Biomedical subjects

K Tsujioka

Publications and source records attributed to K Tsujioka.

At least 19 recordsLinked to original sources

PubMed1998

In vivo observations of the intramural arterioles and venules in beating canine hearts.

1. To evaluate the effects of cardiac contraction on intramyocardial (midwall) microvessels, we measured the phasic diameter change of left ventricular intramural arterioles and venules using a novel needle-probe videomicroscope with a CCD camera and compared it with the diameter change in subepicardial and subendocardial vessels. 2. The phasic diameter of the intramural arterioles decreased from 130 +/- 79 ìm in end-diastole to 118 +/- 72 micron (mean +/- S.D.) in end-systole by cardiac contraction (10 +/- 6 %, P < 0.001, n = 21). 3. The phasic diameter in the intramural venules was almost unchanged from end-diastole to end-systole (85 +/- 44 vs. 86 +/- 42 micron, respectively, 2 +/- 6 %, n. s., n = 14). 4. Compared with intramural vessels, the diameters of subendocardial arterioles and venules decreased by a similar extent (arterioles: 10 +/- 8 %, P < 0. 001; venules: 12 +/- 10 %, P < 0.001) from end-diastole to end-systole, respectively, whereas the diameter of the subepicardial arterioles changed little during the cardiac cycle, and subepicardial venule diameter increased by 9 +/- 8 % (P < 0.01) from end-diastole to end-systole. These findings are consistent with our previous report. 5. We suggest that the almost uniform distribution of the cardiac contractility effect and arteriolar transmural pressure between the subendocardium and the midmyocardium, which together constitute the systolic vascular compressive force, accounts for the similarity in the arteriolar diameter changes in both myocardial layers. The smaller intravascular pressure drop from deep to superficial myocardium relative to the larger intramyocardial pressure drop explains the difference in the phasic venular diameter changes across the myocardium.

Animals↗

PubMed1998

[Effects of brovincamine fumarate on choroidal blood volume in rabbits].

We examined the effects of brovincamine fumarate, a Ca(2+)-channel blocker, on choroidal blood flow. We measured the choroidal blood volume continuously for 1 hour using laser Doppler flowmetry, as well as systemic blood pressure, heart rate, and intraocular pressure in six urethane-anesthetized rabbits after intravenous administration of 0.1 mg/kg or 0.5 mg/kg brovincamine. As a control, ten rabbits receiving no medication were used. All the data were recorded and analyzed using MacLab on a computer. In both the 0.1 mg/kg and 0.5 mg/kg brovincamine-injected groups, the choroidal blood volume decreased significantly after administration, but showed no significant difference from controls. Vascular resistance in the choroid showed a significant increase over the value before administration and over the control group. The heart rate decreased significantly compared to the value before injection and to the control group. The mean blood pressure in both dose groups and the intraocular pressure in the 0.5 mg/kg injected group were significantly higher than the controls. These results indicate that intravenous administration of 0.1 mg/kg or 0.5 mg/kg brovincamine does not cause an increase in the choroidal blood volume in urethane-anesthetized rabbits.

Animals↗

PubMed1997

Decrease in the amount of focal adhesion kinase (p125(FAK)) in interleukin-1beta-stimulated human umbilical vein endothelial cells by binding of human monocytic cell lines.

Monocytes in the blood circulation migrate across endothelial cell monolayers lining the blood vessels and infiltrate into the underlying tissues in inflammation. However, little is known about the mechanisms by which leukocytes migrate across the endothelial barrier after binding and what molecules participate in the process. Addition of the human monocytic cell line THP-1 to interleukin-1beta (IL-1beta)-stimulated human umbilical vein endothelial cells (HUVEC) induced a decrease in the amount of focal adhesion kinase (p125(FAK)) protein, a tyrosine kinase localized at focal contacts and essential for cell attachment to the extracellular matrix, whereas little change was observed in the amount of other molecules associated with cell adhesion such as vascular cell adhesion molecule-1, alpha-catenin, and talin. A maximum decrease in the amount of p125(FAK) was observed 15-30 min after addition of THP-1 cells to HUVEC, after which the level of p125(FAK) gradually recovered. A reduction in the density of actin stress fibers in IL-1beta-activated HUVEC was observed in parallel with the decrease in p125(FAK). The p125(FAK) decrease was partially inhibited by preventing THP-1 binding to HUVEC using a mixture of antibodies to adhesion molecules. We suggest that the decrease in p125(FAK) triggered by binding of monocytes in inflammation facilitates the transendothelial migration of the monocytes by altering the adhesiveness of endothelial cells to the extracellular matrix.

