Biomedical subjects

F Kajiya

Publications and source records attributed to F Kajiya.

At least 19 recordsLinked to original sources

PubMed2004

Regional myocardial perfusion under exchange transfusion with liposomal hemoglobin: in vivo and in vitro studies using rat hearts.

The purpose of this study was to test the hypothesis that exchange transfusion with liposomal hemoglobin (LH) reduces the microheterogeneity of regional myocardial flows while sustaining cardiac function. Neo Red Cell mixed with albumin was used as the LH solution, in which the LH volume fraction was 17 approximately 18% and hemoglobin density was nearly two-thirds smaller than in rat blood. Regional myocardial flows in left ventricular free walls were measured by tracer digitalradiography (100-mum resolution) in anesthetized rats with or without 50% blood-LH exchange transfusion. Within-layer flow distributions showed lower heterogeneity with (n = 8) than without (n = 8) LH transfusion. No extravasation of hemoglobin was confirmed by 3,3-diaminobenzidin staining (n = 2). Carotid flow increased by 68% due to LH transfusion, whereas arterial pressure and heart rate remained unchanged. On the other hand, cross-circulated rat hearts (n = 7) were used to evaluate the effects of 50% blood-LH exchange on coronary flow and tone preservation under 300-beats/min pacing and 100-mmHg perfusion pressure. Blood-LH exchange caused a 71% increase of coronary flow and 10% decrease of percent flow increase during hyperemia after 30-s flow interruption. Myocardial O(2) supply and consumption increased by 9% and 10%, respectively, whereas myocardial O(2) extraction remained unchanged. The large increases of in vivo carotid flow and coronary flow in cross-circulated hearts due to LH coperfusion could be explained by the reduction of apparent flow viscosity. These results suggest that under LH coperfusion, the microheterogeneity of myocardial flows decreases with increased coronary flow while fairly preserving coronary tone and cardiac function.

Animals↗

PubMed2004

Load independence of temperature-dependent Ca2+ recirculation fraction in canine heart.

Intramyocardial Ca(2+) recirculation fraction (RF) critically determines the economy of excitation-contraction coupling. RF is obtainable from the exponential decay of the postextrasystolic potentiation of left ventricular (LV) contractility. We have shown that RF remains unchanged despite increasing LV volume (LVV) at normothermia, but decreases with increasing temperature at a constant LVV. However, it remains unknown whether the temperature-dependent RF was not due to the simultaneously changed peak LV pressure (LVP) at a constant LVV. We hypothesized that this temperature-dependent RF would be independent of the simultaneous change in LVP. We used nine excised, cross-circulated canine hearts and allowed their LVs to contract isovolumically. During stable regular beats at 500 msec intervals, we inserted an extrasystolic beat at 360 msec interval followed by the postextrasystolic beats (PESs) at 500 msec intervals. We equalized the temperature-dependent peak LVPs of the regular beats at 36 degrees C and 38 degrees C to the peak LVP level of the stable regular beat at 33 degrees C by adjusting LVV. We fitted the same equation: nEmax = a.exp[-(i - 1)/tau(e)] + b.exp[-(i - 1)/tau(s)]cos[pi(i - 1)] + 1, used before to the normalized Emax (maximum elastance) values of PESi (i = 1-6) relative to the regular beat Emax. RF given by exp(-1/tau(e)) decreased by 19% to 38 degrees C from 33 degrees C. The temperature coefficient (Q(10)) of 1/RF was significantly greater than 1.3. The present results indicated a similar temperature dependence of RF and its Q(10) to those we observed previously without equalizing peak LVP. Thus, the temperature-dependent RF is independent of ventricular loading conditions.

Animals↗

PubMed2004

Arterial and left ventricular pressures illude transient alternans of contractility during postextrasystolic potentiation.

