Elastase-induced aneurysms in rabbits: effect of postconstruction geometry on final size.

BACKGROUND AND PURPOSE: Elastase-induced aneurysms in rabbits have become an accepted model to study endovascular treatment. The size and shape of the resulting aneurysms may vary widely. Our goal was to predict the final aneurysm morphology on the basis of immediate postinduction geometry. METHODS: Thirty New Zealand white rabbits were used. Aneurysms were created at the origin of the right common carotid artery (CCA). Intraluminal incubation of elastase was applied to the origin of CCA with proximal balloon occlusion of the artery. The aneurysms were allowed to mature for 3 weeks and evaluated by digital subtraction angiography. We retrospectively measured neck diameter, dome height, and aneurysm diameter, as well as the angle between the parent artery and the main axis of the aneurysm neck. We performed correlation analysis with immediate postinduction geometry. RESULTS: The diameter of the origin of the CCA measured immediately after elastase incubation correlated positively to the mature aneurysm neck (P < .01). Moreover, the aneurysm neck both after the aneurysm creation and at 3-week follow-up had a positive correlation with the final dome height (P < .05). Finally, the dome height was related to the angle between the centerline of the innominate artery and axis of the aneurysm neck for dome diameter-to-neck ratio of <1.5 (P < .05). CONCLUSION: These results indicate that neck width immediately after creation and the curvature of the parent artery are linked to the final aneurysm dimensions, and we may be able to predict the size of aneurysm on the day of creation.

Acute and chronic swine rete arteriovenous malformation models: effect of ethiodol and glacial acetic acid on penetration, dispersion, and injection force of N-butyl 2-cyanoacrylate.

BACKGROUND AND PURPOSE: Liquid embolic agents are increasingly gaining importance in the embolization of cerebral arteriovenous malformations (AVMs). Currently, the most commonly used agent is N-butyl 2-cyanoacrylate (NBCA). Various NBCA mixtures, arterial hypotension, and Valsalva maneuver (increased positive end-expiratory pressure) during the injection of the acrylate have been used to address hemodynamic and architectural variations of an AVM; however, the precise in vivo polymerization, distribution, and kinetics of NBCA mixtures are unknown. We investigated the effect of different acrylate/Lipiodol mixtures and the addition of glacial acetic acid (GAA) on the penetration, dispersion, and injection force of NBCA. METHODS: A swine rete AVM model that has been described elsewhere was used for the embolization. In one subgroup of animals, embolization was performed immediately after construction of the AVM model. In a second subgroup, a chronic AVM model was used. GAA was added to the NBCA mixture to decrease the pH value of the solution and prolong the polymerization time. The addition of GAA allowed us to reduce the amount of Lipiodol, thereby reducing the viscosity of the mixture. A total of 30 swine were used for both the acute (n = 23) and chronic (n = 7) subgroups. The following mixtures of Lipiodol/NBCA and GAA (% vol/%vol + microL) were used for embolization: 80/20 + 0; 50/50 + 0; 50/50 + 5; 50/50 + 10; and 50/50 + 20. A total of six retia per mixture were used for the analysis. Glue injection pressure profiles were recorded in each experiment. High-resolution radiographic images obtained from the harvested retia were used to correlate the dispersion and depth of glue penetration with the AVM hemodynamics. The effect of different amounts of GAA on the glue dispersion and depth of penetration of the mixtures was also studied. RESULTS: Using the same pressure gradients, less viscous NBCA + GAA mixtures led to a deeper nidal penetration. The addition of 20 microL of GAA resulted in a three times higher penetration and dispersion of the NBCA mixture that was more homogenous. CONCLUSION: The viscosity of the liquid embolic agent used is an important limiting factor for an AVM embolization. Reducing the amount of Lipiodol improves nidus penetration. Quicker polymerization can be overcome by adding GAA, which reduces the pH of the mixture.

Acute and chronic swine rete arteriovenous malformation models: hemodynamics and vascular remodeling.

