Pulsed Doppler Flowmetry Research Articles

Stress and cocaine elicit similar cardiac output responses in individual rats.

Cocaine use and behavioral stress elicit variable cardiovascular responses in individuals. In the present study, we examined the effects of cocaine or stress on arterial pressure, heart rate, and cardiac output in conscious rats. Rats were instrumented for determination of ascending aortic blood flow as an index of cardiac output using pulsed Doppler flow-metry. Cocaine administration elicited consistent decreases in cardiac output in some rats, whereas others had increases. In contrast, the pressor and heart rate responses were similar in these two groups of animals. Air jet stress also elicited a decrease in cardiac output only in a subset of conscious rats, yet produced equivalent pressor responses in all rats. Cardiac output responses to cocaine and air jet stress were closely correlated in individual rats, indicating that these stimuli evoke similar hemodynamic responses in individual rats. These observations suggest that the rat may provide a model for understanding differential cardiovascular sensitivity to cocaine and/or stress in humans.

Continuous measurement of rat gastric blood flow using Doppler flowmeter.

We describe the use of pulsed Doppler flowmetry to permit continuous measurement of gastric blood flow in the anesthetized rat. The aims of this study were: 1) to assess the stability of blood flow during Doppler flowmetry; 2) to assess the ability of Doppler flowmetry to record rapid, transient blood flow changes; and 3) to validate Doppler flowmetry against an established blood flow measurement technique using labeled microspheres. Measurements over 3-h periods with a Doppler probe placed on the left gastric artery showed that there was an initial 30-min stabilization period; after this the mean percentage coefficient of variation, indicating intraindividual variability for blood flow, was < 10% for the remaining 150 min. The infusion of norepinephrine produced rapid, transient blood flow changes, including the typical "autoregulatory escape" and "postinfusion hyperemia," both of which were detected by Doppler flowmetry. The accuracy of pulsed Doppler flowmetry in measuring gastric blood flow was established by the demonstration of a highly significant agreement between blood flow measured by the Doppler flowmetry and microsphere techniques. These data indicate that pulsed Doppler flowmetry is an accurate method for the continuous measurement of left gastric artery blood flow in the rat.

Effects of the single and repeated administration of benazepril on systemic and forearm circulation and cardiac function in hypertensive patients

The hemodynamic and cardiac effects of the new angiotensin-converting enzyme inhibitor, benazepril, were studied in 28 hypertensives in a double blind, placebo-controlled, between-patient study. Hemodynamic studies were performed noninvasively by means of M-mode echo (central hemodynamics and left ventricular systolic function), 2-D echo-Doppler (left ventricular diastolic function), and pulsed Doppler flowmetry (forearm circulation). Examinations were done at the end of a placebo run-in period and 3 hours after benazepril administration, both on the first day and after 6 weeks of treatment (10 or 20 mg once daily, according to patient response). In comparison with placebo, benazepril reduced systolic (p = 0.04) and diastolic (p = 0.003) blood pressure, because of a significant reduction in systemic vascular resistance (p = 0.03), while cardiac output was unchanged. Forearm vascular resistance was reduced and brachial artery compliance increased, although not to a statistically significant level (both p = 0.07). Both systolic and diastolic left ventricular function were positively influenced by the afterload reduction: End-systolic stress was reduced by 12% (p = 0.07), as was the late diastolic peak flow velocity (p = 0.02). All hemodynamic changes were evident after acute benazepril administration, and no differences was observed between acute and repeated treatment. We conclude that, similar to other ACE-inhibitors, benazepril reduces blood pressure through a reduction in vascular resistance, while cardiac output and heart rate are unaffected. These hemodynamic effects occur as early as after the first administration and exert a favorable influence on left ventricular dynamics.