We have previously found that the postextrasystolic (PES) potentiation (PESP) of the left ventricular (LV) contractility (Emax) decays typically in transient alternans even in the normally ejecting canine heart. This contradicted the general expectation that arterial pressure (AP) and LV pressure (LVP) usually decay exponentially during PESP. We hypothesized this contradiction to be due to the different cardiodynamic behaviors of AP and LVP from LV Emax during PESP. We tested this hypothesis by measuring AP, LVP, LV volume, Emax, effective arterial elastance (Ea) as an index of afterload, and pulse pressure (PP) during PESP in eight anesthetized open-chest dogs by using the conductance catheter system. We changed Ea by changing the total peripheral resistance (TPR) with methoxamine hydrochloride (iv) and repeated the measurements. Although the Emax alternans patterns during PESP were comparable between the normal and high afterloads, LVP and PP were slightly potentiated and alternated under the normal afterload, whereas LVP and PP were obviously potentiated and alternated under the high afterload. We also simulated the effects of Ea/Emax on the transient alternans of AP and LVP on a computer. Despite the same alternans pattern of Emax, a higher Ea/Emax, which is typical in heart failure, caused a larger PP alternans, whereas a lower Ea/Emax, which is typical in normal hearts, almost eliminated it. These results suggest that a transient alternans of LV contractility during PESP could be overlooked when AP and LVP are monitored in in situ normal hearts.

Animals↗

PubMed2001

Microheterogeneity of myocardial blood flow.

Myocardial blood flow exhibits the most marked heterogeneity at the microvascular level. Its within-layer spatial distribution can be described from subepi- to subendocardium with resolutions of 0.1 x 0.1 to 1 x 1 mm2 by quantitative digital radiography based on the technique of desmethylimipramine deposition. In the subendocardium, flow heterogeneity is the highest, whereas local flow randomness is the lowest, showing the clustered pattern of high- or low-flow regions. The resolution-dependence of flow heterogeneity is characterized by its fractality, which holds consistently down to the microvascular level through the vascular structural transition from the treelike arteriolar to the non-treelike capillary network. Flow heterogeneity is adjustable in a transmurally different manner to local metabolic changes. The redistribution of flow is considered as a result of adaptive coordination of microperfusion between adjacent microcirculatory units, which are perfused by a single precapillary arteriole.

Animals↗

PubMed2001

In vivo visualization of angiotensin II- and tubuloglomerular feedback-mediated renal vasoconstriction.

BACKGROUND: A noninvasive technique to monitor renal microcirculation would be a useful tool for investigation of renal disease and the effects of drugs on the renal system. We have developed a novel, less invasive technique to visualize renal microcirculation in vivo using an intravital tapered-tip (1 mm phi) lens-probe (pencil lens-probe) videomicroscopy, which only requires insertion of the probe into superficial renal cortex in situ. METHODS: To assess validity of this technique, the effects of angiotensin II (Ang II) and intrarenal sodium chloride loading (activator of tubuloglomerular mechanism) were examined. The renal microvasculature was successfully visualized and monitored. RESULTS: Administration of Ang II (1, 3, 10 and 30 ng/kg/min) produced a dose-dependent constriction of afferent and efferent arterioles in similar degrees; at 30 ng/kg/min, Ang II elicited 52 +/- 3 (N = 9) and 53 +/- 3% decreases in diameter (N = 9), respectively. The Ang II-induced arteriolar constriction was completely prevented by losartan, an Ang II type 1 (AT1) antagonist. The intrarenal hypertonic saline administration elicited transient increments (from 98 +/- 8 to 122 +/- 7 mL/min, N = 6, P < 0.05), followed by a marked reduction in renal blood flow (RBF; 78 +/- 7 mL/min, P < 0.05). This response was accompanied by prominent constriction of afferent (from 15.0 +/- 1.1 to 8.5 +/- 1.1 microm, N = 6, P < 0.05), but not efferent (from 14.3 +/- 1.2 to 13.8 +/- 1.0 microm, N = 3) arterioles. Furthermore, this response was completely inhibited by furosemide, a tubuloglomerular feedback inhibitor. CONCLUSION: : The intravital pencil lens-probe videomicroscopy can be a powerful tool for in vivo observation of renal microcirculation, with intact renal microvascular responses to two important renal homeostatic mechanisms, angiotensin II and tubuloglomerular feedback.

Adult↗

PubMed2001

Dual action of nitric oxide on purely isolated retinal ganglion cells.