BACKGROUND AND PURPOSE: An acute and a chronic arteriovenous malformation (AVM) model were developed by using the swine rete to study hemodynamics and vascular remodeling. The models were also used to study in vivo polymerization kinetics and the distribution of various N-butyl 2-cyanoacrylate (NBCA) and Lipiodol mixtures. METHODS: In the acute swine AVM model, retrograde flow through the left side of the rete was created by the placement of an endovascular shunt through the ipsilateral ascending pharyngeal artery. In the chronic model, flow was redirected retrograde through the left side of rete and ascending pharyngeal artery by creating an arteriovenous fistula between the ipsilateral jugular vein and the common carotid artery. After a period of at least 6 months, the entire head with the rete was connected to a perfusion loop driven by a peristaltic pump. A total of 30 swine were used for both the acute (n = 23) and chronic groups (n = 7). Hemodynamic parameters, including the flow and pressure drop across the rete, were recorded before NBCA embolization. Image processing was used on high-resolution radiographs of the explanted retia to measure the total rete length. Measurements of rete vessel calibers were based on histology. RESULTS: The pressure gradients across retia were higher in the chronic model than in the acute model, but they did not reach the level of statistical significance (23.7 +/- 12.0 mm Hg vs 15.4 +/- 1.4 mm Hg). The rete blood outflow was significantly higher in the chronic model compared with the acute one (139.9 +/- 100.3 mL/min vs 32.5 +/- 17.6; P = .03). The rete length in the chronic model was significantly higher than in the acute model (593.1 +/- 39.9 vs 401.3 +/- 65.2 pixel; P < .001). The average vessel diameter of the rete in the chronic group was 520 microm and 320 microm in the control animals. CONCLUSION: Increased pressure gradients and flow in the chronic swine rete AVM model may be related to increased size and decreased impedance. The resulting hemodynamic changes reflect a true flow-induced vascular remodeling rather than a simple change related to aging and size of the animal.

Compliance of the main pulmonary artery during the ventilatory cycle.

Transmural pulmonary arterial pressure (Ppa), diameter (D), and length (L) of a segment of the main pulmonary artery (MPA) were measured simultaneously in anesthetized open-chest dogs. The instantaneous volume was calculated from D and L. Pulmonary arterial elasticity for diameter (EpD) was calculated as the ratio of the amplitude of Ppa to D oscillation normalized by the mean D. Similar indexes were calculated for L (EpL) and V (Epv). Compliance per unit length was calculated from the dimensions and elasticity of the MPA. Under control conditions with 5 cmH2O positive end-expiratory pressure, EpD, EpL, and Epv at cardiac frequency were 175 +/- 27, 147 +/- 27, and 55 +/- 7 cmH2O, respectively. EpD increased with positive end-expiratory pressure, but EpL decreased and Epv was unaffected. EpD, EpL, Epv, and compliance per unit length were not significantly different between the start of inspiration and the start of expiration. In addition, there were no significant phase differences between the oscillations of Ppa and V at respiratory frequency. We conclude that the previously reported time variation of pulmonary arterial compliance during the ventilatory cycle is not due to time-varying properties of the MPA.

Time-varying pulmonary arterial input impedance via wavelet decomposition.

Wavelet decomposition is proposed as a novel approach for determining pulmonary arterial input impedance throughout the breathing cycle. The canine pulmonary arterial input impedance was evaluated throughout the ventilatory cycle at 5, 10, and 15 cmH2O of positive end-expiratory pressure. The impedance spectrum was obtained by Fourier transformation of wavelets generated by decomposing the pulmonary arterial pressure and flow waveforms. With wavelet decomposition, each heart beat is viewed individually as a transient pulse rather than as an interval within a continuous function of pressure and flow. The advantage of using this approach is the ability to obtain stable estimates of input impedance spectra with high-frequency resolution over the entire frequency range with only a limited data set of pressure and flow decomposed to wavelets as short as singular extrapolated cardiac cycles. This method was used to define the changes of input impedance that occur during the ventilatory cycle. Results show that the impedance spectrum undergoes notable changes during the breathing cycle and demonstrate the utility of the proposed method.

Beat-by-beat changes of viscoelastic and inertial properties of the pulmonary arteries.

We tested the hypothesis that pulmonary arterial input impedance varies during the ventilatory cycle due to alterations not only of the viscoelastic components of the pulmonary vasculature but also due to changes of the inertial components. A four-element lumped-parameter model was used to fit the pulmonary arterial pressure-flow recordings in the time domain in 10 anesthetized dogs. The four elements consisted of a resistor (R) that represents input resistance, a second resistor (R1) and a capacitor (C1) that represent the viscoelastic properties of the pulmonary vasculature, and an inductor (L1) that represents inertial properties of blood within the pulmonary vasculature. The parameters were evaluated at each heartbeat throughout the ventilatory cycle at three levels of positive end-expiratory pressure. All four parameters varied significantly during the ventilatory cycle. R, C1, L1, and R1 varied by up to 97, 33, 13, and 17%, respectively. Changes in parameter values were most apparent at the start of expiration when the most rapid changes of lung volume occur. This pattern of the results is consistent with the hypothesis that the time variation of pulmonary arterial impedance is due to dynamic shifts of blood volume between the extra-alveolar and alveolar arteries.