Calcium Channel Antagonists Reduce the Cocaine-Induced Decrease in Cardiac Output in a Subset of Rats

Intravenous (i.v.) cocaine administration elicits a decrease in cardiac output (CO) in some but not all rats. In the present study, we examined the effects of L-type calcium channel antagonists on cardiovascular responses in conscious freely moving rats with a cocaine-induced decrease in CO. Arterial blood pressure (ABP), heart rate (HR), and CO (pulsed Doppler flowmetry) were measured, and estimates of changes in systemic vascular resistance (SVR), stroke volume (SV), and rate-pressure product (RPP) were calculated from these values. After recovery, rats were treated with cocaine (5 mg/kg, i.v.) to ascertain their myocardial responses. Some rats demonstrated a decrease in CO, usually during the peak pressor response after cocaine administration, whereas others experienced only slight increases in CO. Rats demonstrating a minimum 15% decrement in CO were pretreated with either verapamil or nifedipine before cocaine was readministered. Verapamil (150 micrograms/kg) or nifedipine (100 micrograms/kg) selectively reduced the peak fall in CO and the increase in SVR after cocaine administration, whereas nifedipine (25 micrograms/kg) had little effect on these parameters. Neither drug affected the pressor response to cocaine. These data suggest that calcium channel antagonists can selectively reduce cocaine-induced decreases in CO and increases in SVR without reducing afterload in a subset of rats sensitive to the cardiodepressive effects of cocaine.

Reversal of cardiac and large artery structural abnormalities induced by long-term antihypertensive treatment with trandolapril

In 15 patients with untreated mild to moderate essential hypertension and left ventricular hypertrophy, we assessed blood pressure, echocardiographic left ventricular mass index, brachial artery compliance (pulsed doppler flowmetry), and calculated forearm vascular resistance (strain gauge plethysmography) before, during (6 and 12 months) and after (1 month washout period) 1 year of satisfactory (blood pressure <- 140/90 mm Hg) antihypertenshre therapy with the angiotensin-converting enzyme inhibitor trandolapril (2.0 mg orally once daily). During the antihypertensive effective treatment, we observed a significant reduction of systolic and diastolic blood pressures, left ventricular mass index, and forearm vascular resistance at both 6 and 12 months. In addition, brachial artery compliance was significantly increased. After washout, systolic (156 ± 3 mm Hg) and diastolic (102 ± 1 mm Hg) blood pressures returned to levels comparable to baseline. However, left ventricular mass index (132 ± 4; p < 0.01) and brachial artery compliance (1.53 ± 0.01; p < 0.01) were still different from baseline. These results demonstrate that chronic antihypertensive treatment with trandolapril is associated with a stable regression of cardiac and vascular abnormalities, which is partially unrelated to the blood pressure lowering effect.

Usefulness of perioperative pulsed Doppler flowmetry in predicting postoperative local ischemic complications after ileocolic esophagoplasty

Regional ischemia may induce cervical anastomosis leakage or stenosis or graft necrosis after esophageal reconstruction by retrosternal interposition of an ileocolic graft. These complications may be related to systemic or local hemodynamic alterations. This study was designed to evaluate the relationship between immediate postoperative arterial blood supply to the graft, arterial patency monitored by angiography, and clinical outcome. Eight patients (mean age 30 +/- 4 years; standard deviation) were studied. Miniaturized Doppler implantable microprobes were sutured to the single artery supplying the graft and connected to an 8 MHz pulsed Doppler flowmeter. Systemic hemodynamic parameters and mesenteric hemodynamic data were collected 3 hours after the end of the surgical procedure. These data were compared with the angiogram of the right superior colic artery supplying the graft, systematically performed on the fifteenth postoperative day, and with the clinical course of follow-up for 3 months. Five patients (group 1) had excellent clinical and angiographic results. Mean mesenteric blood flow in these patients was 51 +/- 49 ml.min-1 (+/- standard deviation, ranging from 9 to 122). Three patients (group 2) had a poor clinical outcome. One had early complete graft necrosis and the two others had leakage of the cervical anastomosis with poor distal arterial vascularization of the graft on the angiogram. Mean mesenteric blood flow was nul in the first patient and, respectively, 24 and 28 ml.min-1 in the two others. Cardiac output and mean arterial pressure were in the same range for all patients. Phasic velocity shape analysis revealed that the three group 2 patients had an end-systolic or end-diastolic reverse flow pattern that was not observed in the five group 1 patients, which suggested a submaximal increase in downstream vascular resistance. This reverse flow pattern seems to be a good predictor of ischemia-related complications. We conclude that perioperative pulsed Doppler blood flow monitoring in an ileocolic graft may be useful for the diagnosis and prevention of ischemic complications.

