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F Kajiya

Publications and source records attributed to F Kajiya.

At least 55 records · Page 3Linked to original sources
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

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↗
PubMed1993

Velocity profiles and phasic flow patterns in the non-stenotic human left anterior descending coronary artery during cardiac surgery.

OBJECTIVE: The aim was to investigate the phasic characteristics of normal human left coronary artery flow and velocity profiles across the vessel. METHODS: The phasic characteristics of flow in the human left anterior descending coronary artery, the centreline flow velocities, and the velocity profiles were measured in 10 patients during corrective surgery for atrial septal defect after closure of the defect. None of these patients had any detectable coronary artery stenosis or left ventricular hypertrophy. Measurements were made with a 20 MHz 80 channel pulsed Doppler velocimeter. RESULTS: The velocity waveform displayed a diastolic-predominant pattern with a systolic to diastolic velocity ratio of 0.29(SD 0.17). Reverse flow was observed in early systole in five patients and in mid to late systole in six patients. The values of peak Reynolds number, unsteadiness parameter, and pulsatility index were 504(198), 2.5(0.6), and 5.9(4.4) respectively. The velocity profiles during diastole showed considerable variability in shape, ranging from symmetrical to skewed to M shaped patterns. The peak wall shear rate was 765(250) s-1 on the epicardial wall of the vessel and 712(301) s-1 on the myocardial wall; the difference was not statistically significant. CONCLUSIONS: The velocity waveform displayed a diastolic-predominant pattern. Considerable variability in shape of the velocity profile was found and was perhaps due to the time evolution of the velocity profile within the diastolic time period.

Adolescent↗
PubMed1993

In vivo observation of subendocardial microvessels of the beating porcine heart using a needle-probe videomicroscope with a CCD camera.

We developed a portable needle-probe videomicroscope with a charge-coupled device (CCD) camera to visualize the subendocardial microcirculation. In 12 open-chest anesthetized pigs, the sheathed needle probe with a doughnut-shaped balloon and a microtube for flushing away the intervening blood was introduced into the left ventricle through an incision in the left atrial appendage via the mitral valve. Images of the subendocardial microcirculation of the beating heart magnified by 200 or 400 on a 15-in. monitor were obtained. The phasic diameter change in subendocardial arterioles during cardiac cycle was from 114 +/- 46 microns (mean +/- SD) in end diastole to 84 +/- 26 microns in end systole (p < 0.001, n = 13, ratio of change = 24%) and that in venules from 134 +/- 60 microns to 109 +/- 45 microns (p < 0.001, n = 15, ratio of change = 17%). In contrast, the diameter of subepicardial arterioles was almost unchanged (2% decrease, n = 5, p < 0.01), and the venular diameter increased by 19% (n = 8, p < 0.001) from end diastole to end systole. Partial kinking and/or pinching of vessels was observed in some segments of subendocardial arterioles and venules. The percentage of systolic decrease in the diameter from diastole in the larger (> 100 microns) subendocardial arterioles and venules was greater than smaller (50-100 microns) vessels (both p < 0.05). In conclusion, using a newly developed microscope system, we were able to observe the subendocardial vessels in diastole and systole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Atrial contractility affects phasic blood flow velocity of atrial small vessels in the dog.

OBJECTIVES: The aim was to evaluate the relative contribution of atrial muscle contraction and atrial pressure to the phasic patterns of left atrial arterial and venous flows. METHODS: Using a laser Doppler velocimeter, blood velocities were measured in the atrial small arteries and veins (outer diameter: 150-500 microns) in anaesthetised open chest dogs (n = 21). The velocity sensor was fixed on the vessel surface with a drop of cyanoacrylate glue when good quality Doppler signals were consistently observed. Left atrial pressure and the contractility of the left atrium were changed by premature ventricular contraction and by intracoronary injection of isoprenaline (0.5 microgram), respectively. RESULTS: Premature ventricular contraction increased left atrial pressure significantly during arterial velocity measurements from 8.1(SD 2.7) to 16.4(1.3) mm Hg and during venous measurements from 8.2(1.2) to 14.3(3.7) mm Hg. However, premature ventricular contraction did not change the blood velocity patterns, the maximum deceleration rate of the systolic velocity wave in arteries, or the maximum acceleration rate of the systolic velocity wave in veins. Although isoprenaline did not change the left atrial pressure, it decreased minimum arterial blood velocity during atrial systole, from 3.3(3.4) to -2.5(3.2) cm.s-1, and increased maximum venous blood velocity from 15.9(5.5) to 19.2(7.4) cm.s-1. Isoprenaline also increased both the maximum arterial systolic velocity deceleration rate, from 90(45) to 234(143) cm.s-2, and the maximum venous systolic velocity acceleration rate from 356(230) to 763(366) cm.s-2. CONCLUSIONS: (1) Left atrial pressure is not a major determinant of the blood flow patterns of the atrial arteries and veins, and therefore it may not closely reflect pressure around mural vessels. (2) Atrial contractility affects the blood flow patterns of the atrial arteries and veins.