Antibodies, Monoclonal↗

PubMed1997

In-vivo measurements of blood flow velocity profiles in canine ilio-femoral anastomotic bypass grafts.

In-vivo velocity profiles were recorded with a 20 MHz 80-channel pulsed Doppler ultrasound velocimeter in canine end-to-side ilio-femoral anastomotic grafts. The geometries were obtained from casts of the anastomotic region, and flow rates were measured with electromagnetic flow probes. Three cases reported here include a "standard" geometry, which was similar to previously studied in vitro models, a stenosed geometry, and a case with below average flow rate. Observed flow features include separation at the hood and toe, movement of the floor stagnation point, and skewed profiles in the proximal outflow segment. Out-of-plane curvature and lateral displacement of the anastomosis inlet appear to have a strong effect on the flow fields. In addition, compliance affects the instantaneous flow rates within the proximal and distal branches.

Anastomosis, Surgical↗

PubMed1997

Alpha-adrenergic vasoconstriction reduces systolic retrograde coronary blood flow.

There is a paradoxical alpha-adrenoceptor-mediated coronary vasoconstriction whenever there is adrenergic activation of the heart, as during cardiovascular reflexes or exercise. A previous study demonstrated that this paradoxical vasoconstriction helps maintain blood flow to the vulnerable inner layer of the left ventricular wall during exercise, but the mechanism for this effect was not elucidated. The purpose of the present investigation was to test the hypothesis that alpha-adrenoceptor-mediated vasoconstriction lessens the to-and-fro oscillation of blood flow that occurs in the coronary arterial tree during systole and diastole. Septal coronary artery blood velocity was measured in anesthetized open-chest dogs with a 20-MHz pulsed Doppler velocimeter. Systolic retrograde velocity and diastolic forward velocity were compared during norepinephrine infusion before and after alpha-adrenoceptor blockade with phenoxybenzamine. Systolic aortic pressure was held constant by aortic banding; heart rate was controlled by pacing at 80, 140, and 200 beats/min; and maximum left ventricular dP/dt was unchanged by alpha-blockade. At each pacing rate, systolic retrograde velocity was significantly greater after alpha-blockade, indicating that alpha-vasoconstriction reduced systolic retrograde flow by changing coronary vascular impedance. Transmural blood flow was measured with microspheres in a second group of dogs during the same experimental conditions, and flow to the inner layer of the left ventricle was diminished by alpha-adrenoceptor blockade at a heart rate of 250 beats/min, demonstrating a beneficial effect of alpha-vasoconstriction. In conclusion, adrenergic alpha-adrenoceptor-mediated coronary vasoconstriction reduces systolic retrograde coronary flow during norepinephrine infusion. This lessens to-and-fro flow oscillation in the coronary circulation and probably is the mechanism whereby alpha-vasoconstriction helps maintain blood flow to the inner layer of the left ventricle during exercise.

Adipose Tissue↗

PubMed1997

Spatial fluctuation of regional myocardial blood flows.

Digital radiography (100 pixels/mm2) combined with the technique of 3H-labeled desmethylimipramine deposition was employed to visualize regional blood flow distributions in rabbit left ventricular myocardium. A fluctuated pattern of myocardial flow and its dependence on arterial oxygen tension (PaO2) was evaluated with the coefficient of variation (CV) computed at each step of coarse-graining; flow images were revisualized by increasing pixel area (PA) step by step from 0.01 to 1 mm2. The CV values decreased with hypoxia at all resolution levels, suggesting that there is a vascular regulatory mechanism for making myocardial perfusion uniform in response to decreased PaO2. In both perfusion states, CV decreased with increasing PA. The relationship between CV and PA fitted the noninteger power law function, implying an apparent fractality of CV.

Animals↗

PubMed1996

Effects of intraaortic balloon pumping on septal arterial blood flow velocity waveform during severe left main coronary artery stenosis.

