Pulsed Doppler Velocity Meter Research Articles

Epinephrine Affects Hemodynamics of Noninnervated Normal and All-Trans Retinoic Acid-Treated Embryonic Chick Hearts

Objective: To study the acute effect of epinephrine on hemodynamics of noninnervated normal and retinoic-acid-treated embryos. Design: Prospective interventional study design. Methods: A total of 190 stage 15 (50–55 h of incubation) chick embryos were randomly treated with 1 µg all-trans retinoic acid and reincubated. At stage 20 (day 3) and stage 24 (day 4), dorsal aortic flow velocities were measured with a 20-MHz pulsed Doppler velocity meter, in normal and retinoic-acid-treated embryos. Flow velocity waveforms were assessed both before and after the administration of epinephrine (5 or 10 µg). Results: Epinephrine caused a significant increase (p < 0.05) in heart rate, peak and mean velocities, peak acceleration, peak and mean blood flows, stroke volume and dorsal aortic area of both stage 20 and stage 24 normal and retinoic-acid-treated chick embryos. However, before epinephrine administration, stage 24 retinoic-acid-treated embryos displayed a significantly lesser increase in all outcome variables with the exception of dorsal aortic area. This was even observed after epinephrine administration. The effect of retinoic acid on cardiac output could not be compensated by epinephrine application. Conclusion: Epinephrine affects hemodynamics in both normal embryos and retinoic-acid-treated embryos prior to sympathetic innervation. A significant difference in hemodynamics exists between stage 24 normal and retinoic-acid-treated embryos. The underlying mechanism for the observed hemodynamic changes will need to be investigated.

Altered hemodynamics in chick embryos after extraembryonic venous obstruction.

To obtain insight into hemodynamics during abnormal cardiac development, a chick model was developed recently in which a spectrum of conotruncal anomalies, in combination with abnormal semilunar valves and/or pharyngeal arch artery malformations, was induced through extraembryonic venous obstruction (venous clip) at stage 17 (70-h incubation). In chick embryos of stage 24 and stage 34 control (n = 8; n = 21) and with venous clip (n = 11; n = 18), we simultaneously measured dorsal flow velocities with a 20-MHz pulsed Doppler velocity meter and dorsal aortic (stage 24) and vitelline artery (stage 34) blood pressures with a servo-null system. After the hemodynamic recordings were collected, all 58 embryos were subjected to morphological examination. The hemodynamic data were correlated with the morphology. Statistical comparison was performed between control and experimental values. At stage 24, venous clip embryos showed impaired looping. Physiologically, only a decrease in peak acceleration was found in these embryos (p < 0.05). At stage 34, a spectrum of conotruncal malformations was seen, that consisted of a ventricular septal defect in combination with abnormal semilunar valves and/or pharyngeal arch malformations. A dextroposed aorta in combination with a ventricular septal defect was diagnosed as double-outlet right ventricle. Hemodynamically, peak systolic and mean velocities, peak systolic and mean blood flows and stroke volume were increased while the heart rate was reduced after placement of the venous clip (p < 0.05). In both stages, pressure readings showed no statistically significant differences between control and experimental embryos. Our findings suggest that the hemodynamic changes seen in venous clip embryos reflect the presence of a compensatory mechanism.

Blood flow acceleration in the carotid and brachial arteries of healthy volunteers: respective contributions of cardiac performance and local resistance.

The influence of local resistance and cardiac performance on peripheral blood acceleration was investigated in 14 healthy male volunteers. Steady and pulsatile flow was studied in the brachial and in the common carotid arteries, ie, two territories that exhibit marked differences in resistive characteristics. Instantaneous blood velocity (V), mean blood velocity (Vm) and artery diameter (D) were evaluated at rest by an ultrasonic range-gated pulsed Doppler flowmeter using a double transducer probe, thus allowing the calculation of mean blood flow (Q). Mean local resistance (R) was obtained by dividing the mean arterial pressure by Q. The peak value of the local acceleration of the blood was obtained by computer-assisted calculation of the first derivative of instantaneous blood velocity (Gmax = +dV/dtmax). Peak aortic blood acceleration (GAo) was simultaneously measured from the suprasternal notch using a pulsed Doppler velocity meter. In the branchial and the common carotid arteries, Gmax was of a similar magnitude (551 +/- 30 and 555 +/- 44 cm/s2, respectively) despite major differences in the respective D, Vm, Q and R values. In neither artery was there a relationship between Gmax and either resting Q or R. At the brachial artery level, Gmax was positively related to GAo (r = 0.79, P = 0.0008). At the common carotid artery level, there was a weak, although non significant relationship between Gmax and GAo (P = 0.08). Our results indicate that the local acceleration of peripheral blood flow in the brachial artery is related rather to upstream central impulse than to downstream hemodynamics, and suggest some regional differences in the hemodynamic determinants of the local acceleration of peripheral blood flow.