PURPOSE: The role of nitric oxide (NO) in the survival of retinal ganglion cells (RGCs) was investigated. METHODS: RGCs were purely isolated from postnatal Sprague-Dawley rats by 2-step panning and were cultured in chemically defined serum free medium. An NO releaser, S-nitroso-N-acetylpenicillamine (SNAP: 500 microM, 250 microM, 100 microM, 10 microM, 1 microM, 100 nM, and 10 nM), an NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5 tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO: 100 microM, 33 microM, 10 microM, 1 microM), mixture of 100 microM SNAP and 33 microM c-PTIO, N(G)-nitro-L-arginine methyl ester (L-NAME: 10 mM, 5 mM, 500 microM, 100 microM or 10 microM), or their vehicles were added to the medium of pure RGC culture for 48 hr. Survival rates of small and large RGCs were determined separately by flow cytometry. RESULTS: At > or = 100 microM, SNAP significantly reduced RGC survival in a concentration dependent manner. At < or = 41 microM, SNAP significantly increased survival, particularly of large RGCs. c-PTIO and L-NAME reduced the survival rates concentration-dependently. A mixture of 100 microM SNAP and 33 microM c-PTIO significantly improved RGC survival compared with when they were added on their own. CONCLUSIONS: These results indicate that NO exhibits neuroprotective and neurotoxic actions on RGCs and that low concentrations of NO may be beneficial for the survival of neonatal RGCs in vitro.

Animals↗

PubMed2001

New double-tracer digital radiography for analysis of spatial and temporal myocardial flow heterogeneity.

A new high-resolution digital radiographic technique based on the deposition of (125)I- and (3)H-labeled desmethylimipramine (IDMI and HDMI, respectively) was developed for the assessment of spatial and temporal myocardial flow heterogeneity at a microvascular level. The density distributions of two tracers, or relative flow distributions, were determined by subtraction digital radiography using two imaging plates of different sensitivity. The regions resolved are comparable in size to vascular regulatory units (400 x 400 microm(2)). This method was applied to the measurement of within-layer myocardial flow distributions in Langendorff-perfused rabbit hearts. The validity of this method was confirmed by the strong correlation between regional densities of two tracers injected simultaneously (r = 0.89 +/- 0.03, n = 8). The temporal flow stability was evaluated by a 90-s continuous IDMI injection and subsequent bolus HDMI injection (n = 8). Regional densities of the two tracers were fairly correlated (r = 0.86 +/- 0.03), indicating that the spatial pattern of flow distribution was stable even at a microvascular level over a 90-s period. The effect of microsphere embolization on the flow distribution was also investigated by the sequential injections of IDMI, 15-microm microspheres, and HDMI at 20-s intervals (n = 8). Microembolization increased the coefficient of variation of tracer density from 19 to 25% (P < 0.05), whereas the regional densities of two tracers were still correlated substantially, as in the case of no embolization (r = 0.84 +/- 0.06). Thus the microsphere embolization enhanced flow heterogeneity with increasing flow differences between control high-flow and control low-flow regions but rather maintained the pattern of flow distribution. In conclusion, double-tracer digital radiography will be a promising method for the spatial and temporal myocardial flow analysis at microvascular levels.

Animals↗

PubMed2001

Stenosis differentially affects subendocardial and subepicardial arterioles in vivo.

The presence of a coronary stenosis results primarily in subendocardial ischemia. Apart from the decrease in coronary perfusion pressure, a stenosis also decreases coronary flow pulsations. Applying a coronary perfusion system, we compared the autoregulatory response of subendocardial (n = 10) and subepicardial (n = 12) arterioles (<120 microm) after stepwise decreases in coronary arterial pressure from 100 to 70, 50, and 30 mmHg in vivo in dogs (n = 9). Pressure steps were performed with and without stenosis on the perfusion line. Maximal arteriolar diameter during the cardiac cycle was determined and normalized to its value at 100 mmHg. The initial decrease in diameter during reductions in pressure was significantly larger at the subendocardium. Diameters of subendocardial and subepicardial arterioles were similar 10--15 s after the decrease in pressure without stenosis. However, stenosis decreased the dilatory response of the subendocardial arterioles significantly. This decreased dilatory response was also evidenced by a lower coronary inflow at similar average pressure in the presence of a stenosis. Inhibition of nitric oxide production with N(G)-monomethyl-L-arginine abrogated the effect of the stenosis on flow. We conclude that the decrease in pressure caused by a stenosis in vivo results in a larger decrease in diameter of the subendocardial arterioles than in the subepicardial arterioles, and furthermore stenosis selectively decreases the dilatory response of subendocardial arterioles. These two findings expand our understanding of subendocardial vulnerability to ischemia.

Animals↗

PubMed2001

In vivo visualization of characteristics of renal microcirculation in hypertensive and diabetic rats.