Time-varying pulmonary arterial compliance.

We tested the hypothesis that pulmonary arterial compliance (Ca) varies during the ventilatory cycle. Pressure and flow in the main pulmonary artery were measured in open-chest dogs under chloralose anesthesia (n = 12) with a positive-pressure volume-cycled ventilator. Input impedance was calculated from the pressure and flow waves of heart cycles obtained immediately after the start of inspiration (SI) and immediately after the start of expiration (SE). A lumped parameter model was used to calculate Ca from the input impedance spectrum of the main pulmonary artery. Three levels of positive end-expiratory pressure (PEEP) were used before and after meclofenamate (n = 6) or vagotomy (n = 6). Ca was significantly greater at SE than at SI at each level of PEEP. PEEP increased Ca at SE but not at SI. None of these changes was altered by meclofenamate or vagotomy, suggesting that these differences of Ca were due to passive mechanical effects rather than an active neurohumoral mechanisms. We conclude that Ca is time varying during the ventilatory cycle because it is altered by the dynamic increase of lung volume between SI and SE, but not with the quasi-static increase of lung volume induced by raising the level of PEEP. These changes of Ca were unaffected by vagal feedback or inhibition of cyclooxygenase. We suggest that the increased Ca just after the start of expiration may result from dynamic shifts of blood volume from the extra-alveolar to the alveolar vessels.

Self-expanding nitinol stents in canine vertebral arteries: hemodynamics and tissue response.

PURPOSE: To evaluate the hemodynamics and tissue response associated with stent placement in low-flow-velocity arteries. METHODS: Six self-expanding nitinol stents (5.5 mm caliber) were implanted transfemorally within the proximal segments of vertebral arteries (2.5 mm diameter) in six adult dogs during anticoagulative protection. RESULTS: Control angiograms demonstrated patency and 20% dilatation of all stented arteries. One artery was partially thrombosed 1 week later and subsequently showed a 50% stenosis. Throughout the observation period (4 to 9 months after stenting), the other five arteries remained patent without significant narrowing (< or = 15%). Small cervical muscle branches originating from the vertebral arteries within the stented segments remained patent. No major branch occlusions of the vertebrobasilar system were detected. Stent migration or kinking did not occur. MR studies of the brain 4 months after implantation revealed no infarcted areas. These findings were confirmed with brain sections. Stented artery specimens showed delayed stent dilatation. A comparison of the total mean thickness of intima covering the five 30- to 40-mm stents removed at 4, 6, and 9 months showed no significant difference (338, 332, and 389 microns, respectively). Histologic findings verified the macroscopic impression of a thicker intima at the inner curve of the stented artery segments and at the junctions of the stent filaments. The shortest (10 mm) stent had the thinnest neointimal growth (155 microns). Stented vessels showed compression of the media with atrophy, but without necrosis or perforation. Scanning electron photomicrographs revealed intact endothelial cell linings with typical elongated cells. CONCLUSIONS: No significant risk of thromboembolic events exists after implanting these nitinol stents in nonatherosclerotic vertebral arteries in dogs. Thicker neointimal growth after stenting may result from either low wall shear stress with possible flow separation or from changes in the shape and size of the stent, or both.

Europium fluorescence to visualize N-butyl 2-cyanoacrylate in embolized vessels of an arteriovenous malformation swine model.

