebral venous outflow pathway in supine humans. In upright humans the positioning of these veins above heart level causes them to collapse. An alternative cerebral outflow pathway is the vertebral venous plexus. We set out to determine the effect of posture and central venous pressure (CVP) on the distribution of cerebral outflow over the internal jugular veins and the vertebral plexus, using a mathematical model. Input to the model was a data set of beat-to-beat cerebral blood flow velocity and CVP measurements in 10 healthy subjects, during baseline rest and a Valsalva manoeuvre in the supine and standing position. The model, consisting of 2 jugular veins, each a chain of 10 units containing nonlinear resistances and capacitors, and a vertebral plexus containing a resistance, showed blood flow mainly through the internal jugular veins in the supine position, but mainly through the vertebral plexus in the upright position. A Valsalva manoeuvre while standing completely re-opened the jugular veins. Results of ultrasound imaging of the right internal jugular vein cross-sectional area at the level of the laryngeal prominence in six healthy subjects, before and during a Valsalva manoeuvre in both body positions, correlate highly with model simulation of the jugular cross-sectional area (R(2) = 0.97). The results suggest that the cerebral venous flow distribution depends on posture and CVP: in supine humans the internal jugular veins are the primary pathway. The internal jugular veins are collapsed in the standing position and blood is shunted to an alternative venous pathway, but a marked increase in CVP while standing completely re-opens the jugular veins.

Adult↗
PubMed2002

The fainting lark.

Explore the source record for details and available documents.

Cerebrovascular Circulation↗
PubMed2001

Cerebrovascular and cardiovascular responses associated with orthostatic intolerance and tachycardia.

Idiopathic orthostatic intolerance syndrome is characterized by postural symptoms of cerebral hypoperfusion without arterial hypotension. Abnormal baroreceptor responses with deranged cerebral autoregulation leading to cerebral vasoconstriction have been proposed as a causative mechanism. The authors report the cerebrovascular and cardiovascular responses in a patient who recovered from orthostatic intolerance and tachycardia. Changes in the orthostatic responses of mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and transcranial Doppler middle cerebral artery (MCA) mean blood flow velocity (Vmean) were assessed at admission and again 6 months after recovery. Normal cardiovascular responses to forced breathing and to standing indicated intact overall baroreflex integrity with normal baroreflex sensitivity (10.2 msec.mm Hg(-1)). After the patient stood for 8 minutes, presyncopal symptoms developed, with unchanged MAP but increased HR (+41 beats/min) and reduced stroke volume (SV) (-69%), CO (-50%), and MCA Vmean (-46%; 57 to 31 cm. s(-1)). After a reconditioning program and recovery, the patient was reexamined. The supine MCA Vmean was larger (79 cm. s(-1)), as were MAP (76 versus 70 mm Hg) and CO (+15%). The orthostatic HR increase was smaller (+5 beats/min), as was the reduction in SV (-44%) and CO (-30%), with an increase in MAP to 93 mm Hg. The orthostatic reduction in MCA Vmean was smaller (-13 versus -26 cm.s(-1)) and standing cerebrovascular resistance decreased (1.41 versus 2.39 mm Hg.cm. s(-1)). In this patient who had intact baroreflex control and no postural decrease in blood pressure, the reduction in MCA Vmean, concomitant with a large decrease in CO, seemed reversible. The result suggests that a symptomatic reduction in cerebrovascular conductance during standing is to be interpreted as being an adaptive response to a critically limited systemic blood flow, rather than to derangement of cerebral autoregulation.

Adult↗
PubMed2001

Comparison of the time courses and potencies of the vasodilator effects of nifedipine and felodipine in the human forearm.

In a previous study we investigated the differential time courses of the vasodilator effect of various calcium antagonists (CA) in small isolated rat mesenteric arteries (van der Lee et al., Fundam Clin Pharmacol, 1998: 12: 607-12). We concluded that the differences observed could be due to differences in lipophilicity between the CA studied. A measure for lipophilicity is the logarithm of the membrane-partition coefficient (log P). The log P values of nifedipine and felodipine are 2.50 and 4.46, respectively. It was the aim of the present study to compare the time courses of nifedipine and felodipine effects by means of forearm venous occlusion plethysmography in healthy subjects. Healthy male non-smoking volunteers (age 31 +/- 7 years, n = 14) were studied. Informed consent was obtained prior to each experiment from all subjects. The study commenced with the vehicle of either CA (NaCl 0.9% or a PEG400-solution for nifedipine and felodipine, respectively). In four subsequent runs, increasing concentrations of CA were studied for 20 min each, at an infusion rate of 0.3 ml/min. During experiments both hands were excluded from the circulation using small wrist cuffs, inflated to at least 40 mmHg over systolic blood pressure. Mean arterial pressure remained stable in all subjects (88 +/- 3 and 83 +/- 3 mmHg for nifedipine and felodipine, respectively), thus a systemic effect of the CA was not likely. Log IC50 values were -7.46 +/- 0.17 and -8.47 +/- 0.14 for nifedipine and felodipine, respectively (p < 0.01). Averaged KD values were 4.3 +/- 0.6 and 4.6 +/- 0.6 for nifedipine and felodipine, respectively (n.s.). In this model, felodipine appears to be a more potent vasodilator than nifedipine. The 100-fold difference in lipophilicity between the two CA tested is apparently not sufficient to cause major differences in K(D) values in the plethysmography experimental set-up.

