Transit-time Ultrasonic Flowmeter Research Articles

Ultrasonic transit-time flowmeters modelled with theoretical velocityprofiles: methodology

Fully developed flow is well defined for most values of Reynoldsnumber but distorted flow is not. Velocity profile is the definition given tothe distribution of velocity in the axial direction over the cross-section ofthe pipe. This distribution is not usually uniform and can vary dramaticallydepending on the properties of the fluid and the configuration of the pipe inwhich it flows. Ultrasonic flowmeters are affected by such distortions in theflow profile, often resulting in erroneous measurements. Transit-timeultrasonic flowmeters are widely used in industry in distorted fluid flows,therefore correction to or prediction of distorted profiles has sparked greatinterest in the design and application of ultrasonic flowmeters. This documentdescribes a method for modelling and analysing the effect of theoreticalasymmetric flow profiles on ultrasonic flowmeters of the transit-time type,thus allowing an understanding of installation effects.

Improved phase-contrast flow quantification by three-dimensional vessel localization

In this paper, a method of three-dimensional (3D) vessel localization is presented to allow the identification of a vessel of interest, the selection of a vessel segment, and the determination of a slice orientation to improve the accuracy of phase-contrast magnetic resonance (PCMR) angiography. A marching-cube surface-rendering algorithm was used to reconstruct the 3D vasculature. Surface-rendering was obtained using an iso-surface value determined from a maximum intensity projection (MIP) image. This 3D vasculature was used to find a vessel of interest, select a vessel segment, and to determine the slice orientation perpendicular to the vessel axis. Volumetric flow rate (VFR) was obtained in a phantom model and in vivo using 3D localization with double oblique cine PCMR scanning. PCMR flow measurements in the phantom showed 5.2% maximum error and a standard deviation of 9 mL/min during steady flow, 7.9% maximum error and a standard deviation of 13 mL/min during pulsatile flow compared with measurements using an ultrasonic transit-time flowmeter. PCMR VFR measurement error increased with misalignment at 10, 20, and 30 degrees oblique to the perpendicular slice in vitro and in vivo. The 3D localization technique allowed precise localization of the vessel of interest and optimal placement of the slice orientation for minimum error in flow measurements.

Flow patterns in an ultrasonic liquid flow meter

Flow visualisation studies have been undertaken for the case of an in-line, ultrasonic transducer housing in a cylindrical cross-section metering duct by direct observation of injected dye and of particles illuminated by a laser sheet. Results are presented for single and three bluff-body strut attachment of the transducer housing to the duct wall at Reynolds numbers (based on mean velocity and meter duct diameter) of 750, 1900 and 7950. Transducer face and wall fillet recirculation zones were dependent on the number of attachment struts and on the flow rate. The results are discussed in terms of their consequences for the performance of an ultrasonic transit time flow meter.

Renal vascular reactivity in mice: AngII-induced vasoconstriction in AT1A receptor null mice.

The present study describes methodology and its application to evaluate renal reactivity in acute studies on anesthetized mice. Renal blood flow (RBF) was measured using an ultrasonic transit-time flowmeter and a non-cannulating V-shaped probe. An intrarenal artery injection technique established feasibility and reproducibility of studies of renal vascular reactivity to angiotensin II (AngII) in adult wild-type mice. The study also examined whether AngII would affect RBF in mice lacking AT1A receptors due to gene targeting. Mean arterial pressure averaged 83 and 62 mmHg, respectively, in mice with and without AT1A receptors. The RBF was similar in both groups, averaging 7 ml/min per g kidney wt. AngII injection (10-microl bolus) into the renal artery produced transient, dose-dependent, selective reductions in RBF in AT1A knockout mice as well as wild-type mice. The response was considerably greater in mice with AT1A receptors: 10% for 0.1 ng, 30% for 1 ng, and 45% for 5 ng AngII in control animals versus respective decreases of 6, 15, and 17% in knockout mice. In other studies, angiotensin-converting enzyme (captopril) or renin (CP-71362-14) was inhibited. During inhibition of AngII formation, renal vascular reactivity to AngII increased twofold in both groups. Coadministration of the AT1 receptor antagonist losartan (1 to 1000 ng) elicited dose-dependent inhibition of AngII effects, with near maximum blockage of 80 to 90% in both groups of mice. The putative AT2 receptor antagonist PD 123319 inhibited 30 to 40% of AngII-induced vasoconstriction, whereas CGP 42112 had no effect in either group. In conclusion, AngII can elicit renal vasoconstriction, albeit attenuated, in AT1A knockout mice. The weaker RBF effects are most likely due to the absence of the AT1A receptor. Inhibition of the response by AT1 receptor antagonist suggests mediation by the AT1B receptor in these animals. The residual constrictor effect observed during AT1 receptor blockade and sensitive to PD 123319 appears to be mediated by a non-AT1 receptor.

Coronary endothelium-derived vasodilation during cooling and rewarming of the in situ heart.

The integrity of coronary vascular endothelial vasodilator function during core cooling and rewarming was investigated in a pentobarbital-anesthetized open-chest dog model. Vasodilator response was assessed as the change from baseline blood flow by injecting the endothelial-dependent vasodilator acetylcholine (ACh) (1.0 microg) or the endothelial-independent vasodilator nitroglycerin (NTG) (50 microg) into the left anterior descending (LAD) coronary artery. Change in blood flow was measured using a transit time ultrasonic volume flowmeter technique. During cooling and rewarming LAD blood flow was significantly decreased. After rewarming, aortic pressure was artificially elevated to reach control. This procedure restored heart work (LV-RPP, left ventricular rate pressure product) and coronary perfusion pressure, but LAD blood flow remained lowered. Ability to dilate the vascular bed supplied by LAD, after injections of ACh or NTG, was present both during cooling and rewarming. At 25 degrees C coronary blood flow (LAD) increased from 3 +/- 1 to 9 +/- 1 mL x min(-1) in response to both ACh and NTG. Posthypothermic blood flow increased from 7 +/- 1 to 19 +/- 2 and 20 +/- 3 mL x min(-1) in response to ACh and NTG, respectively. Measured as the percent change from baseline LAD blood flow, the response was not significantly different from the one obtained in prehypothermic hearts. In conclusion, coronary vasodilator function, both endothelium dependent and endothelium independent, is present but not maintained at the same level during cooling to 25 degrees C and rewarming. In spite of the deterioration of cardiac function, no selective defect in the endothelium-dependent response was detected, either during hypothermia or after rewarming.