Distribution of blood flow between embryo and vitelline bed in the stage 18, 21 and 24 chick embryo

We defined the distribution of blood flow between the embryo and the extraembryonic vascular bed as an initial step in understanding the control of flow distribution in the early developing heart. Dorsal aortic blood flow of stage 18, 21, and 24 chick embryo (n > or = 7 at each stage) was measured with a 20 MHz pulsed-Doppler velocity meter. Analog waveforms were digitally sampled at 500 Hz. 1-5 x 10(3) yellow microspheres in saline suspension were injected into the vitelline vein. The embryo and the extraembryonic vascular bed were harvested and separated from each other. The dye on the microspheres from each portion was extracted and extrapolated from the standard curve of the absorbance of dye concentrations per number of microspheres quantified by spectrophotometry. Blood flow was calculated from the integral of blood velocity and aortic cross-sectional area multiplied by the fraction distribution of microspheres in the embryo and extraembryonic vascular bed. Data were presented as mean +/- standard error of the mean. The proportion distribution of microspheres between embryo and extraembryonic vascular bed shifted from 18.7 +/- 2.5 vs. 81.3 +/- 2.5% at stage 18, 25.1 +/- 3.0 vs. 74.9 +/- 3.0% at stage 21, and 34.2 +/- 2.4 vs. 65.8 +/- 2.4% at stage 24. Indices of blood flow normalized to wet weight (mean +/- 95% confidence interval) were similar between the embryo and the extraembryonic vascular bed, but increased throughout the stages. During embryogenesis, blood flow per unit mass is evenly distributed between the metabolically active embryo and the extraembryonic vascular bed.

Effect of atrial natriuretic peptide on diastolic filling in the stage 21 chick embryo.

Atrial natriuretic peptide (ANP) exerts hemodynamic effects by direct venodilation in the chick embryo. We hypothesized that ANP-induced venodilation affects ventricular diastolic filling resulting in reduced ventricular preload. Chick ANP (0.1 microgram in 10 microL of normal saline) was suffused onto the vitelline vascular bed in stage 21 (3 1/2 d) chick embryos. Equivalent aliquots of normal saline were suffused as sham controls, and normal embryos received no suffusion. We measured simultaneously dorsal aortic blood velocity and atrioventricular blood velocity with a 20-MHz pulsed-Doppler velocity meter. Analog wave forms were digitally sampled at 500 Hz, and the dorsal aortic cross-sectional area was used to calculate dorsal aortic blood flow. Passive ventricular filling volume equaled dorsal aortic stroke volume multiplied by the fraction of passive area; active filling volume equaled dorsal aortic stroke volume multiplied by the fraction of active area. Data were summarized as mean +/- SEM (n > or = 7 per group) and analyzed by analysis of variance. Cycle lengths were similar in ANP-suffused, sham control, and normal embryos. Dorsal aortic blood flow decreased from 0.49 +/- 0.04 mm3/S at baseline to 0.27 +/- 0.05 mm3/S at 4 min post-ANP suffusion (p < 0.05) and was unchanged in sham control and normal embryos (p > 0.05). Passive ventricular filling was reduced by ANP suffusion, whereas active filling was unaffected, resulting in a decreased passive/active filling ratio from 0.64 +/- 0.07 at baseline to 0.32 +/- 0.08 at 4 min in ANP-suffused embryos (p < 0.05). Passive/active ratio was unchanged in sham control and normal embryos. Thus, ANP-mediated vasodilation reduces cardiac output via decreased passive ventricular filling in the embryonic heart.