Adolescent↗
PubMed2001

Muscle tensing during standing: effects on cerebral tissue oxygenation and cerebral artery blood velocity.

BACKGROUND AND PURPOSE: When standing up causes dizziness, tensing of the leg muscles may alleviate the symptoms. We tested the hypothesis that leg tensing improves orthostatic tolerance via enhanced cerebral perfusion and oxygenation. METHODS: In 10 healthy young adults, the effects of leg tensing on transcranial Doppler-determined middle cerebral artery (MCA) mean blood velocity (V(mean)) and the near-infrared spectroscopy-determined frontal oxygenation (O(2)Hb) were assessed together with central circulatory variables and an arterial pressure low-frequency (LF) (0.07 to 0.15 Hz) domain evaluation of sympathetic activity. RESULTS: Standing up reduced central venous pressure by (mean+/-SEM) 4.3+/-2.6 mm Hg, stroke volume by 49+/-7 mL, cardiac output by 1.9+/-0.4 L/min, and mean arterial pressure at MCA level by 9+/-4 mm Hg, whereas it increased heart rate by 30+/-4 beats per minute (P<0.05). MCA V(mean) declined from 67+/-4 to 56+/-3 cm/s, O(2)Hb decreased by 7+/-2.8%, and LF spectral power increased (P<0.05). Leg tensing increased central venous pressure by 1.4+/-2.7 mm Hg and cardiac output by 1.8+/-0.4 L/min with no significant effect on blood pressure, whereas heart rate decreased by 11+/-3 beats per minute (P<0.05). MCA V(mean) increased to 63+/-3 cm/s and O(2)Hb increased by 2.1+/-2.6%, whereas LF power declined (P<0.05). Within 2 minutes after leg tensing, these effects had disappeared. CONCLUSIONS: During standing, tensing of the leg muscles attenuates a reduction in cerebral perfusion and oxygenation as it stabilizes central circulatory variables and reduces sympathetic activity.

Adult↗
PubMed2001

Mechanisms underlying the impairment in orthostatic tolerance after nocturnal recumbency in patients with autonomic failure.

In the present study, we have assessed in patients with neurogenic orthostatic hypotension the haemodynamics underlying the reduced tolerance to standing after prolonged recumbency at night. In 10 patients with neurogenic orthostatic hypotension (age 33-68 years), of which seven were being treated with fludrocortisone and/or sleeping in the 12 degrees head-up tilt position, 24 h continuous non-invasive finger blood pressure was recorded by a Portapres device. Beat-to-beat blood pressure, heart rate, stroke volume, cardiac output and total peripheral vascular resistance obtained by pulse contour analysis were assessed during 5 min of standing in the evening (at 22.30 hours) and in the morning (at 06.30 hours). On average, the inverse of the normal 24 h blood pressure profile was found, with a large diversity in blood pressure profiles among patients. Supine blood pressure values were similar, but standing blood pressure values were lower in the morning than in the evening (P<0.01). This resulted from larger falls in stroke volume and cardiac output upon standing in the morning compared with the evening, while total peripheral resistance did not change. There was no relationship between the decrease in body weight during the night (mean 0.9 kg; range 0.2-1.6 kg) and the evening-morning difference in standing blood pressure. We conclude that, in patients with neurogenic orthostatic hypotension, the impaired tolerance to standing in the morning is due to larger falls in stroke volume and cardiac output. Not only nocturnal polyuria, but also a redistribution of body fluid, are likely mechanisms underlying the pronounced decreases in stroke volume and cardiac output after prolonged recumbency at night.

Adult↗
PubMed2000

Fludrocortisone and sleeping in the head-up position limit the postural decrease in cardiac output in autonomic failure.