Animals↗
PubMed1992

Blood velocity patterns in poststenotic regions and velocity waveforms for myocardial inflow associated with coronary artery stenosis in dogs.

Velocity profiles across a vessel were investigated in poststenotic regions of the canine left coronary artery by our 80-channel 20 MHz ultrasound velocimeter. The velocity waveform in a small artery just before its penetration into myocardium was measured by our laser Doppler method. The poststenotic velocity configuration was characterized by a narrow region of high velocity with diastolic reverse flow near the wall which may dissipate energy. The velocity waveform in the distal small arteries exhibited increased systolic reverse flow with decreased diastolic forward flow, resulting in a remarkable reduction of coronary inflow into the myocardium.

Animals↗
PubMed1992

Phasic characteristics of arterial inflow and venous outflow of right ventricular myocardium in dogs.

To clarify the characteristics and causes of phasic blood flow in coronary circulation of the right ventricle we measured blood velocities in peripheral portions of the right coronary artery and vein in dogs under three conditions: control, transient pulmonary stenosis, and isoproterenol administration. An optical fiber sensor of a laser Doppler velocimeter was fixed onto the vessels (150-500 microns OD) with cyanoacrylate. The phasic pattern of distal arterial velocity was compared with the proximal velocity in the right coronary artery measured with an ultrasound pulsed Doppler velocimeter. Systolic-to-total velocity area ratio in the small epicardial artery [0.38 +/- 0.03 (SE)] was found to be smaller than in the large epicardial artery (0.51 +/- 0.02, P less than 0.01), indicating a capacitive filling of the epicardial artery during systole. The velocity waveform in small right coronary veins was predominantly systolic; i.e., it increased with a rise of right ventricular pressure and decreased with right ventricular relaxation. Comparison of the waveforms during isoproterenol infusion and pulmonary stenosis indicates that contraction of the ventricle is more important than right ventricular systolic pressure in retarding arterial inflow and accelerating venous outflow.

Animals↗
PubMed1992

Blood velocity distributions within intact canine arterial bifurcations.

As local variations in blood flow are implicated in atherogenesis at bifurcations, we measured in vivo blood velocities in different planes within exposed iliofemoral arterial bifurcations in 8 dogs using 20-MHz, 80-channel Doppler ultrasound velocimetry. Cardiac frequency was fixed at 2 Hz by pacing. Local geometry was characterized using 25-MHz, B-mode ultrasound images, photographs, and methacrylate casts. The bifurcations were asymmetrical and planar to within 5 degrees, the diameter ratios of the daughter vessels ranged from 1.47 to 2.00, and the angles between them ranged from 40 to 76 degrees. Measured velocities indicated that just upstream of the bifurcation mean peak Reynolds numbers ranged from 196 to 564 and Womersley (frequency) parameters ranged from 2.00 to 4.1. At the level of the bifurcation, secondary flows were insignificant in the normal plane but strong in the plane of the bifurcation. As a result, two-dimensional velocity fields, reconstructed by vector addition of velocities measured in the plane of the bifurcation, differed markedly from the one-dimensional profiles calculated assuming flow parallel to the vessel axis. In the two-dimensional velocity fields, forward flow was directed toward the flow divider and reversal occurred earliest near the outer wall. Wide spatial and temporal variations in the shear stress at the endothelium are implied by these detailed, in vivo measurements of the bifurcation velocity fields.

Animals↗
PubMed1992

Effect of coronary stenosis on phasic pattern of septal artery in dogs.

To analyze the effect of coronary stenosis on the phasic pattern of blood flow velocity into the myocardium, we measured septal artery blood velocities under control conditions, i.e., no stenosis (N), with moderate (S1) and severe (S2) proximal coronary arterial stenosis, and during complete occlusion. In eight anesthetized open-chest dogs, the blood velocity measurements were performed using our 20-MHz multichannel pulsed Doppler method before and after intracoronary adenosine administration. Under N, the coronary perfusion pressure was set to approximately 100 mmHg, with S1 the poststenotic pressure was approximately 60 mmHg, and with S2 it was decreased to 35 mmHg. Septal arterial blood velocity area, which is the time-integrated envelope of the velocity, was divided into three components; systolic retrograde velocity area, systolic anterograde velocity area, and diastolic anterograde velocity area. There were no significant changes from N to S1 in any of the three velocity areas, which is a measure of the flow. Total inflow decreased from N to S2 by 52% (P less than 0.05). Diastolic anterograde flow decreased from N to S2 by 32% (P less than 0.05). Systolic retrograde flow increased from N to S2 by 75% (P less than 0.05). Systolic anterograde flow was almost unchanged by increasing stenosis. After complete occlusion, the septal artery exhibited a to-and-fro flow pattern. Adenosine-induced vasodilation reduced poststenotic pressure (P less than 0.05) and enhanced systolic retrograde flow without a significant increase in diastolic anterograde flow. Systolic retrograde flow increased at S1 by 49% (P less than 0.05) and at S2 by 27% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

Effect of intracoronary nitroglycerin administration on phasic pattern and transmural distribution of flow during coronary artery stenosis.