BACKGROUND AND PURPOSE: Standard tissue staining using the lipid dye Oil-Red-O has been previously applied to stain vessel specimens, which were embolized with a mixture of n-butyl 2-cyanoacrylate (NBCA) and oil (Lipiodol). That technique, however, results in nonspecific and nonquantitative staining that does not provide the necessary differentiation between NBCA and Lipiodol. We present an innovative staining procedure that quantifies NBCA within treated tissues. METHODS: An arteriovenous malformation (AVM) model in swine was used to evaluate the polymerization characteristics of various ratios of Lipiodol/NBCA/glacial acetic acid (GAA) mixtures. To determine the depth of NBCA penetration within the AVM model and to characterize the polymerization patterns of various mixtures within the vessel, histologic cross- and longitudinal sections were prepared for microscopy. These paraffin-embedded tissue sections were stained with a europium aryl-beta-diketone complex (TEC) to improve differentiation between NBCA and Lipiodol. Quantification of NBCA and Lipiodol within the lumen of rete cross-sections was accomplished using image analysis software to determine percent luminal area occluded by embolization. RESULTS: Upon application of TEC, intense europium fluorescence was seen when the tissue samples were excited by low-power UV light (excitation at 365 nm; emission at 614 nm). The area of europium intensity within the lumen corresponded to NBCA concentration, and addition of GAA aided the NBCA distribution throughout the lumen without affecting fluorescence intensity. It was seen that NBCA could be easily differentiated from Lipiodol and that quantification could be readily performed on these sections because of the improved differentiation. For the case of a 50:50 (vol. %) mixture with an added 20 microL of GAA, luminal area distribution of Lipiodol, NBCA, and blood products was 42.6 +/- 3.5%, 33.8 +/- 5.7%, and 23.7 +/-2.7%, respectively. CONCLUSION: The rare earth metal europium, when added as a fluorescent chelate compound to histologic tissue sections, allowed for differentiation between NBCA and Lipiodol with good detail. These results have facilitated further characterization of NBCA polymerization for the use of AVM embolization.

Modification of a previously described arteriovenous malformation model in the swine: endovascular and combined surgical/endovascular construction and hemodynamics.

BACKGROUND AND PURPOSE: The rete mirabile in swine has been proposed as an arteriovenous malformation (AVM) model for acute experimental studies through surgical creation of a large carotid-jugular fistula. This report describes two endovascular modifications to simplify the surgical creation and provides hemodynamic parameters for the AVM model. METHODS: An AVM model was created in 29 animals to study n-butyl 2-cyanoacrylate polymerization kinetics. The common carotid artery (CCA) was punctured and a guiding catheter was inserted tightly into the origin of the ascending pharyngeal artery (APA). The CCA was ligated proximal to the catheter to create a pressure drop across the rete, which represented the AVM nidus. The catheter hub was opened whenever needed and served as the venous drainage of the AVM nidus. The contralateral APA served as the arterial feeder. Instead of the surgical ligation of the CCA, a temporary balloon occlusion was performed in three animals. RESULTS: A mean pressure gradient of 14.9 +/- 10.5 mm Hg (range, 4-42 mm Hg) was measured across the rete. The mean flow rate was 30.4 +/- 14.2 mL/min (range, 3.5-46 mL/min), as measured at the venous drainage. CONCLUSION: The endovascular and combined surgical-endovascular rete AVM model in swine is easy to construct and is less time-consuming than are the currently used models for acute experimental studies. Hemodynamic parameters can be monitored during the entire experiment and correspond to values found in human cerebral AVMs.

Microdroplet tracking using biplane digital subtraction angiography for cerebral arteriovenous malformation blood flow path and velocity determinations.

High-speed biplane angiography is used to determine the path and velocity of microdroplets of contrast material in three dimensions. By allowing more accurate determination of detailed blood flow in feeding vessels and draining veins of cerebral arteriovenous malformations than available with standard angiography, the new method offers the potential for more accurate treatment and further study of neurovascular/cerebrovascular hemodynamics. The first study of the method is presented.

A novel approach to flow quantification in brain arteriovenous malformations prior to enbucrilate embolization: use of insoluble contrast (Ethiodol droplet) angiography.

