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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.

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.

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.

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.

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.

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)

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.

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%.

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)

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.

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)

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.

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.

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.

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.

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.

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)

To obtain a smaller sample volume and a suitable sample position for the measurement of blood velocity, we fabricated a laser Doppler velocimeter (LDV) with a dual-fiber pickup. The two fibers (clad: 62.5 micron and core: 50 micron) were placed side by side. An He-Ne laser was introduced into the blood through one fiber and the backscattered light was collected by the other fiber. The Doppler signal was analyzed by a spectrum analyzer. The spectrum of the Doppler shift frequency showed a sharp peaked pattern for both forward and reverse flows and exhibited an excellent correlation with the known blood velocity. The blood velocity in the poststenotic portion of canine coronary artery was successfully measured by the dual-fiber LDV. These results indicate that the dual-fiber LDV is useful for measuring blood velocity accurately with a small sample volume even in disturbed flow fields.

In order to evaluate the functional characteristics of the intramyocardial capacitance vessels during prolonged diastole, we analyzed the response of coronary vein flow after stepwise changes of coronary artery pressure in anesthetized open-chest dogs by using our newly developed laser Doppler velocimeter with an optical fiber. The peripheral portion of the great cardiac vein was isolated and the optical fiber tip was inserted into the vessel. The left anterior descending coronary artery was cannulated and connected to a reservoir to regulate coronary perfusion pressure. Intracoronary adenosine administration was carried out to avoid any change in coronary vasomotor tone. After 15 seconds of occlusion of the perfusion route, the heart was arrested by pacing-off. Two seconds later, coronary perfusion pressure was increased stepwise to a preset target pressure. This procedure was repeated by changing target pressure at 4 (or 5) different pressure levels (31-105 mm Hg). The great cardiac vein flow became zero due to the cardiac arrest and remained at zero for a moment (dead time) after the initiation of reperfusion. Then the flow reappeared and increased with first order time delay. The presence of dead time indicates the existence of unstressed volume, and the first order time delay represents the product of resistance and capacitance. The unstressed volume with a minimal vasomotor tone for perfusion pressure of 60-90 mm Hg was 5.2 +/- 2.2 ml per 100 g left ventricle, which is comparable to coronary blood flow for several beats. The capacitance at perfusion pressure of 60-90 mm Hg was 0.08 +/- 0.04 ml/mm Hg per 100 g left ventricle, while that at low perfusion pressure (30-50 mm Hg) was 0.14 +/- 0.09 ml/mm Hg per 100 g left ventricle. These results indicate that the intramyocardial capacitance vessels have two functional components, and that the phasic nature of coronary vein flow is solely the result of the myocardial squeezing of the blood in the capacitance vessels.

In the present study, characteristics of the phasic flow pattern in the great cardiac vein and the mechanism of such pattern formation were investigated using a laser Doppler velocimeter with an optic fiber probe. The laser Doppler velocimeter allowed measurements of venous blood velocity under more physiological conditions than were possible with previous methods. Moreover, venous blood flow measurement in the great cardiac vein mirrors the effects of myocardial contraction on the venous flow more directly than does measurement in the coronary sinus. Thus, our method is considered very useful. Results obtained from the present study are as follows: 1) Measurement of the phasic flow in the great cardiac vein was made in 11 anesthetized dogs using our laser Doppler method. The blood velocity curve obtained in the great cardiac vein was always characterized by a prominent systolic flow wave (SFW). The mean value for the maximum velocities under control conditions in 11 cases was 40 +/- 13 cm/s. The blood velocity increased with the onset of left ventricular ejection and decreased gradually after the peak formation at mid- or late systole.--2) Besides the above SFW, one or two small wave components were frequently observed during the atrial contraction period and/or during the isovolumic contraction phase. On the waveform during the atrial contraction period, two cases showed forward flow, while one case showed reverse flow. The small reverse flow waves during the isovolumic contraction phase were found in seven cases.(ABSTRACT TRUNCATED AT 250 WORDS)

To evaluate local blood flow velocities accurately at many sampling points in small vessels, especially in human coronary arteries, we have developed an 80 channel 20 MHz pulsed Doppler velocimeter. Doppler signals from 80 channels are detected by a zero-cross method and a signal from an optional channel is analyzed by a fast-Fourier transform method, both in real time. Basic experiments using a model and animals have demonstrated the accuracy and utility of our method of measurement of blood flow velocity for both nondisturbed and disturbed flow. Velocity waveforms in a native coronary artery beyond a vein bypass graft insertion were measured during cardiac surgery. They showed a diastolic-predominant pattern with a small systolic component. During transient graft occlusion, the waveforms changed to a systolic-predominant pattern in a patient with severe stenosis and to a to-and-fro pattern in a patient with total occlusion. In a patient with severe aortic regurgitation, the coronary arterial velocity waveforms exhibited a systolic-predominant pattern with a broad velocity spectrum. After aortic valve replacement, however, a diastolic-predominant pattern with a narrow spectrum was observed.