We developed a videomicroscope system with a charge-coupled device camera and evaluated it in the investigation of the glomerular microcirculation in normal [Wistar-Kyoto (WKY)], spontaneously hypertensive (SHR), and streptoyotocin-induced diabetic rats (STZ). In WKY, the diameter of the afferent arterioles (Af) was 11.9 +/- 0.7 microm and that of the efferent arterioles (Ef) was 8.9 +/- 0.7 microm. Af and Ef in each glomerulus could be visualized simultaneously with continuous recording of blood pressure and renal blood flow. In SHR, Af diameter was constricted to approximately 60% of that in WKY. A dose-dependent dilation of Af and Ef was observed after administration of barnidipine (1-10 microg/kg iv), a calcium channel antagonist, in all three groups. No change was seen in the Af-to-Ef diameter ratio (Af/Ef ratio) in WKY. In SHR, the Af/Ef ratio increased significantly because of the marked dilation of Af after barnidipine administration. In contrast, barnidipine dilated Ef in STZ, causing a significant reduction in the Af/Ef ratio. This system can analyze in vivo glomerular microcirculation and systemic macrocirculation simultaneously, allowing more direct investigation of the characteristics of and acute changes in glomerular microcirculation in pathological animals.

Animals↗

PubMed2001

New calculation of internal Ca(2+) recirculation fraction from alternans decay of postextrasystolic potentiation.

In our previous studies, we calculated the internal Ca(2+) recirculation fraction (RF) after obtaining the beat decay constant (tau(e)) of the monoexponential component in the postextrasystolic potentiation (PESP) of the alternans decay by curve fitting. However, this method sometimes suffers from the sensitive variation of tau(e) with small noises in the measured contractilities of the 5th and 6th postextrasystolic (PES) beats in the tail of the exponential component. We now succeeded in preventing this problem by a new method to calculate RF without obtaining tau(e). The equation for the calculation in the new method expresses an alternans decay of PESP as a recurrence formula of PESP. It can calculate RF directly from the contractilities of the 1st through the 4th PES beats without any fitting procedure. To evaluate the reliability of the new method, we calculated RF from the alternans decay of PESP of the left ventricle (LV) of the canine excised cross-circulated heart preparation by both the original fitting and the new method. Although there was no significant difference in the mean value of the obtained RF between these two methods, the variance of RF was smaller with the new method than with the original method. Thus the new method proved useful and more reliable than the original fitting method.

Animals↗

PubMed2000

Effect of dietary control on plasma nitrate level and estimation of basal systemic nitric oxide production rate in humans.

It is of great interest and value to evaluate the systemic nitric oxide (NO) production rate in humans under various conditions. However, the currently available estimation methods are troublesome and time-consuming. We thus aimed at developing a simple method to estimate the basal systemic NO production rate in humans based on a steady-state analysis, i.e., a balance between the systemic NO production rate and the total nitrate elimination rate. Plasma nitrate concentrations of young healthy volunteers (n = 7 in group 1: n = 9 in group 2) were measured for 2 days. In group 1, all subjects had the same meals for 7 days prior to the plasma nitrate measurement. In group 2, all subjects were allowed free diets. The plasma nitrate concentrations were highly influenced by dietary nitrite/nitrate intake in both groups and reached the steady-state levels after 14-h fasting. Accordingly, the basal systemic NO production rates were estimated from the plasma nitrate concentrations after 14-h fasting (group 1, 630 +/- 37 nmol min(-1) = 0.78 +/- 0.03 micromol kg(-1) h(-1); group 2, 597 +/- 45 nmol min(-1) = 0.66 +/- 0.05 micromol kg(-1) h(-1), P = not significant vs group 1). These estimated values were comparable to the values obtained by other methods. In conclusion, the present estimation method with 14-h fasting using a single-compartment analysis was found to be a simple approach to quantitative evaluation and intra- and interindividual comparisons of the basal systemic NO production rates in humans.

Adult↗

PubMed2000

Intramyocardial influences on blood flow distributions in the myocardial wall.

Flow velocity wave forms of coronary arterial inflow and venous outflow of myocardium are influenced by cardiac contraction and relaxation: arterial flow is exclusively diastolic; venous outflow is systolic. We first discuss the intramyocardial microvascular flow dynamics, then present some results of visualization of transmural microvessels by our needle-probe charge coupled device (CCD) microscope, along with an interpretation of the arteriolar and venular hemodynamics through a cardiac cycle. After describing a hierarchical system of coronary microvessels (small artery, arteriole, and capillary), we emphasize the importance of spatial heterogeneity of blood supply to myocardium with reference to a minimal vascular control unit (approximately 400 microm). An understanding of mechanoenergetic interaction is fundamentally important to an understanding of intramyocardial coronary circulation, and the Physiome Project will provide powerful tools for understanding the integrated role of the intramyocardial microcirculation system.