Hemodynamics and Ventricular Function in the Day-12 Rat Embryo: Basic Characteristics and the Responses to Cardiovascular Drugs

We investigated the basic characteristics of the rat embryonic circulation and also looked at the hemodynamic effects of alpha- and beta-agonists, digitalis, and atrial natriuretic peptide, using a modified organ culture system in which the embryo was placed in oxygenated Hanks' balanced salt solution, blood pressure was measured by a servo-null micropressure system, and blood flow pattern was obtained by a 20-MHz pulsed Doppler velocity meter. The peak pressure was 0.5 +/- 0.04 (SEM) mm Hg at the atrium (n = 6), 2.3 +/- 0.10 mm Hg at the ventricle (n = 15), 1.6 +/- 0.03 mm Hg at the truncus (n = 7), and 1.0 +/- 0.05 mm Hg at the umbilical artery (n = 21). There was a pressure drop from the ventricle to the truncus and then a smaller pressure decrease to the umbilical artery. The atrial a-wave was 20% of ventricular pressure and ventricular inflow blood flow pattern showed very low early-to-late filling ratio, indicating that the ventricle was stiff. These findings were essentially the same as in the chick embryo. We recorded the ventricular image by using a high-speed video system with a frame rate of 200/s, and the ventricular pressure-area loop showed a triangular shape with short isovolumetric phases, which was different from that of the chick embryo at a similar stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of dynamic atrial dimension and function during early cardiac development in the chick embryo.

Although atrial morphologic changes are well documented, the description of early atrial function is limited. We used videomicroscopic methods to define the function of the contracting atrium in stage 16 to 24 white Leghorn chick embryos. We exposed the embryo in ovo (right side up) and imaged the ventricle, then repositioned the embryo (left side up) and imaged the atrium (n greater than or equal to 8 per stage). We traced the atrial endocardial border and then measured atrial perimeter (mm) and cross-sectional area (mm2). A 20-MHz pulsed Doppler velocity meter was used to measure atrioventricular blood velocity during atrial imaging in an additional six stage 21 embryos. Data were tested by analysis of variance and regression analysis. Mean heart rate change after repositioning was -4 +/- 1%. Atrial maximum and minimum area increased linearly versus embryo stage (y = 0.10x - 1.41, r = 0.89, p less than 0.05 and y = 0.05x - 0.67, r = 0.82, p less than 0.05, respectively). Shortening fraction (percentage of reduction) of atrial perimeter and area decreased from 32.3 +/- 2.0% to 27.5 +/- 1.8% (p less than 0.05) and 56.2 +/- 3.0% to 47.7 +/- 2.0% (p less than 0.05), respectively, from stage 16 to 24. During atrial contraction, the velocity of circumferential wall shortening increased linearly with stage (y = 0.22x - 2.08, r = 0.81, p less than 0.01); however, the velocity of lengthening was similar between stages (p = 0.45). Simultaneous atrial imaging and pulsed Doppler velocity measurement showed that passive atrioventricular flow occurred late in atrial lengthening and active atrioventricular flow occurred during atrial contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Diastolic Filling Characteristics in the Stage 12 to 27 Chick Embryo Ventricle

Cardiac output is affected by the diastolic filling characteristics of the ventricle. We hypothesized that the relative contributions of passive and active filling change as the ventricle develops from a smooth-walled tube to a trabeculated four-chamber heart. In stage 12 to 27 white Leghorn chick embryos, we simultaneously measured ventricular pressure with a servo-null micropressure system and dorsal aortic and atrioventricular velocities with a 20-MHz pulsed-Doppler velocity meter. The analog waveforms were sampled at 500 Hz and converted to digital format via an analog/digital board. We partitioned diastole into passive and active components. The passive phase began with the return of the pressure curve to baseline and extended to the onset of the a-wave. The active phase began with the upstroke of the atrial velocity curve and extended to the upstroke of the ventricular pressure curve at end-diastole. Data are presented as mean +/- SEM (n greater than or equal to 6 at each stage) and analyzed by analysis of variance and regression analysis. At similar cycle lengths ranging from 480 to 600 ms (p greater than 0.05), end-diastolic pressure increased from 0.24 +/- 0.02 mm Hg at stage 12 to 0.55 +/- 0.01 mm Hg at stage 27. Passive and active filling volumes were 92 (0.0038 +/- 0.0005 mm3) and 8% (0.0004 +/- 0.0002 mm3), respectively, at stage 12 and changed to 24 (0.23 +/- 0.08 mm3) and 76% (0.62 +/- 0.08 mm3), respectively, at stage 27. The ratio of passive to active filling volume decreased from 7.89 to 0.35.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Atrial Natriuretic Peptide on Hemodynamics of the Stage 21 Chick Embryo