BACKGROUND: Nitroglycerin is effective in relieving myocardial ischemia; however, intracoronary nitroglycerin often fails to relieve angina and has been reported to have deleterious effects on subendocardial blood flow. To understand the mechanisms involved, we evaluated the direct effect of nitroglycerin on coronary circulation of the ischemic hearts. METHODS AND RESULTS: We measured the phasic pattern of intramyocardial coronary arterial flow with an 80-channel, 20-MHz pulsed Doppler ultrasound flowmeter under moderate to severe coronary artery stenosis (distal perfusion pressure approximately 45 mm Hg group 1, n = 6) and transmyocardial blood flow distribution using radioactive microspheres while maintaining coronary pressure at a low constant level (40 mm Hg, group 2, n = 6). In anesthetized open-chest dogs, the left main coronary artery was perfused directly from the right carotid or femoral artery. In this bypass circuit, pressure was controlled with an occluder or a reservoir was connected to the circuit. In group 1, the systolic and diastolic pressures distal to the stenosis decreased significantly after intracoronary administration of nitroglycerin at maximal coronary flow from 66.5 +/- 18.5 to 56.5 +/- 13.8 mm Hg (p less than 0.01) and from 36.6 +/- 14.4 to 27.5 +/- 8.9 mm Hg (p less than 0.01), respectively. The phasic pattern of the septal artery flow was predominantly diastolic and was characterized by systolic reverse flow even in the absence of stenosis. Coronary stenosis increased systolic reverse flow. Nitroglycerin increased diastolic forward flow (p less than 0.05) but augmented systolic reverse flow markedly (p less than 0.001). In group 2, nitroglycerin increased subepicardial flow (p less than 0.05) but failed to increase subendocardial flow. With the administration of nitroglycerin, the subendocardial-to-subepicardial flow ratio decreased significantly from 0.73 +/- 0.19 to 0.32 +/- 0.14 (p less than 0.01). CONCLUSIONS: The increased systolic reverse flow after intracoronary administration of nitroglycerin may be closely related to failure of subendocardial blood flow to increase with increase subepicardial flow.

Animals↗
PubMed1991

Effect of left ventricular hypertrophy secondary to systemic hypertension on left coronary artery flow dynamics.

STUDY OBJECTIVE: The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. DESIGN: Measurements of blood velocities in the left anterior descending coronary artery were made with a 20 MHz Doppler catheter with a top mounted annular crystal. All patients had normal coronary arteriograms. PATIENTS: 23 hypertensive patients [systolic/diastolic pressure: 181(SD 15)/100(4) mm Hg)] with left ventricular hypertrophy, and 13 atypical chest pain patients without left ventricular hypertrophy or any abnormal haemodynamic findings (normal controls) entered the study. MEASUREMENTS AND MAIN RESULTS: The left anterior descending coronary artery blood velocity waveform in pressure overloaded left ventricular hypertrophy was characterised by delayed early diastolic inflow. The diastolic rise time of coronary flow (TDR), ie, the time from the beginning of diastole to peak velocity, was higher in patients with hypertensive left ventricular hypertrophy than in normal controls, at 145(56) v 66(15) ms, p less than 0.001. In patients with hypertensive left ventricular hypertrophy, TDR correlated well with the degree of hypertrophy (r = 0.83, p less than 0.01) and also with peak left ventricular systolic pressure (r = 0.62, p less than 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, decreased with prolongation of TDR (r = 0.58, p less than 0.02). CONCLUSIONS: (1) Impairment of early diastolic coronary arterial inflow is the most remarkable characteristic in pressure overloaded left ventricular hypertrophy; (2) preceding systolic vascular compression and impaired left ventricular relaxation correlate with the delayed early diastolic inflow; (3) the delayed inflow is an important possible cause of the decreased coronary flow reserve in the hypertensive left ventricular hypertrophy.

Adult↗
PubMed1991

[Left ventricular hypertrophy secondary to systemic hypertension: its effect on coronary hemodynamics].