Cyclosporine causes sympathetically mediated elevations in arterial pressure in rats.

Cyclosporine-induced immunosuppression has emerged as a new cause of hypertension, but the underlying mechanisms are poorly understood. In patients, this hypertension is accompanied by sympathetic neural activation. We therefore hypothesized that increased sympathetic nerve discharge is an important mechanism by which cyclosporine raises blood pressure. To test this hypothesis, we examined effects of acute administration of cyclosporine (5 mg/kg i.v.) or vehicle on renal and lumbar sympathetic nerve activity, renal and femoral blood flow velocity (pulsed Doppler flowmetry), and arterial pressure in chloralose-anesthetized rats. Vehicle had no effect on sympathetic nerve activity, whereas cyclosporine caused renal and lumbar sympathetic nerve activity to increase progressively over 60 minutes to levels that were 362 +/- 46% and 388 +/- 70%, respectively, of the baseline values (p less than 0.05). These increases in sympathetic nerve activity were accompanied by proportional increases in renal and femoral vascular resistance and sustained increases in mean arterial pressure (+19 +/- 3 mm Hg, p less than 0.05 versus baseline). The cyclosporine-induced increases in regional vascular resistance and arterial pressure were greatly attenuated, or abolished, by ganglionic blockade or by clonidine (central sympatholysis) but were unaffected by angiotensin converting enzyme inhibition. These findings demonstrate that in an anesthetized animal preparation, the vasoconstrictor and blood pressure-raising effects of cyclosporine are caused by sympathetic neural activation.

Effect of bisoprolol on blood pressure and arterial hemodynamics in systemic hypertension

Blood pressure, heart rate, common carotid and brachial arterial hemodynamics using pulsed Doppler flowmetry and pulse wave velocity determinations were evaluated using a double-blind crossover design versus placebo in 14 patients with sustained essential hypertension treated by the selective β 1 blocking agent bisoprolol. Blood pressure and heart rate significantly decreased after bisoprolol, whereas no significant change occurred in the diameter, the blood flow and in the vascular resistance of the carotid and brachial circulations. Pulse wave velocity significantly decreased in the brachioradial and the carotid femoral areas. The decrease in the latter was −1.6 ± 0.8 m/s with bisoprolol and −0.06 ± 0.80 m/s with placebo (p = 0.001). Brachial artery compliance significantly increased from 117 ± 49 to 205 ± 84 cm 4· dynes −1· 10 9 (p = 0.001), indicating that the antihypertensive effect of β 1 blockade is associated with an improvement in the viscoelastic properties of the brachial artery wall.

Restriction of regional blood flow and diaphragmatic contractility

We have tested the hypothesis that the diaphragmatic head-to-head arterial anastomosis system should maintain adequate diaphragmatic function even during occlusion of some of its arteries. In six anesthetized open-chest dogs, left phrenic vein blood flow (Qphv) was measured by pulsed Doppler flowmetry. Contractility was measured by sonomicrometry in the left costal and crural diaphragm. The diaphragm was paced for 15 min by continuous bilateral supramaximal phrenic nerve stimulation. In five separate runs the following arteries were occluded at minute 5: 1) left phrenic artery, 2) internal mammary artery (IMA), 3) left phrenic artery and IMA, 4) descending aorta, and 5) descending aorta and IMA. Occlusion was then released at minute 10 of the run. In runs 1-3 there were no changes in contractility in costal or crural diaphragm and no changes in Qphv. However, in runs 4 and 5, Qphv decreased to 55.2 +/- 7.4 and 24.0 +/- 6.5% of control values, respectively. In run 4, percent maximum shortening from functional residual capacity (%LFRC) of the crural diaphragm decreased by 39.1%, while %LFRC of the costal diaphragm increased by 41.4% and abdominal pressure decreased by 47.0%. In run 5, abdominal pressure decreased by 53.5% and %LFRC of the crural and costal diaphragm decreased by 45.5 and 5.8%, respectively. Also relative postocclusion hyperemia was greater in run 5 (64.8%) than in run 4 (40.2%).(ABSTRACT TRUNCATED AT 250 WORDS)