OBJECTIVES: We sought to evaluate the effect of intraaortic balloon pumping on the phasic blood velocity waveform into myocardium with severe coronary artery stenosis. BACKGROUND: In the presence of severe coronary artery stenosis, it is not clear whether intraaortic balloon pumping augments intramyocardial inflow during diastole or changes systolic retrograde blood flow from the myocardium to the extramural coronary arteries. METHODS: Using anesthetized open chest dogs (n=7), we introduced severe stenosis in the left main coronary artery to reduce the poststenotic pressure to approximately 60 mm Hg (>90% diameter stenosis). Septal arterial blood flow velocities were measured with a 20-MHz, 80-channel ultrasound pulsed Doppler velocimeter. Left anterior descending arterial flow, aortic pressure and poststenotic distal coronary pressure were measured simultaneously. The diastolic anterograde flow integral and systolic retrograde flow integral were compared in the presence and absence of intraaortic balloon pumping. RESULTS: Although intraaortic balloon pumping augmented diastolic aortic pressure, this pressure increase was not effectively transmitted through stenosis. Septal arterial diastolic flow velocity was not augmented, and left anterior descending arterial flow was unchanged during intraaortic balloon pumping. CONCLUSIONS: In the presence of severe coronary artery stenosis, intraaortic balloon pumping failed to increase diastolic inflow in the myocardium and did not enhance systolic retrograde flow from the myocardium to the extramural coronary artery. Thus, the major effect of intraaortic balloon pumping on the ischemic heart with severe coronary artery stenosis may be achieved by reducing oxygen demand by systolic unloading.

Analysis of Variance↗

PubMed1996

Evaluation of intramyocardial coronary blood flow waveform during intraaortic balloon pumping in the absence or presence of coronary stenosis.

Our aim was to evaluate the effects of intraaortic balloon pumping (IABP) on the blood velocity waveform in the absence or presence of coronary artery stenosis. Using anesthetized open-chest dogs, the septal arterial blood flow velocities were measured with a 20 MHz 80-channel ultrasound pulsed Doppler velocimeter in the absence (n = 5) or presence (n = 3) of left main coronary artery stenosis. The blood velocity waveform was analyzed by calculating the systolic retrograde velocity integral (SR) and the diastolic antegrade velocity integral (DA). A slosh ratio was defined as SR/DA. The left anterior descending arterial flow (CBF), aortic pressure (AoP), and poststenotic distal coronary pressure (DiP) were also measured simultaneously. We compared the effect of IABP on the velocity waveforms in the absence and in the presence of coronary artery stenosis. In the absence of stenosis, IABP increased DiP during diastole and augmented DA while it also increased SR. IABP augmented the net CBF because of the greater increase in DA than SR. In the presence of stenosis, however, IABP did not increase DiP and resulted in no significant effect on the net CBF.

Animals↗

PubMed1996

Microheterogeneity of myocardial blood flow in rabbit hearts during normoxic and hypoxic states.

The goal of this study was to evaluate microheterogeneity of myocardial blood flow and its dependence on arterial O2 tension (PaO2). We measured within-layer distribution of regional blood flows in the left ventricles of anesthetized rabbits in both normoxic and hypoxic states with myocardial region sizes in the range of 0.01-1.0 mm2. A novel method of digital radiography combined with the technique of 3H-labeled desmethylimipramine deposition enabled us to visualize and accurately quantitate regional blood flow at such high levels of resolution. To analyze myocardial blood flow patterns, we computed the coefficient of variation (CV) and the correlation between adjacent regional flows (CA). The CA values were larger in the hypoxic state (PaO2 = 26 +/- 5 mmHg) than in the normoxic state (PaO2 = 97 +/- 20 mmHg) at all levels of resolution (P < 0.001). In the normoxic state, there was a transmural difference in CA (P < 0.001); CA increased with depth of the left ventricle (from subepicardium to subendocardium). However, the relation between CA and the depth of the left ventricle was not statistically significant in the hypoxic state. The CV values were smaller in the hypoxic state than in the normoxic state at all levels of resolution (P < 0.001). When the degree of resolution was reduced from 0.01 to 1.0 mm2, CV decreased by 75% in the normoxic and by 69% in the hypoxic state. Thus we conclude that 1) the decrease in PaO2 increases similarity of blood flows in nearby regions and decreases myocardial blood flow heterogeneity, and 2) similarity of regional blood flows increases with depth of the left ventricle in the normoxic state, but this transmural difference disappears in the hypoxic state.