OBJECT: Successful therapeutic embolization of arteriovenous malformations (AVMs) of the brain with liquid polymers (glues) requires precise knowledge of highly variable AVM structure and flow velocities and transit times of blood through the AVM nidus. The goal of this study was to improve AVM flow measurement and visualization by the substitution of the insoluble Ethiodol (ethiodized oil) contrast agent for the soluble contrast media normally used in angiographic studies. METHODS: Before enbucrilate embolization of 24 AVM feeding pedicles in 13 patients, standard contrast medium was superselectively injected into each target pedicle, followed by infusion of 20 microl of Ethiodol microdroplets. Transport of contrast material was assessed using high-speed biplane pulsed digital subtraction angiography (DSA) operating at 15 frames per second. The mean blood flow transit times through AVMs after administration of Ethiodol were found to be approximately half as long as in those measured after injection of soluble contrast materials (0.22 +/- 0.10 seconds compared with 0.46 +/- 0.19 seconds [mean +/- standard deviation]; p < 0.0001). The discrete Ethiodol microdroplets travel with the core flow, more closely approximating the dynamic behavior of enbucrilate, allowing the AVM structure to be traced with high spatial and temporal resolution. There were no inadvertent vessel occlusions or pulmonary complications related to the use of Ethiodol for DSA. CONCLUSIONS: Because of diffusion and convection, forces that decrease concentration, visualization of the contrast front is reduced, often resulting in deceptively long transit times when soluble contrast materials are used. Overestimation may prove dangerous when planning embolizations. The Ethiodol droplet DSA method provides accurate transit time measurements and precise, detailed, and dynamic AVM visualization. Further development of this method will improve the safety and precision of AVM treatments.

The decomposition of apparent stresses in disturbed pulsatile flow in the presence of large scale organized structures.

Flow disturbance phenomena that occur in unsteady-in-the-mean flows (i.e. pulsatile or oscillating) at moderate Reynolds numbers are analyzed in both the time domain and the frequency domain. The analysis utilizes variable decomposition into a time-varying underlying waveform and flow disturbances which are composed of large scale organized structures and random fluctuations. A practical technique which incorporates time domain phase conditioning, trend removal, and frequency domain matched filtering, is presented and examined using simulated data of known statistical behavior. The applicability of the method is shown by the decomposition of the simulated data and the technique is then applied to experimental data obtained in pulsatile flow through a constricted tube by means of a laser Doppler anemometer. The cross-sectional area reduction at the constriction throat was 90%. The Womersley parameter in the experiments was 5.3 and the Reynolds number based on the average flow rate per cycle was 300 with a minimum/maximum value of 55/600 based on the instantaneous flow rate. Measurements were taken in the flow region downstream of the constriction throat which included several interesting flow disturbance phenomena. The results of the decomposed flow phenomena demonstrate the significant role of large scale organized structures in such flows. This is particularly important when analyzing blood flow in the large arteries in the presence of severe stenosis or behind prosthetic devices in an attempt to estimate the 'turbulent' stress which act on cellular elements. Estimation of the apparent stress tensor is of importance in an effort to elucidate the mechanical factors which influence the durability of red blood cells under abnormal conditions.

Apparent stresses in disturbed pulsatile flows.

Traditional attempts at decomposing measured velocities into repeatable and random components are examined for a set of velocity data measured under pulsatile flow conditions distal to a 90% axisymmetric constriction. The Reynolds numbers, which are typical of those found in the human carotid artery, are such that transitional phenomena occur during portions of the pulsatile cycle at several axial stations. The implications of the method selected for velocity decomposition upon the computation of fluctuating or 'apparent' stresses is a point of major focus. It is shown that the usual estimation of Reynolds stresses in a pulsatile flow by subtracting the ensemble-averaged velocity from the instantaneous velocity leads to an underestimation of the apparent stress when coherent or repeatable disturbances exist in the flow. An alternative decomposition using a frequency domain approach is presented which combines both random and coherent stresses into a single apparent stress, and it is proposed that this approach is preferable to the traditional ensemble averaging method when estimating fluctuating stresses in arterial flows.

Post-stenotic core flow behavior in pulsatile flow and its effects on wall shear stress.

Arteries of several species, including man, tend to adjust their diameters such that the mean wall shear stress is in the range of 10-20 dynes cm-2. Additionally, intimal thickening in the human carotid bifurcation correlates well with the reciprocal of wall shear stress as determined in model studies. The correlation indicates that wherever the local mean wall shear stress exceeds approximately 10 dynes cm-2, the artery tends to be spared from intimal thickening. However, it is not known whether mean shear stress, i.e. the time-averaged value, or the instantaneous shear stress is the appropriate correlative variable. Each of these variables suggests different mechanisms for the reaction of the artery wall to its hemodynamic environment. It is therefore important to devise means by which the effects of mean shear and pulsatile shear can be separated in the study of atherogenesis. The present investigation examines the post-stenotic flow field in Plexiglas models under pulsatile conditions approximating those in the aortas of the cynomolgus monkey, an animal often employed in atherogenesis research. Behavior of the core flow and its effects on wall shear stress are studied for stenoses of 75 and 90% area reductions using laser velocimetry. The results show that the post-stenotic field contains regions in which the mean wall shear stress is low, but the pulsatile excursions are large.(ABSTRACT TRUNCATED AT 250 WORDS)

The utility of neural network in the diagnosis of Cheyne-Stokes respiration.