Cicletanine Modulates Endothelin-Induced Renal Vasoconstriction in the Rat

Endothelin (ET-1), a recently discovered endothelium-derived peptide, has been reported to produce potent vasoconstriction in various isolated vessels of experimental animals. Cicletanine (CIC) is a novel antihypertensive agent. This study concerns the effect of CIC on the vascular actions of ET-1 (0.2 nM/kg) and epinephrine (1 microgram/kg) in normotensive Wistar rats. The hemodynamic effects of ET-1 and epinephrine were also tested in the presence of molsidomine (MOL), a vasodilator that releases nitric oxide. Rats were treated for 15 days with CIC (10 mg/kg/day) or gum arabic p.o. Subsequently, the animals were anesthetized and renal and aortic blood flow (BF) determined by pulsed Doppler flowmetry. ET-1 or epinephrine was injected. After return to the basal level, MOL (5 mg/kg) was injected; 10 min later, the mean arterial pressure (MAP) was decreased and then ET-1 or epinephrine was administered. The vascular resistance was calculated by the MAP/BF ratio and expressed as a percentage. In CIC-treated rats, ET-1 induced a renal vasoconstriction smaller than in control rats (+27.2 +/- 5.95 and +60.4 +/- 11.95%, respectively, p less than 0.01). In the presence of MOL, ET-1 produced a smaller increase in MAP (+9.7 +/- 1.34 and +16.9 +/- 2.49 mm Hg, p less than 0.05). Epinephrine injected after MOL in CIC-treated rats induced a smaller renal vasoconstriction than in control rats (+98.8 +/- 29.83 and 185 +/- 30.33%, p less than 0.05). Thus, CIC partially reduced the hypertensive and renal vasoconstrictor effects of ET-1. A combination of CIC and MOL diminished the renal effects of epinephrine. In conclusion, CIC could be used to attenuate the hypertensive status or renal ischemia disorders where ET-1 seems to be implicated.

Influence of diuretics on brachial artery diameter and distensibility in hypertensive patients

Blood pressure, brachial artery diameter and pulse wave velocity were determined before and after diuretic treatment in 2 groups of hypertensive patients treated either by indapamide (2.5 mg per d) or by canreonate (50 mg per d). Brachial artery diameter, measured from pulsed Doppler flowmetry, and pulse wave velocity, evaluated from mechanography, did not alter significantly despite a significant blood pressure reduction. The study indicates that, in hypertensive patients of middle age, diuretics did not change brachial artery diameter and distensibility, whether the drug caused an increase or a decrease in plasma potassium levels.

A comparison of the haemodynamic profiles of Ro 31-6930, cromakalim and nifedipine in anaesthetised normotensive rats

The regional haemodynamic profiles of Ro 31-6930, cromakalim and nifedipine were compared using pulsed Doppler flowmetry in the anaesthetised rat. In order of potency, Ro 31-6930 (0.1–300 μg/kg), cromakalim (1–300 μ/kg) and nifedipine (1–1000 μ/kg) produced dose related falls in mean arterial pressure. The hypotensive effects of Ro 31-6930 and cromakalim were accompanied by reflex tachycardia. All three agents reduced renal vascular resistance by 30–50%. Cromakalim exerted a selective action on this vascular bed. Similar maximal reductions in mesenteric vascular resistance (37–50%) were observed; however, cromakalim was the least potent on this vascular bed. Maximal reductions in iliac vascular resistance (65–78%) were observed, with an order of potency as observed on mean arterial pressure. Qualitative differences in the regional haemodynamic profiles of Ro 31-6930, cromakalim and nifedipine are evident from this study. The different profiles of Ro 31-6930 and cromakalim may reflect structural differences between the pharmacophores of these compounds.