Treatment with head-up tilt sleeping and low-dose fludrocortisone effectively minimizes orthostatic symptoms and increases orthostatic blood pressure in patients with neurogenic orthostatic hypotension. The aim of the present study was to examine whether the improvement in orthostatic blood pressure during combined treatment with low-dose fludrocortisone and nocturnal head-up tilt in patients with neurogenic orthostatic hypotension can be attributed to expansion of plasma volume or to increased total peripheral resistance. The effects of a 3-week treatment with fludrocortisone and nocturnal head-up tilting on the postural changes in arterial pressure, heart rate, and cardiac output (pulse contour) were evaluated in eight consecutive patients with orthostatic hypotension. The period during which the patients were able to remain in the standing position without orthostatic complaints increased minimally from 3 to 10 minutes. The decrease in arterial pressure after 1 minute of standing--(means with standard deviations in parentheses) systolic, 49 (20) mm Hg; diastolic, 18 (11) mm Hg--before treatment was produced by a greater than normal decrease in cardiac output: 37% (10%) in patients with neurogenic orthostatic hypotension versus -14% (8%) in control subjects. Treatment increased upright arterial pressure from 83 (19) mm Hg systolic and 55 (13) mm Hg diastolic to 114 (22) mm Hg systolic and 60 (16) mm Hg diastolic by limiting the decrease in cardiac output. Body weight increased but hematocrit did not change. Leg pressure-volume relationship decreased in the two patients studied. The responses of plasma renin activity and aldosterone to orthostatic stress prior to treatment were subnormal and became even lower after treatment. The improvement in upright blood pressure in orthostatic hypotension during treatment with fludrocortisone and nocturnal head-up sleeping is the result of a reduction in the orthostatic decrease in cardiac output. Preliminary data suggest that the expanded body fluid volume is allocated to the perivascular space rather than to the intravascular space.

Adult↗
PubMed2000

Middle cerebral artery blood velocity during a valsalva maneuver in the standing position.

Occasionally, lifting of a heavy weight leads to dizziness and even to fainting, suggesting that, especially in the standing position, expiratory straining compromises cerebral perfusion. In 10 subjects, the middle cerebral artery mean blood velocity (V(mean)) was evaluated during a Valsalva maneuver (mouth pressure 40 mmHg for 15 s) both in the supine and in the standing position. During standing, cardiac output decreased by 16 +/- 4 (SE) % (P < 0.05), and at the level of the brain mean arterial pressure (MAP) decreased from 89 +/- 2 to 78 +/- 3 mmHg (P < 0.05), as did V(mean) from 73 +/- 4 to 62 +/- 5 cm/s (P < 0.05). In both postures, the Valsalva maneuver increased central venous pressure by approximately 40 mmHg with a nadir in MAP and cardiac output that was most pronounced during standing (MAP: 65 +/- 6 vs. 87 +/- 3 mmHg; cardiac output: 37 +/- 3 vs. 57 +/- 4% of the resting value; P < 0.05). Also, V(mean) was lowest during the standing Valsalva maneuver (39 +/- 5 vs. 47 +/- 4 cm/s; P < 0.05). In healthy individuals, orthostasis induces an approximately 15% reduction in middle cerebral artery V(mean) that is exaggerated by a Valsalva maneuver performed with 40-mmHg mouth pressure to approximately 50% of supine rest.

Adult↗
PubMed2000

Orthostatic tolerance, cerebral oxygenation, and blood velocity in humans with sympathetic failure.

BACKGROUND AND PURPOSE: Patients with orthostatic hypotension due to sympathetic failure become symptomatic when standing, although their capability to maintain cerebral blood flow is reported to be preserved. We tested the hypothesis that in patients with sympathetic failure, orthostatic symptoms reflect reduced cerebral perfusion with insufficient oxygen supply. METHODS: This study addressed the relationship between orthostatic tolerance, mean cerebral artery blood velocity (V(mean), determined by transcranial Doppler ultrasonography), oxygenation (oxyhemoglobin [O(2)Hb], determined by near-infrared spectroscopy), and mean arterial pressure at brain level (MAP(MCA), determined by finger arterial pressure monitoring [Finapres]) in 9 patients (aged 37 to 70 years; 4 women) and their age- and sex-matched controls during 5 minutes of standing. RESULTS: Supine MAP(MCA) (108+/-14 versus 86+/-14 mm Hg) and V(mean) (84+/-21 versus 62+/-13 cm. s(-1)) were higher in the patients. After 5 minutes of standing, MAP(MCA) was lower in the patients (31+/-14 versus 72+/-14 mm Hg), as was V(mean) (51+/-8 versus 59+/-9 cm. s(-1)), with a larger reduction in O(2)Hb (-11. 6+/-4 versus -6.7+/-4.5 micromol. L(-1)). Four patients terminated standing after 1 to 3.5 minutes. In these symptomatic patients, the orthostatic fall in V(mean) was greater (45+/-6 versus 64+/-10 cm. s(-1)), and the orthostatic decrease in O(2)Hb (-12.0+/-3.3 versus -7.6+/-3.9 micromol. L(-1)) tended to be larger. The reduction in MAP(MCA) was larger after 10 seconds of standing, and MAP(MCA) was lower after 1 minute (25+/-8 versus 40+/-6 mm Hg). CONCLUSIONS: In patients with sympathetic failure, the orthostatic reduction in cerebral blood velocity and oxygenation is larger. Patients who become symptomatic within 5 minutes of standing are characterized by a pronounced orthostatic fall in blood pressure, cerebral blood velocity, and oxygenation manifest within the first 10 seconds of standing.