The aim of this study was to design a diagnostic model to identify patients with Cheyne-Stokes respiration (CSR-CSA) based on indices of oximetric spectral analysis. A retrospective analysis of oximetric recordings of 213 sleep studies conducted over a one-year period at a Veterans Affairs medical facility was performed. A probabilistic neural network (PNN) was developed from salient features of the oximetric spectral analysis, desaturation events and the delta index. A fivefold cross-validation was used to assess the accuracy of the neural network in identifying CSR-CSA. When compared to overnight polysomnography, the PNN achieved a sensitivity of 100% (95% confidence interval [CI] 85%-100%) and a specificity of 99% (95% 97%-100%) with a corresponding area under the curve of 99% (95% CI 99%-100%). When combined with overnight pulse oximetry, PNN offers an accurate and easily applicable tool to detect CSR-CSA.

Angiogenesis is confined to the transient period of VEGF expression that follows adenoviral gene delivery to ischemic muscle.

Therapeutic angiogenesis involves the introduction of exogenous growth factor proteins and genes into ischemic tissues to augment endogenous factors and promote new vessel growth. Positive results from studies in animal models of peripheral arterial disease (PAD) and coronary artery disease over the past decade have supported the implementation of clinical trials testing vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) proteins and genes. Although several clinical trials reported positive results, others have been disappointing and results of a recent Phase II trial of VEGF delivered by adenovirus (the RAVE trial) were negative. It has been suggested that the duration of gene expression following delivery by adenovirus may be insufficient to produce stable vessels. Here we present direct evidence in support of this using the rabbit ischemic hindlimb model injected with adenovirus encoding VEGF165. Immunohistology indicated an activation of endothelial cell cycling and proliferation 2-3 days after VEGF delivery that coincided closely with transient VEGF expression. Ki-67-positive endothelial nuclei were evident at high levels in capillaries and large vessels in muscles from treated animals. Angiography indicated increased density of both large and small vessels in Ad-VEGF-treated muscle at 1 week, but no significant differences thereafter. The early burst of endothelial proliferation was accompanied by increased nuclear fragmentation and condensation in VEGF-treated muscles, suggesting coincident apoptosis. No further endothelial cell proliferation took place after 1 week although there was still evidence of apoptosis. The results suggest that angiogenesis is confined to the short period of VEGF expression produced by adenovirus and early gains in collateralization rapidly regress to control levels when VEGF production ceases.

Estimation of organ transport function: model-free deconvolution by recursive quadratic programming optimization.

A model-free deconvolution method is proposed for evaluating the frequency distribution function of organ transit times. The deconvolution is treated as a nonlinear constrained optimization problem and it is solved by using a modified constrained variable metric approach. The only constraint implemented in the solution is that all the discrete transport function values are not allowed to become negative. The method is tested on model mathematical systems of known analytical transport functions. The tests are performed on systems that included noise in both the input and output functions. The criteria of successful deconvolution are the reconvolution error and, most importantly, the deviation of the computed transport function from the known analytical one. The proposed method is then applied, as a pilot experiment, to biological data obtained from an isolated, perfused rabbit lung preparation contained within a plethysmograph. The results indicate that this type of deconvolution produces stable estimates which faithfully follow the analytical function while negating the need to assume either any functional form for the behavior of the transport function or any educated initial guess of its values.

Oscillatory flow in a symmetric bifurcation airway model.

Flow in a symmetric bifurcation model of analytically known geometry was investigated experimentally under oscillatory flow conditions. The duration of the inspiratory and expiratory phases were set to be equal during the oscillatory period. A two velocity component laser Doppler anemometer was used to interrogate the flow field. Three different flow rates through the bifurcation were investigated. The peak Reynolds numbers, based on peak flow rates, were 700, 1278, and 2077. The Womersley number was set to 4.3 and it was kept at the same value for the three different flow rates. The results suggest that under the conditions studied a quasisteady flow assumption for oscillatory flow is valid for only about 50% of the oscillatory period, or it is limited to represent the oscillatory flow only in the vicinity of peak inspiration and peak expiration. Complex transport phenomena that occur during the transition between the respiratory phases cannot be elucidated and analyzed by quasisteady equivalents.