Fetal renal arterial blood velocity waveforms detected with color‐flow mapping and pulsed Doppler flowmetry in intrauterine growth retardation

Fetal renal arterial blood velocity waveforms detected with color‐flow mapping and pulsed Doppler flowmetry in intrauterine growth retardation

Experimental thrombosis and thrombolysis in freely moving rats, using directional pulsed doppler flowmetry

Experimental thrombosis and thrombolysis in freely moving rats, using directional pulsed doppler flowmetry

Responses to hypotension in conscious rats with chronic portal venous hypertension

Heart rate, mean arterial pressure, and vascular conductance response to intravenous nitroprusside were compared in conscious, unrestrained portal vein-stenosed and sham-operated rats chronically instrumented for pulsed Doppler flowmetry. Ten to twelve days after portal vein stenosis, portal venous pressures were elevated and resting heart rates were greater. Portal vein-stenosed animals' depressor responses to nitroprusside were similar to those of sham-operated animals, despite a 41% reduction in their tachycardic response to arterial hypotension. Skeletal muscle vascular bed reflex responses to nitroprusside-induced hypotension were significantly attenuated in the portal vein-stenosed group, whereas their renal artery and superior mesenteric artery responses resembled that of the sham-operated group. After ganglionic blockade, tachycardic responses to hypotension were abolished, but portal vein-stenosed rats' heart rates remained greater than sham-operated rats. Comparisons of arterial pressure changes, renal artery, abdominal aorta, and superior mesenteric artery vascular conductance changes after ganglionic blockade revealed no differences in neurogenic vascular tone between groups. Ganglionic blockade enhanced nitroprusside depressor responses and increased vascular conductance responses to nitroprusside in both treatment groups while abolishing the between group difference in the skeletal muscle baroreflex response. These findings indicate that chronic prehepatic portal vein stenosis with portal venous hypertension results in reduced reflex tachycardic and skeletal muscle baroreflex responses to nitroprusside-induced hypotension.

β-Blockade and Brachial Artery Hemodynamics in Hypertension

The effect of systemic adrenergic blockade on hypertensive brachial arteries was studied in humans with pulsed Doppler flowmetry. Blockade of beta-receptors by the nonselective beta-blocking agent propranolol did not modify the brachial artery diameter, whereas pindolol increased this parameter for the same degree of blood pressure reduction. The beta1-selective blocking agents atenolol and bisoprolol caused similar decreases in blood pressure and a reduction in the diameters of the brachial artery and abdominal aorta, respectively. The combination of alpha- and beta-blockade produced a rapid drop in blood pressure but did not change the brachial arterial diameter. Thus, following beta-blockade, the arterial diameter increased, did not change, or even decreased despite an adequate blood pressure reduction. It is suggested that beta-blockade in some instances resets the pressure-diameter curve and therefore has a direct action on the arterial wall independent of the mechanical effect of blood pressure reduction.

β-Blockade and Brachial Artery Hemodynamics in Hypertension

The effect of systemic adrenergic blockade on hypertensive brachial arteries was studied in humans with pulsed Doppler flowmetry. Blockade of β-receptors by the nonselective β-blocking agent propranolol did not modify the brachial artery diameter, whereas pindolol increased this parameter for the same degree of blood pressure reduction. The β1-selective blocking agents atenolol and bisoprolol caused similar decreases in blood pressure and a reduction in the diameters of the brachial artery and abdominal aorta, respectively. The combination of α- and β-blockade produced a rapid drop in blood pressure but did not change the brachial arterial diameter. Thus, following β-blockade, the arterial diameter increased, did not change, or even decreased despite an adequate blood pressure reduction. It is suggested that β-blockade in some instances resets the pressure-diameter curve and therefore has a direct action on the arterial wall independent of the mechanical effect of blood pressure reduction.