Atrial natriuretic peptide (ANP) is important in the modulation of hemodynamics and fluid balance in the mature subject, but its hemodynamic effects at early stages of morphogenesis are not defined. We studied the effect of rat atriopeptin III on hemodynamics in chick embryos at Hamburger-Hamilton stage 21. The cardiovascular system is not yet innervated, nor is the kidney formed in these embryos. The vitelline arterial and venous blood pressures were measured with a servo-null, micro-pressure system and the dorsal aortic blood flow was measured with a 20 MHz pulsed Doppler velocity meter. The peptide was infused into the vitelline vein with a microinjector at doses of 0.1, 1.0, and 10 ng. Doses normalized by body wt of embryos averaged 0.003, 0.035, and 0.32 ng/mg (n = 61), respectively. Vitelline arterial blood pressure decreased in a dose dependent manner [y = 55.8 - 9.9x; r = -0.49; p less than 0.01 (y = % of baseline, x = log ng/mg)], and dorsal aortic blood flow, a measure of cardiac output, decreased similarly (y = 39.6 - 16.2x; r = -0.47; p less than 0.01). Heart rate did not change. Ten ng of ANP increased the vitelline venous diameter, determined directly under a microscope, from 125 +/- 47 (SD) microns to 139 +/- 49 microns (n = 11; p less than 0.01), and decreased vitelline venous pressure from 0.34 +/- 0.05 mm Hg to 0.10 +/- 0.07 mm Hg (n = 5). We conclude that ANP exerts its hemodynamic effect by direct venodilation in the noninnervated and anephric circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamics of the stage 12 to stage 29 chick embryo.

The heart is the first functioning organ in the embryo and provides blood flow during cardiac morphogenesis from a muscle-wrapped tube a few cells thick to the four-chambered pump. We described the hemodynamics of the chick embryo from stage 12 (50 hours of a 21-day incubation) to stage 29 (6 days), during which the embryo weight increased 120-fold. We measured ventricular, embryo and extraembryonic vascular bed wet weights, dorsal aortic blood flow with a directional pulsed-Doppler velocity meter, and ventricular and vitelline arterial blood pressures with a servo-null micropressure system. The data are reported as mean +/- SEM. With rapid development and morphogenesis, dorsal aortic blood flow increased from 0.015 +/- 0.004 to 2.40 +/- 0.20 mm3/sec parallel to the geometric increase of wet embryo weight from 2.22 +/- 0.10 to 267.5 +/- 9.7 mg. Dorsal aortic blood flow normalized for embryo and extraembryonic weight remained relatively constant (Y = 2.13 + 0.02X, r = 0.23, SEE = 0.03). Stroke volume increased from 0.01 +/- 0.003 to 0.69 +/- 0.03 mm3, and heart rate doubled from 103 +/- 2 to 208 +/- 5 beats/min. Systolic, diastolic, and mean vitelline arterial pressure increased linearly from 0.32 +/- 0.01, 0.23 +/- 0.01, and 0.28 +/- 0.01 mm Hg at stage 12 to 2.00 +/- 0.06, 1.22 +/- 0.03, and 1.51 +/- 0.04 mm Hg, respectively, at stage 29. Ventricular peak systolic and end-diastolic pressure increased from 0.95 +/- 0.04 and 0.24 +/- 0.02 at stage 12 to 3.45 +/- 0.10 and 0.82 +/- 0.03 at stage 29, respectively. The hemodynamic waveforms were similar to those found in the four-chamber heart of the mature animal. These data are integral to understanding the interrelation of function and form during cardiac development.