Adult↗
PubMed1999

Estimation of beat-to-beat changes in stroke volume from arterial pressure: a comparison of two pressure wave analysis techniques during head-up tilt testing in young, healthy men.

OBJECTIVE: The aim of this study was to compare beat-to-beat changes in stroke volume (SV) estimated by two different pressure wave analysis techniques during orthostatic stress testing: pulse contour analysis and Modelflow, i.e., simulation of a three-element model of aortic input impedance. METHODS: A reduction in SV was introduced in eight healthy young men (mean age, 25; range, 19-32 y) by a 30-minute head-up tilt maneuver. Intrabrachial and noninvasive finger pressure were monitored simultaneously. Beat-to-beat changes in SV were estimated from intrabrachial pressure by pulse contour analysis and Modelflow. In addition, the relative differences in Modelflow SV obtained from intrabrachial pressure and noninvasive finger pressure were assessed. RESULTS: Beat-to-beat changes in Modelflow SV from intrabrachial pressure were comparable with pulse contour measures. The relative difference between the two methods amounted to 0.1+/-1% (mean +/- SEM) and was not dependent on the duration of tilt. The difference between Modelflow applied to intrabrachial pressure and finger pressure amounted to -2.7+/-1.3% (p = 0.04). This difference was not dependent on the duration of tilt or level of arterial pressure. CONCLUSIONS: Based on different mathematical models of the human arterial system, pulse contour and Modelflow compute similar changes in SV from intrabrachial pressure during orthostatic stress testing in young healthy men. The magnitude of the difference in SV derived from intrabrachial and finger pressure may vary among subjects; Modelflow SV from noninvasive finger pressure tracks fast and brisk changes in SV derived from intrabrachial pressure.

Adult↗
PubMed1999

Continuous cardiac output in septic shock by simulating a model of the aortic input impedance: a comparison with bolus injection thermodilution.

BACKGROUND: To compare continuous cardiac output obtained by simulation of an aortic input impedance model to bolus injection thermodilution (TDCO) in critically ill patients with septic shock. METHODS: In an open study, mechanically ventilated patients with septic shock were monitored for 1 (32 patients), 2 (15 patients), or 3 (5 patients) days. The hemodynamic state was altered by varying the dosages of dopamine, norepinephrine, or dobutamine. TDCO was estimated 189 times as the series average of four automated phase-controlled injections of iced 5% glucose, spread equally over the ventilatory cycle. Continuous model-simulated cardiac output (MCO) was computed from radial or femoral artery pressure. On each day, the first TDCO value was used to calibrate the model. RESULTS: TDCO ranged from 4.1 to 18.2 l/min. The bias (mean difference between MCO and TDCO) on the first day before calibration was -1.92 +/- 2.3 l/min (mean +/- SD; n = 32; 95% limits of agreement, -6.5 to 2.6 l/min). The bias increased at higher levels of cardiac output (P < 0.05). In 15 patients studied on two consecutive days, the precalibration ratio TDCO:MCO on day 1 was 1.39 +/- 0.28 (mean +/- SD) and did not change on day 2 (1.39 +/- 0.34). After calibration, the bias was -0.1 +/- 0.8 l/min with 82% of the comparisons (n = 112) < 1 l/min and 58% (n = 79) < 0.5 l/min, and independent of the level of cardiac output. CONCLUSIONS: In mechanically ventilated patients with septic shock, changes in bolus TDCO are reflected by calibrated MCO over a range of cardiac output values. A single calibration of the model appears sufficient to monitor continuous cardiac output over a 2-day period with a bias of -0.1 +/- 0.8 l/min.

Adult↗