The important role of left ventricular relaxation and left atrial pressure in the left ventricular filling velocity profile

To evaluate the determinants of left ventricular filling, left ventricular filling velocity was measured by pulsed Doppler flowmetry during catheterization of the right and left sides of the heart in 37 patients with cardiac disease before and during leg elevation. During leg elevation, despite no significant change in the time constant of isovolumic relaxation (T), the peak rapid filling velocity (PVRF) increased in association with an increase in pulmonary wedge pressure (PWP), but the peak atrial filling velocity was unchanged. The PVRF correlated with the pulmonary wedge V wave — left ventricular minimum pressure difference ( r = 0.68) and in multivariate regression with both T and mean PWP (R = 0.73). These results indicate that left ventricular filling is determined by both left ventricular relaxation and left atrial pressure and that an increase in left atrial pressure changes the left ventricular filling velocity profile in a manner that mimics the pattern with normal diastolic function.

Pressor responses in conscious rats with chronic portal venous hypertension.

Heart rate, mean arterial pressure (MAP), and vascular conductance responses to graded phenylephrine (PE) infusions were compared in conscious, unrestrained portal vein-stenosed (PS), and sham-operated (SO) rats chronically instrumented for pulsed Doppler flowmetry. Ten days after stenosis, MAP was lower in PS than in SO, and PS heart rates were higher. Pressor sensitivity to PE was attenuated 70%, and bradycardic responses to increases in MAP were 47% greater in PS. Abdominal aorta vascular bed conductance sensitivity was reduced 84%, and renal artery sensitivity was reduced 29% in PS compared with SO, whereas the superior mesenteric artery conductance response was unaffected by portal vein stenosis. After ganglionic blockade, the heart rate of PS remained greater than that of SO, and comparisons of renal artery, abdominal aorta, and superior mesenteric artery vascular conductances revealed no significant differences in neurogenic vascular tone. Differences between PS and SO pressor responses were abolished by ganglionic blockade, as were differences in vascular bed conductance responses. These findings suggest that a greater bradycardic response and greater baroreflex-mediated withdrawal of sympathetic tone from skeletal muscle and renal vascular beds were responsible for the decreased pressor sensitivity observed in PS animals.

Portal vein blood flow measurements using pulsed doppler and electromagnetic flowmetry in dogs: A comparative study

Comparative measurements of portal vein blood flow were performed at laparotomy in anesthetized dogs using either a pulsed Doppler echo system or electromagnetic flowmeters. Three hundred four simultaneous determinations were obtained under baseline conditions and during vasopressin and glucagon infusions. In each dog, serial triplicate measurements were taken within 10 min of each other. In all the cases, flow changes induced by vasoactive drugs followed the same direction regardless of the method used. Portal vein blood flow as measured by electromagnetic flowmetry ranged from 85 to 1570 ml/min. Portal vein blood flow values obtained with Doppler and electromagnetic flowmeters were not significantly different (609 ± 335 vs. 600 ± 370 ml/min; p = NS) and were highly correlated (r = 0.918, p < 0.001). The difference between values obtained by the two techniques was −3 ± 159 ml/min or −1.0% ± 21.2% (mean ± SD). This difference was not influenced by the portal vein diameter but increased slightly as a function of the angle of insonation. When considering the mean of triplicate measurements, we also found a highly significant correlation between data obtained by the two techniques (r = 0.934, p < 0.001; n = 63). The mean difference was 11 ml/min, but limits of agreement between these methods were −267 and +239 ml/min. This relative discrepancy was explained by a coefficient of variation higher in Doppler measurements than in electromagnetic measurements (10.9% vs. 5.9%). These data demonstrate that under our experimental conditions, Doppler flowmetry is probably not an ideal method to measure absolute portal vein blood flow values, and that more sophisticated equipment is needed to improve its reproducibility and accuracy. In humans, however, this method might be a useful tool to assess the direction of portal flow changes in the same individual.