Effect of increased pressure on ventricular growth in stage 21 chick embryos.

We studied the effect of increased ventricular pressure on heart growth in the stage 21 (3.5-day) chick embryo. Ventricular pressure was increased by constricting the conotruncus with a loop of 10-0 nylon tied in an overhand knot. The embryos were reincubated, and physiology and cellular morphology were evaluated at successive stages of development, stages 21, 24, 27, and 29. Ventricular pressure was measured with a servo-null pressure system, and cardiac output was measured with a 20-MHz pulsed Doppler velocity meter. Ventricular and embryo dry weights were measured on an electronic microbalance, myocyte organelle composition was measured by a point counting technique, and cell growth response was measured by DNA and protein assay. The conotruncal loop increased ventricular pressure in experimental compared with control embryos, i.e., at stage 24, 2.88 +/- 0.13 vs. 1.96 +/- 0.05 (SE) mmHg (P less than 0.05), respectively, without affecting cardiac output. Ventricular dry weight increased in experimental vs. control embryos, i.e., at stage 24, 114 +/- 7 vs. 85 +/- 4 micrograms (P less than 0.05), respectively, whereas embryo weights were similar between the two groups. The difference in ventricular weights was due to myocyte hyperplasia, since organelle proportion of myofibrils and mitochondria, DNA-to-protein ratio, and myocyte area were similar in experimental voice control embryos. Thus the adjustment of myocardial mass to ventricular work occurs even during the earliest stages of embryonic development. Cardiac growth and morphogenesis are parallel but separable processes.

Aortic impedance and hydraulic power in the chick embryo from stages 18 to 29.

Little is known about the hemodynamic properties of the rapidly expanding arterial bed during embryonic development. Using a servo-null pressure system and 20-MHz pulsed Doppler velocity meter, we recorded simultaneous dorsal aortic pressure and velocity waveforms. The waveforms were digitized at 3-msec intervals and subjected to Fourier analysis. We calculated hydraulic energy and the impedance spectrum to 10 Hz. From stages 18 to 29, heart rate (148 +/- 3 to 193 +/- 9 beats/min), systolic pressure (1.14 +/- 0.12 to 3.04 +/- 0.10 mm Hg), and mean dorsal aortic blood flow (21 +/- 2 to 214 +/- 19 mm3/min) increased. Peripheral vascular resistance (Z0: 30.4 +/- 4.8 to 6.4 +/- 0.7 dyne x sec/mm5), and the impedance moduli (Z1: 6.5 +/- 1.0 to 1.7 +/- 0.2 dyne x sec/mm5; Z2: 6.1 +/- 1.2 to 1.7 +/- 0.1 dyne x sec/mm5; Z3: 7.3 +/- 1.1 to 1.7 +/- 0.2 dyne x sec/mm5) decreased. Total hydraulic power increased from 48 +/- 7 to 2,606 +/- 96 nW, while the proportion of oscillatory energy increased from 29 +/- 2% to 65 +/- 4%. With development hydraulic load decreases, total external work increases and the dorsal aorta and embryonic vascular bed becomes more compliant. A greater proportion of total energy is expanded in pulsatile blood flow, suggesting that ventricular-arterial coupling is less efficient later in development.

Pulsed Doppler Determinations of Cardiac Output in Neonates: Normal Standards for Clinical Use

Noninvasive monitoring of cardiac output can greatly facilitate the clinical assessment and management of neonates with cardiovascular compromise. To assess normal values of cardiac output in neonates, mean blood flow velocity was measured in the ascending aorta from a suprasternal approach using a range-gated, pulsed Doppler velocity meter, and aortic root diameter was determined from an M-mode echocardiogram. These techniques were combined, and cardiac output was evaluated in 59 healthy premature and 62 term newborn infants during the first week of life. Birth weights ranged from 780 g to 4,740 g and gestational age from 27 to 42 weeks. Cardiac output values increased linearly with advancing birth weight (r = +.94, P less than 0.001) and gestational age (r = +.95, P less than .001). Mean cardiac output values (+/- SD) per kilogram of body weight were 249 +/- 34 mL/min/kg and decreased with advancing birth weight: less than 1,500 g = 265 +/- 32 mL/min/kg; 1,500 to 2,500 g = 253 +/- 34 mL/min/kg; and greater than 2,500 g = 241 +/- 33 mL/min/kg. For clinical use, 325 mL/min/kg and 200 mL/min/kg can be used as upper and lower limits of normal, respectively. Doppler cardiac output estimates compared favorably with studies using invasive techniques.