Blood Flow Velocity↗

PubMed2000

Quantitative blood velocity mapping in glomerular capillaries by in vivo observation with an intravital videomicroscope.

We have evaluated rat glomerular microcirculation under in-vivo condition with an intravital videomicroscope. To measure erythrocyte velocities, a line segment was set along the glomerular capillaries in time-sequential videotaped images and then a spatiotemporal image was constructed along that segment. The angle of striped pattern in the spatiotemporal image which reflects the erythrocyte velocity, was estimated to compute erythrocyte velocity vector mapping. We found that erythrocyte velocities in rat glomeruli were significantly faster in diabetic rats than in control rats (p < 0.05). In conclusion, we have succeeded in quantitatively evaluating the in-vivo renal microcirculation with our videomicroscope system and by spatiotemporal image analyzing method.

Animals↗

PubMed2000

Direct in vivo visualization of glomerular microcirculation by intravital pencil lens-probe CCD videomicroscopy.

There have been developed several types of experimental techniques for evaluation of renal microcirculation. Although each methodology possesses excellent and unique characteristics, it requires substantial artificial manipulation that might alter the renal microvascular responsiveness. To circumvent such limitations of previous ex vivo or in vitro approaches to glomerular microcirculation, we have developed a pencil lens probe CCD intravital videomicroscopic system that allows us to evaluate both systemic hemodynamics and renal microcirculation. Furthermore, real time images of afferent and efferent arterioles as well as glomeruli can be continuously assessed, which would facilitate the functional characterization of these microvessels in vivo. Finally, the tapered nature of the CCD probe of this videomicroscopy may allow direct observation of the renal microvasculature in small animals. In conclusion, this novel technique is a valuable tool for unveiling the in vivo, in situ, and intact renal microvascular behavior, and may provide further approaches to the understanding of renal microcirculation.

Animals↗

PubMed1999

Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced.

BACKGROUND: Because coronary blood flow is impeded during systole, the duration of diastole is an important determinant of myocardial perfusion. The aim of this study was to show that coronary flow modulates the duration of diastole at constant heart rate. METHODS AND RESULTS: In anesthetized, open-chest dogs, diastolic time fraction (DTF) increased significantly when coronary flow was reduced by lowering perfusion pressure from 100 to 70, 55, and 40 mm Hg. On average, DTF increased from 0.47+/-0.04 to 0.55+/-0.03 after a pressure step from 100 to 40 mm Hg in control, from 0.42+/-0.04 to 0.47+/-0.04 after administration of adenosine, and from 0.46+/-0.07 to 0.55+/-0.06 after L-NMMA (mean+/-SD, 6 dogs for control and adenosine, 4 dogs for L-NMMA, all P<0.05). Flow normalized to its value at full dilation and pressure of 90 mm Hg (375+/-25 mL/min) increased during the period of reduced pressure at 40 mm Hg; control, from 0.005+/-63 (2 seconds after pressure step) to 0.09+/-0.06 (15 seconds after pressure step); with adenosine, from 0.19+/-0.06 to 0. 22+/-0.06; and with L-NMMA, from 0.013+/-0.007 to 0.12+/-0.02 (all P<0.05). The increase in DTF at low pressure may be explained by a decrease in interstitial volume at low pressure, which either decreases the preload of the myocytes or reduces the buffer capacity for ions determining repolarization, thereby causing an earlier onset of relaxation. CONCLUSIONS: Because the largest increase in DTF occurs at pressures below the autoregulatory range when blood flow to the subendocardium is closely related to DTF, modulation of DTF by coronary blood flow can provide an important regulatory mechanism to match supply and demand of the myocardium when vasodilatory reserve is exhausted.

Adenosine↗

PubMed1999

Flow dependence and time constant of the change in nitric oxide concentration measured in the vascular media.