To clarify the characteristics of the phasic blood velocity pattern in small arteries and veins on the left atrial surface, we used our newly developed fiber-optic laser Doppler velocimeter. We intended particularly to examine the influence of atrial contraction and relaxation on velocity waveforms to obtain some insight into the nature of the mechanical force acting on the atrial intramyocardial vascular beds. In 14 anesthetized open-chest dogs, the left atrial appendage was gently displaced to expose small branches of the artery and vein. Vessels with an outer diameter of about 150-500 microns were chosen for the measurements because their walls are transparent to laser light. The fiber tip (velocity sensor) was fixed on the vessel surface with a drop of cyanoacrylate when good-quality Doppler signals were consistently observed. Additional experiments with three dogs were performed to observe the blood velocities in the atrial artery and vein during arrhythmia. The blood velocity waveform in the artery was similar to the pattern of aortic pressure during ventricular ejection (peak velocity, 18.8 +/- 7.8 cm/sec) but was characterized by a pronounced dip during atrial contraction. The temporal coincidence between the dip formation and atrial contraction was confirmed during atrial flutter with an atrioventricular block. After isoproterenol administration (2 micrograms i.v.), the acceleration rate of the forward flow velocity increased by 176% (p less than 0.05), and reverse flow appeared during atrial contraction in five cases out of eight (p = 0.013). The blood flow velocity in atrial small veins, on the other hand, was predominant during atrial contraction (peak velocity, 15.6 +/- 5.8 cm/sec). Isoproterenol increased the acceleration rate of this forward flow velocity by 121% (p less than 0.01). Nitroglycerin did not change the blood velocity waveform significantly in atrial arteries or in veins. The phase opposition between arterial inflow into and venous outflow from the atrial myocardium indicates that a large portion of the coronary inflow to the atrial myocardium may be stored due to the presence of atrial myocardial vascular capacitance. We conclude that atrial myocardial contraction impedes atrial inflow and promotes venous outflow from atrial capacitance vessels.

The dose-response relation of contrast medium-induced hyperemic response in coronary blood flow (contrast hyperemia) was investigated to determine the optimal dose of contrast medium (CM, Urografin-76) for the assessment of coronary flow reserve in man. The great cardiac venous flow (GCVF) was determined with the continuous thermodilution method during the contrast hyperemia induced by the intracoronary injection of CM of three different doses, ie, 2, 4, and 6 ml/60 kg of body weight, into left coronary artery. Submaximal coronary vasodilation could be obtained by intracoronary injection of 4 ml of CM with minimal changes in systemic hemodynamics. The contrast hyperemia with this dose of CM was reproducible and also closely correlated with that obtained during pacing-induced angina. Thus, we conclude that the contrast hyperemic technique with intracoronary injection of 4 ml of Urografin-76 could be a reliable method to assess the coronary flow reserve.

In this paper we describe a laser Doppler velocimeter (LDV) with an optical fiber that measures blood flow velocities accurately in a small sample volume. The principle, optical arrangement, spatial and the temporal resolutions and accuracy for blood flow measurements are delineated, followed by a report of the results of measurements of coronary artery and vein blood flow velocities in dogs. Finally, we touch upon some recent progress made in the LDV with an optical fiber pickup.

To analyze the origin of the coronary artery inflow and the coronary vein outflow, we measured the intramyocardial artery flow and the epicardial small vein flow by means of a laser Doppler velocimeter with an optical fiber. The functional characteristics of the intramyocardial capacitance vessels were investigated by analyzing the responses of coronary vein flow after stepwise changes in coronary artery pressure during long diastole. Then the effect of the intramyocardial capacitance vessels on coronary artery inflow and vein outflow was evaluated. Intramyocardial artery flow was found to be almost exclusively diastolic with frequent systolic reverse flow, whereas peripheral coronary vein flow was almost systolic exclusively. The intramyocardial capacitance vessels have two functional components, unstressed volume and ordinary capacitance. When the unstressed volume was saturated, the intramyocardial displacable blood volume impeded the coronary artery inflow, but promoted vein outflow.

A high resolution laser Doppler velocimeter using an optical fiber was developed to evaluate detailed characteristics of phasic blood flow in the coronary artery. Local blood flow velocities were measured in the proximal (0.27 +/- 0.05 cm i.d.) and the distal portion (0.09 +/- 0.02 cm i.d.) of the left circumflex coronary artery of anesthetized, open-chest dogs. The velocity waveform in the central axial region of the vessel and the velocity profile across the vascular lumen were compared in the proximal and the distal portions.