Blood velocities in the uterine artery in humans during labour.

Blood velocities in the uterine arteries were measured during labour in humans, by means of the pulsed ultrasound Doppler velocity meter (UNIDOP). The uterine arteries were approached through the abdominal wall at the lateral border of the uterus and through the lateral vaginal fornix. At a depth of 0.5-1.5 cm from the lateral vaginal fornix there were three different arteries in each woman. One of these arteries had similar velocity spectra to the uterine artery as measured through the abdominal wall higher up along the uterus, and the velocities were in the same range. The mean velocities were high and the velocities in diastole were high compared to those in systole. During uterine contractions the velocities were reduced during diastole, reducing mean velocities by 20-40% as measured through the vagina and by 50-60% when measured higher up through the abdominal wall. A second artery, which we believe is a branch of the uterine artery traversing the myometrium, had lower mean velocities and a greater difference between systole and diastole. During contractions the velocities were reduced by 100%. A third artery, which we believe is the descending branch of the uterine artery, supplying the cervix and vagina, had the lowest mean velocities, with backflow during diastole. During contractions the velocities increased 100-140%.

152 BLOOD FLOW IN THE ASCENDING AND THE DESCENDING AORTA IN TERM NEWBORN INFANTS

The combination of 2-dimensional real-time and pulsed Doppler echocardiography provides a noninvasive method of measuring blood flow and has been used to study blood flow at the lower thoracic level of the descending aorta (DA) in the human fetus. Using these techniques, we evaluated the proportion of cardiac output distributed through the DA in 13 term newborn infants (mean±SEM BW 3551±95 g, GA 40.1±0.3 w). Blood flow velocity was measured using a 3.5 MHz, range gated, pulsed Doppler velocity meter with the transducer positioned in the suprasternal notch. Blood flow in the ascending aorta (AA) was measured at the aortic root level and descending flow below the isthmus. The internal diameter of the AA was assessed at the level of the aortic valve using M-mode echocardiography and the diameter of the DA in the posterior atrioventricular groove with the use of the 2-D long axis view. Blood flow in the AA was 789±42 ml/min and in the DA 499±26 ml/min indicating that 63.5% of the left ventricular output is distributed through the DA. The mean blood flow velocity was comparable at both sites, whereas the mean diameter of the DA was 19% smaller than the diameter of the AA. In healthy term newborn infants approx. 2/3 of cardiac output is directed to the DA and 1/3 to brachial and carotid arteries. The changes in aortic blood flow are correlated with the changes in aortic diameter.

150 DEVELOPMENTAL CHANGES IN THE FRANK-STARLING RELATION SHIP IN THE CHICK EMBRYO

We are studying control mechanisms in the embryonic cardiovascular system. We hypothesize that stroke volume increases directly with preload as the chick embryo develops from stage 18 (3 days) to 29 (6 days), a 16-fold increase in embryo weight. Mean dorsal aortic blood velocity (V) was measured with a 20 MHz pulsed-Doppler velocity meter; mean blood flow (Q) was calculated using V and aortic diameter. Q+HR equals stroke volume index. dV/dt was electronically derived. Peak stroke volume was measured in response to intravenous injection of increasing volumes of chick Ringer's solution. Volumes ranged from 6.8 to 157 μL per gram embryo wet weight, permitting comparison of the volume response at different stages. A minimum of 5 embryos were studied for each volume. Data were tested by ANOVA and regression analysis. Heart rate decreased less than 6% for all stages. Stroke volume changed less than 3% in controls. With volume infusion maximum peak stroke volume increased 29% for stage 18, 83% for stage 24, and 46% for stage 29. Stroke volume increased linearly in all stages with slopes of 3.9 at stage 18, 4.7 at stage 24, and 5.5 at stage 29. dV/dt increased with volume infusion for all 3 stages. Although there is considerable change in embryo and ventricular weight, heart geometric shape, and myofibril myocyte volume and alignment, the relationship between preload and stroke volume is similar at each stage. We conclude that the Frank-Starling mechanism functions over a broad range of development in the preinnervated embryonic heart.