Animals↗

PubMed1996

Blood velocity profiles in the human renal artery by Doppler ultrasound and their relationship to atherosclerosis.

Blood velocity profiles were measured in the renal branch (diameter 5.9 +/- 1.3 mm) of the aortorenal bifurcation using a 20-MHz 80-channel pulsed Doppler velocimeter during retroperitoneal surgery in 10 patients. The peak Reynolds number was 1145 +/- 140 and the frequency parameter (Wormersley parameter) was 3.0 +/- 0.8. Immediately distal to the ostium of the renal artery, reverse flow, indicating flow separation, was observed near the cranial wall mainly during the first part of the cardiac cycle. There were flows from the cranial to the caudal side of the artery at this location, indicating the presence of strong secondary flows. Two diameters downstream of the ostium, the velocity profiles were skewed to the caudal side in all patients. Four diameters downstream, the flow profile was symmetrical (3 patients) or only slightly skewed (7 patients) and virtually parabolic throughout the cardiac cycle. These observations mean that the flow on the cranial side of the renal branch of the human aortorenal bifurcation is characterized by (1) a bidirectional oscillation of the flow, (2) separation of the flow during systole, and (3) low time-averaged shear rate. These blood velocity patterns may be related to the localization and development of atheromatous plaque that occurs preferentially in this region of the renal artery. Conversely, the unidirectional, axisymmetrical flow found in more distal parts of the renal artery are associated with a very low incidence of lesions.

Adult↗

PubMed1995

Direct in vivo observation of subendocardial arteriolar response during reactive hyperemia.

To study the vasodilatory capacity of subendocardial (ENDO) arterioles, we evaluated the reactive hyperemic responses of ENDO as well as subepicardial (EPI) arterioles in 40 dogs by our needle-probe intravital microscope. We also examined the individual and combined effects of an ATP-sensitive K+ channel blocker (glibenclamide, 200 micrograms/kg), an inhibitor of nitric oxide synthase (NG-monomethyl-L-arginine [L-NMMA], 2 mumol/min, 20 minutes), and an adenosine-receptor antagonist (8-phenyltheophylline [8PT], 0.75 mumol/min, 15 minutes). The percent increase in end-diastolic diameter of ENDO arterioles was larger (P < .01) than that of EPI arterioles during reactive hyperemia, especially for the arterioles larger than 120 microns (P < .01). The diastolic-to-systolic vascular pulsation amplitude at the peak flow was greater in ENDO than EPI arterioles (25% versus 6%, P < .05). Compared with control conditions, the presence of both glibenclamide and L-NMMA suppressed the vasodilation responses of ENDO arterioles (P < .01 for both) and EPI arterioles (P < .05 for both). The effect of L-NMMA was greater in ENDO arterioles (P < .01), but that of glibenclamide was not different between ENDO and EPI arterioles. 8PT influenced the hyperemic response, although statistical significance was found only in the flow response. The effect of combined infusion of L-NMMA and glibenclamide with or without 8PT was greater than that of individual infusions in both ENDO and EPI arterioles. Conclusions are as follows: (1) The vasodilatory response of ENDO arterioles was even larger than that of EPI arterioles. Thus, the smaller flow reserve of ENDO arterioles may be caused by other factors, including the greater effects of myocardial compression and nitric oxide on the ENDO arterioles. (2) The vascular responses of ENDO and EPI arterioles were modulated by both endothelium-independent and -dependent vasodilative factors, and the effect of each factor including adenosine was associated with the effects of others.

Adenosine↗

PubMed1994

Influence of heart rate and vasoactive drugs on blood flow patterns at the canine ilio-femoral bifurcation.