To clarify the characteristics and possible causes of phasic blood velocity patterns in pressure overload hypertrophy, we measured blood flow velocities in the left anterior descending coronary arteries in 16 patients with left ventricular hypertrophy secondary to systemic hypertension. These measurements were made with a 20MHz Doppler catheter. All patients had normal coronary arteriograms. The blood flow velocity patterns were characterized by the decrease in the rise of early diastolic inflow velocity. Prolongation in the time from the onset of diastole to peak velocity (TDPV) correlated with the degree of left ventricular hypertrophy. TDPV was prolonged in proportion to the increase in the peak left ventricular systolic pressure and left ventricular ejection fraction. The flow reserve calculated from the ratio of the diastolic mean velocity after the intracoronary injection of papaverine to the resting flow showed a trend toward the decrease proportional to the prolongation in TDPV due to an increase of wall thickness. In conclusion, preceding systolic vascular compression and systolic vascular strain can be factors causing early diastolic inflow disturbance in left ventricular hypertrophy secondary to hypertension. The decrease of coronary reserve may partially be attributable to the decrease in the rise of early diastolic inflow velocity.

Adult↗
PubMed1990

Accuracy of 20-MHz Doppler catheter coronary artery velocimetry for measurement of coronary blood flow velocity.

The accuracy of 20-MHz Doppler catheter coronary artery velocimetry (Millar Instruments) was evaluated by model experiments using a turntable and a flow tube. In the turntable experiments, the flow away from the catheter tip (away flow) was significantly lower than that toward the catheter (toward flow), but the measured velocities for both away and toward flows were always lower than the known velocities. Nevertheless, the blood velocities measured at a sampling point 4 mm from the catheter tip showed excellent correlation with the known velocities irrespective of flow direction. The shape of the FFT spectra of the Doppler shift frequency from blood was broadened, and the frequency corresponding to the known velocity was always close to the maximum Doppler shift frequency. We concluded that zero-cross detection of blood velocity by the 20-MHz pulsed Doppler catheter provides a reliable measure for evaluating relative velocity changes, although it underestimates the blood velocity.

Blood Flow Velocity↗
PubMed1990

A laser Doppler catheter for monitoring both phasic and mean coronary vein flow.

A new catheter-type laser Doppler velocimeter has been developed to monitor coronary vein flow. A thin graded-index multimode optical fiber (outer diameter of 125 microns) is set inside a 5-F catheter, and eight elastic silicon rubber spikes are arranged radially toward the vessel wall to fix the catheter tip in or near the axial region of the coronary vein. He-Ne laser light (wave length = 632.8nm) is introduced into the blood through the optical fiber, and reflected light is collected by the same fiber. The Doppler signal is detected by a spectrum analyzer. To avoid any effect by the spikes on flow, the fiber is extended from the catheter tip by 3 mm at the time of measurement. Straight and curved tubing was used to examine the accuracy of flow measurement. The flow velocities recorded by the catheter, which were measured by an electromagnetic flowmeter, exhibited excellent linearity (r = straight; 0.982, curved: 0.996). The blood flow velocity in the great cardiac vein was measured by this method in five dogs. The predominantly systolic waveform, which is a characteristic of the coronary vein flow, was observed in all of the dogs. The great cardiac vein velocity increased around the beginning of the ventricular ejection and decreased gradually after the peak formation at mid- or end-diastole. In addition to this main peak, small flow components were frequently observed during isovolumic contraction and the atrial contraction phase, although these flow components varied in individual dogs. Following left anterior descending artery occlusion, the great cardiac vein flow velocity decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effect of blood filling in intramyocardial vessels on coronary arterial inflow.

The influence of the filling condition of the unstressed volume (UV) of intramyocardial vessels on the diastolic coronary arterial pressure-flow relationship was analyzed. UV is defined as the blood volume at zero transmural pressure. In seven anesthetized, paced dogs with induced heart block, coronary artery inflow was occluded so that blood in the UV was displaced into the coronary vein by myocardial contraction. After pacing was turned off, coronary perfusion pressure was increased stepwise to seven target pressures (20-90 mmHg). After reperfusion, left anterior descending coronary arterial (LAD) flow reached an initial quasi-steady level, but great cardiac venous (GCV) flow was absent (UV-unfilled phase). With reappearance of the GCV flow (UV-filled phase), LAD flow decreased to a final steady level. Pressure-flow relationships during both phases were linear (r = 0.97-0.99). The inverse of the slope of the pressure-flow relationship during the UV-filled phase, 0.69 +/- 0.08 mmHg.min.ml-1, was significantly higher than that during the UV-unfilled phase, 0.55 +/- 0.06 mmHg.min.ml-1 (P less than 0.01), although the zero-flow pressure intercepts were similar (18.9 +/- 1.8 mmHg for UV filled vs. 19.9 +/- 2.2 for UV unfilled). These results indicate that diastolic coronary arterial inflow is impeded by a blood volume within intramyocardial vessels that exceeds the UV.

Animals↗