25 + 1 channel pulsed ultrasound Doppler velocity meter for quantitative flow measurements and turbulence analysis

25 + 1 channel pulsed ultrasound Doppler velocity meter for quantitative flow measurements and turbulence analysis

The effect of isoproterenol on cardiovascular function in the stage 24 chick embryo.

The developing cardiovascular system of the chick embryo is susceptible to teratogenic effects of catecholamines. Yet the mechanism for the teratogenetic action is unclear. Since catecholamines affect cardiovascular physiology, we studied the acute effect of the beta-agonist isoproterenol on mean atrial pressure, heart rate, mean dorsal aortic blood flow, mean arterial pressure and vascular resistance in stage 24 chick embryos. Dorsal aortic blood velocity was measured with a 20-MHz pulsed-Doppler velocity meter and intravascular pressure was measured with a servo-null pressure system. Isoproterenol in doses of 2 X 10(-4) micrograms (2.5 micrograms/kg), 8 X 10(-4) micrograms (10 micrograms/kg), and 1.2 X 10(-3) micrograms (15 micrograms/kg) was injected intravenously in 5-microliters aliquots of chick Ringer's solution. Additional groups of embryos were treated with the beta-antagonist propranolol, and isoproterenol plus propranolol. Control embryos received 5 microliters chick Ringer's solution to assess the hemodynamic effects of a volume injection. We found that isoproterenol caused no change in mean atrial pressure, heart rate, or mean arterial pressure. However, isoproterenol caused a dose-related decrease in dorsal aortic blood flow and a 2.5-fold increase in vascular resistance. The effects of isoproterenol were blocked by propranolol, which suggested that the increase in vascular resistance was mediated by beta-receptor stimulation.

A hemodynamic evaluation of cuffed microarteriorrhaphy.

A cuffing technique and a standard interrupted suturing technique of microarteriorrhaphy were compared in the rat femoral artery. The comparison was based on hemodynamic variables, which were measured by 20-MHz pulsed ultrasound Doppler velocity meter (PUDVM) method. The hemodynamic variables included measured blood velocity and vessel lumen diameters, and calculated volumetric flows. Measurements were completed at 5-, 10-, and 20-minute intervals after vessel repair. Data from 26 experimental animals were suitable for analysis, with 15 animals in the standard repair group and 11 animals in the cuffed group. All variables were statistically similar prior to the surgical procedure, indicating that the study groups were appropriate for comparison. The measured lumen diameters were not statistically different at any time interval (P = .06). However, the velocities and the volumetric flow were statistically different (P less than .05) between groups at all time intervals. These values returned toward normal preoperative values over time. The cuffing technique used in this study was not as efficacious as the standard technique of microarteriorrhaphy, when evaluated by 20-MHz PUDVM-derived hemodynamic criteria.

Microarteriorrhaphy: Blood flow after wound healing

The present study tests the hypothesis that early wound healing effects blood flow after experimental microarteriorrhaphy. Hemodynamic variables were measured in the rat femoral artery prior to and 3 weeks after both interrupted and continuous microarteriorrhaphy techniques. The hemodynamic variables (blood velocities, lumen geometry, and calculated blood flow) were measured by 20-MHz pulsed ultrasonic Doppler velocity meter (PUDVM) methods. The control values (N = 22) and the 3 weeks postoperative values, for both the interrupted (N = 11) and continuous groups (N = 11), were not statistically different (P greater than .01). The average calculated blood flows were as follows: control group 10.85 +/- 1.45 cc/min, interrupted group 12.01 +/- .92 cc/min, and continuous group 8.50 +/- 1.45 cc/min. Three weeks of wound healing after microarteriorrhaphy did not significantly change blood flow variables compared to preoperative values.