It has been considered that the concentration of endothelium-derived nitric oxide (NO) in the arterial vascular wall changes in response to flow-induced shear stress. In the present study, using an NO-sensitive electrode, the aim was to directly evaluate the relationship between perfusion rate and NO concentration in the arterial vascular wall. The NO microelectrode (diameter: 100 microns) was inserted into the vascular media of isolated canine femoral arteries, and the vessel was perfused with a Krebs-Henseleit buffer solution. A flow-related change in NO concentration in the vascular media was then evaluated by changing perfusion rate. NO concentration attained a peak value with a first-order time delay by a stepwise increase in perfusion rate, and the peak-level NO concentration was linearly correlated with perfusion rate in each vessel (10-154 pA at 2.1-72.3 ml min-1; n = 7, r2 = 0.89-0.99, p < 0.03). The average time constant for an increase in NO current with a stepwise increase in perfusion rate was 24 +/- 3 s (n = 5). NO production was increased by perfusing a solution containing 1 mmol l-1 L-arginine and was attenuated by 100 mumol l-1 NG-nitro-L-arginine, indicating the intactness of the endothelium, proper insertion of the NO electrode and selective detection of NO by the electrode. It is concluded that the NO microelectrode is applicable to NO measurement in the vascular media where NO controls vascular tone and that the concentration of NO in the arterial vascular media changes with perfusion rate in a rate-dependent manner as well as with a time constant of about 24 s for a stepwise increase in flow.

Animals↗

PubMed1999

Endothelium-derived nitric oxide enhances the effect of intraaortic balloon pumping on diastolic coronary flow.

BACKGROUND: High shear rate with pulsation is one of the major stimuli for the release of endothelium-derived nitric oxide leading to coronary arteriolar dilation. Intraaortic balloon pumping mechanically enhances shear rate and diastolic-to-systolic flow oscillation. We aimed to evaluate whether or not coronary blood flow augmentation during intraaortic balloon pumping is mediated by coronary arteriolar dilation through endothelium-derived nitric oxide release. METHODS: Using a charge-coupled device intravital videomicroscope, we observed epicardial coronary arterioles (40 to 220 microm in diameter) in anesthetized open-chest dogs (n = 10) during 2:1 mode of intraaortic balloon pumping. Endothelium-derived nitric oxide-mediated vasodilatory effects of intraaortic balloon pumping were evaluated by comparing end-diastolic arteriolar diameters between the coupled beats of on and off intraaortic balloon pumping before and after intracoronary endothelium-derived nitric oxide synthesis inhibition with Nomega-nitro-L-arginine (L-NNA, 2 micromol/min) administration. RESULTS: Intraaortic balloon pumping increased coronary arteriolar diameters and coronary blood flow by 11.4%+/-1.8% (p < 0.0001) and 33.4%+/-4.1% (p < 0.001), respectively. Vasodilation was greater in small arterioles (<110 microm; 15.4%+/-2.2%) than in large arterioles (> or =110 microm; 4.2%+/-1.2%, p < 0.0001). L-NNA attenuated the intraaortic balloon pumping-induced vasodilation and augmentation of coronary blood flow to 4.6%+/-1.0% (p < 0.001) and to 20.8%+/-2.1%, (p < 0.05), respectively. Attenuation of vasodilatory effect by L-NNA was observed mainly in small arterioles (from 15.4%+/-2.2% to 5.9%+/-1.2%). CONCLUSIONS: Intraaortic balloon pumping augmented coronary blood flow by dilating coronary arterioles in diastole, more significantly in small arterioles than in large arterioles. Endothelium-derived nitric oxide inhibition markedly attenuated these effects. We conclude that, in a canine model, endothelium-derived nitric oxide contributes to mechanical enhancement of the coronary blood flow with diastolic arteriolar vasodilation during intraaortic balloon pumping.

Acetylcholine↗

PubMed1999

Measurement accuracy of the flow velocity in pulsed ultrasound Doppler velocimeter.

This paper presents a numerical simulation method for evaluating the measurement accuracy of the high-frequency pulsed ultrasound Doppler velocimeter (PUDV). The frequency distribution of the Doppler signal from a sample volume is calculated by dividing the sample volume into small cells and using the statistics of the velocities of the cells. The distribution is used to analyze the accuracy of the poststenotic velocity measurements of a 20-MHz 80-channel PUDV. The target flow field is obtained by solving Navier-Stokes equations numerically. It was shown that the velocities evaluated by the zero-cross and Fourier transform methods agreed well with the given velocities, and that flow separation was successfully detected. It was also shown that the tube diameter should be at least twice as large as the diameter of the sample volume to obtain accurate measurements.

Blood Flow Velocity↗