OBJECTIVE: The aim was to study the effects of altered heart rate and vasoactive drugs on the blood velocity patterns in the region of an arterial bifurcation. METHODS: Blood velocity profiles were measured in an exposed iliofemoral bifurcation of paced dogs using a pulsed Doppler ultrasound velocimeter with high temporal and spatial resolution. RESULTS: Decrease of the heart rate from 120 beats.min-1 (2 Hz) to 60 beats.min-1 (1 Hz) increased the peak forward velocity (30%), the peak reverse velocity (20%), and the duration of reverse flow (25%). Each drug caused qualitatively similar changes in velocity patterns at both heart rates. The systemic administration of angiotensin II reduced peak forward velocity (-26% at 2 Hz and -33% at 1 Hz) and forward flow duration (-15% at 1 Hz), the peak reverse velocity (-30% at 1 Hz), and reverse flow duration (-20% at 2 Hz and -28% at 1 Hz). Glyceryl trinitrate also reduced the peak forward velocity (-19% at both 2 and 1 Hz) but prolonged forward flow duration (28% at 2 Hz and 17% at 1 Hz) and that of reverse flow (45% at 2 Hz and 24% at 1 Hz), and also decreased the degree of oscillation (-16% at 2 Hz). Barnidipine hydrochloride (a calcium channel antagonist) also increased the duration of forward flow (48% at 1 Hz) and of reverse flow (31% at 2 Hz) but reduced the peak reverse velocity (-29% at 1 Hz) and flow oscillation (-22% at 2 Hz and 20% at 1 Hz). CONCLUSIONS: These dramatic changes in the pattern of blood flow, including alterations in the amplitudes and durations of the different phases of the flow cycle, are expected to have important consequences on the shear dependent responses of endothelial cells in the region of the bifurcation.

Angiotensin II↗

PubMed1994

Effects of nitroglycerin on diameter and pulsation amplitude of subendocardial arterioles in beating porcine heart.

We examined the effect of nitroglycerin (NTG) on the diameter and diastolic-to-systolic pulsation amplitude of large (ID > 100 microns) and small (ID < 100 microns) subendocardial arterioles with their segmental responses. In 10 open-chest, anesthetized pigs, subendocardial arterioles of beating hearts (n = 18) were videorecorded using a needle-probe videomicroscope. Subendocardial arteriolar diameter was determined before and 1-2 min after NTG administration (25 micrograms/kg i.v.). In an additional experiment using three pigs, we monitored the transient response of subendocardial small arterioles (n = 5) from the time before NTG administration until 3 min after NTG. NTG dilated large subendocardial arterioles by 13 +/- 4% (means +/- SD, n = 10, P < 0.001) at about 1.5 min after NTG, but not small subendocardial arterioles (2 +/- 2%, n = 8, not significant). However, the small arterioles responded transiently to NTG in an earlier phase, especially to a higher dose. The percent diameter change of large subendocardial arterioles between diastole and systole at 1.5 min after NTG administration was 32 +/- 4%, which was larger than that under control conditions (19 +/- 8%, P < 0.05). The pulsation amplitude of small subendocardial arterioles at this time was almost unchanged by NTG (16 +/- 8 vs. 17 +/- 6%, NS) but increased transiently in an earlier phase. In conclusion, NTG dilated large subendocardial arterioles on the plateau phase of its impulse (intravenously) response (approximately 1.5 min after NTG).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Diameters of subendocardial arterioles and venules during prolonged diastole in canine left ventricles.

Using a needle-probe videomicroscope with a charge-coupled device (CCD) camera, we measured the diameter of subendocardial arterioles and venules during prolonged diastole beyond the time point at which coronary blood flow reached zero. In seven open-chest heart-blocked dogs, a sheathed needle probe with a doughnut-shaped balloon was introduced from the left atrial appendage and advanced into the left ventricle through the mitral valve. The tip of the probe was placed gently on the endocardial surface. Diameters of arterioles (n = 16) and venules (n = 16) at the beginning of long diastole ranged from 40 to 126 microns and from 32 to 192 microns, respectively. After cardiac arrest, the arteriolar diameter gradually declined with aortic pressure. Arteriolar diameters at zero flow decreased by 28 +/- 9% (mean +/- SD) compared with the initial diameter (P < .01). However, none of the subendocardial arterioles collapsed at zero flow or at 12 seconds after the beginning of prolonged diastole (8 to 9 seconds after zero flow) in an additional experiment (n = 5). In contrast to arteriolar diameter, venular diameter increased during prolonged diastole. Venular diameter at zero flow increased by 14 +/- 12% compared with the initial diameter (P < .01). We conclude that during prolonged diastole, when coronary arterial inflow ceases, subendocardial arteriolar diameter decreases without any visible collapse, whereas venular diameter increases.

Animals↗

PubMed1993

[Visualization of coronary arteries with helical scanning CT: diastolic reconstruction].

The purpose of this study was the visualization of coronary arteries by the diastolic reconstruction method with helical scanning (HES) CT. We chose diastolic phase images from the image data acquired with the HES technique using a continuous nutate-rotate fast CT scanner, because few motion artifacts are induced by cardiac pulsation during the slow filling diastolic phase. We assessed coronary diseases using this method based on HES-CT, and evaluated its clinical effectiveness. We also studied the clinical value of multiplanar reconstruction and three-dimensional surface reconstruction. The subjects consisted of 31 patients with coronary disease, aged 41-77 years. When a diastolic reconstruction HES-CT was employed, the average rate of visualization of the coronary arteries was 72%. An examination can be completed during a 30-second single breath-hold, permitting the acquisition of coronary artery images with excellent continuity. Calcified coronary arteries can be identified.

Adult↗

PubMed1993

[Clinical usefulness of helical scanning CT (HES-CT) for orbital lesion].

Helical scanning CT (HES-CT) was applied to multiplanar reconstruction (MPR) and 3-D imaging for the diagnosis of 65 patients with orbital lesions. We employed the the Toshiba TCT-900S, a fourth-generation high-speed CT scanner equipped with a slip-ring system. In HES-CT, scanning was performed with continuous rotation of the X-ray tube for 30 s, while the couch top was simultaneously moved at a constant speed of 1 to 2 mm/s. Images were reconstructed from continuous raw data to obtain a slice pitch of 1 mm in the longitudinal direction. HES-CT was found to have some advantages over conventional thin slice CT: 1) a wide area could be scanned in a short time (30 s) without motion artifact, 2) small lesions could be easily detected because slice images could be generated with a fine pitch at arbitrary positions from continuous raw data, 3) MPR images had good continuity in the longitudinal direction, and 4) high contrast of structures was obtained in the orbital region. HES-CT was considered to be useful for the detection of orbital lesions.

Child↗

PubMed1993

Endocardial coronary microcirculation of the beating heart.

Direct and continuous observation of subendocardial (deep myocardial) microcirculation provides essential information on coronary circulation, since cardiac contraction affects subendocardial vessels most vigorously. To achieve this aim, we developed a portable needle-probe video-microscope with a charge-coupled-device (CCD) camera to visualize the subendocardial microcirculation. Images of the subendocardial microcirculation of a porcine beating heart were successfully observed in all cases. The vascular compression by cardiac contraction decreased the diameter of subendocardial arterioles and venules by about 20%.

Animals↗

PubMed1993

Decreased mid-to-late diastolic decay of diastolic coronary artery flow velocity in pressure-overloaded left ventricular hypertrophy.

This study was carried out to investigate the characteristics of coronary arterial flow in left ventricular hypertrophy secondary to systemic hypertension. The blood velocities in the left anterior descending coronary artery (LAD) were measured by a No. 3F 20 MHz Doppler catheter in 23 hypertensive patients with left ventricular hypertrophy (systolic/diastolic pressure: 181 +/- 15/100 +/- 4 mmHg) and 13 patients with atypical chest pain, but without left ventricular hypertrophy and any abnormal hemodynamic findings. All patients had normal coronary arteriograms. The LAD blood velocity waveforms in pressure overloaded left ventricular hypertrophy were characterized by both a decreased mid-to-late diastolic deceleration rate (delta V/delta T) and a normalized value of delta V/delta T by peak diastolic velocity [delta V/(delta T.Vpeak)], as well as delayed early diastolic inflow (time for diastolic rise; TDR). The values of the delta V/(delta T.Vpeak) in the patients with hypertensive left ventricular hypertrophy and in the normotensive controls were 1.26 +/- 0.61 and 3.03 +/- 1.18/s, respectively (P < 0.001). The TDR was 145 +/- 56 and 66 +/- 15 ms (P < 0.001). In patients with hypertensive left ventricular hypertrophy, the delta V/(delta T.Vpeak) correlated well with the degree of hypertrophy (r = 0.75, P < 0.01) and with the TDR (r = 0.82, P < 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity increased with the delta V/(delta T.Vpeak) (r = 0.68, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