Coronary endothelium-derived vasodilation during cooling and rewarming of the in situ heart

The integrity of coronary vascular endothelial vasodilator function during core cooling and rewarming was investigated in a pentobarbital-anesthetized open-chest dog model. Vasodilator response was assessed as the change from baseline blood flow by injecting the endothelial-dependent vasodilator acetylcholine (ACh) (1.0 µg) or the endothelial-independent vasodilator nitroglycerin (NTG) (50 µg) into the left anterior descending (LAD) coronary artery. Change in blood flow was measured using a transit time ultrasonic volume flowmeter technique. During cooling and rewarming LAD blood flow was significantly decreased. After rewarming, aortic pressure was artificially elevated to reach control. This procedure restored heart work (LV-RPP, left ventricular rate pressure product) and coronary perfusion pressure, but LAD blood flow remained lowered. Ability to dilate the vascular bed supplied by LAD, after injections of ACh or NTG, was present both during cooling and rewarming. At 25°C coronary blood flow (LAD) increased from 3 ± 1 to 9 ± 1 mL·min-1 in response to both ACh and NTG. Posthypothermic blood flow increased from 7 ± 1 to 19 ± 2 and 20 ± 3 mL·min-1 in response to ACh and NTG, respectively. Measured as the percent change from baseline LAD blood flow, the response was not significantly different from the one obtained in prehypothermic hearts. In conclusion, coronary vasodilator function, both endothelium dependent and endothelium independent, is present but not maintained at the same level during cooling to 25°C and rewarming. In spite of the deterioration of cardiac function, no selective defect in the endothelium-dependent response was detected, either during hypothermia or after rewarming.Key words: rewarming shock, cold, temperature, coronary blood flow, acetylcholine, nitroglycerin.

Effects of Prostaglandin E1 on Hepatic Blood Flow in Conscious Dogs with Chronic Biliary Obstruction

To evaluate the effects of prostaglandin E₁ (PGE₁) on the hepatic circulation in cholestasis, hepatic arterial blood flow (HAF), portal venous blood flow (PVF), cardiac output, and heart rate during PGE₁ infusions were investigated before and 2 weeks after biliary obstruction in conscious dogs by a transit-time ultrasonic flowmeter. In the control period, HAF and PVF increased dose dependently with the infusion of PGE₁ from 0.05 to 0.5 µg/kg/min. During the biliary obstruction period, a lower dose of PGE₁ increased HAF and PVF. The plasma concentration level of PGE₁ during the infusion of PGE₁ was significantly higher at each dose in the cholestatic animals. These results suggest that the metabolism of PGE₁ is attenuated by cholestasis. Plasma PGE₁ concentrations should be useful in deciding the optimal dose of PGE₁.

Technical note: measuring portal blood flow in sheep using an ultrasonic transit time flow probe.

Our objective was to validate the use of an ultrasonic transit-time flowmeter for the measurement of portal blood flow (PBF) in sheep. Data recorded with this technique were compared with those obtained with an indicator dilution method, and probes were calibrated in vivo. Wethers were fitted with catheters in the portal, jejunal, and ruminal veins and in a mesenteric artery. Ultrasonic flow probes were implanted around the portal vein: S-series probes in three wethers, and A-series probes in four wethers. The PBF measured with A-series probes was within 10% of that measured by indicator dilution, but PBF measured with S-series probes were 52 to 77% of that determined by indicator dilution. In vivo calibration indicated that A-series probes provided accurate measurement of PBF (absolute accuracy: 5%+/-zero flow error). In conclusion, an ultrasonic transit-time flowmeter, with an A-series probe, can be used to reliably measure PBF in sheep.

PEEP decreases oxygenation of the intestinal mucosa despite normalization of cardiac output.

To evaluate if normalization of cardiac output reverses the attenuation of local intracapillary hemoglobin saturation (HbO2) of gastric mucosa by PEEP (positive end-expiratory pressure) during IPPV (intermittent positive pressure ventilation). Four healthy, chronically instrumented, anesthetized dogs were repeatedly studied (n = 7). Local HbO2 of gastric mucosa was measured continuously by tissue lightguide spectrophotometry and cardiac output (CO) was recorded continuously by means of a precalibrated ultrasonic transit time flowmeter chronically implanted around the pulmonary artery. After obtaining baseline values during IPPV and ZEEP (zero end-expiratory pressure) 15 cmH2O PEEP was added. To compensate the reduction of CO during PEEP ventilation, HES (hydroxyethyl starch 6%) was infused until CO reached baseline values during ZEEP. Despite of unimpaired systemic oxygen saturation, PEEP reduced HbO2 of gastric mucosa from 55.1 +/- 4.2% to 42.1 +/- 4.7% (mean +/- SEM) and CO dropped from 67.7 +/- 4.9 ml.kg-1.min-1 to 33.9 +/- 4.6 ml.kg-1.min-1. Whereas infusion of HES during PEEP ventilation normalized CO to 65.1 +/- 6.2 ml.kg-1.min-1, HbO2 reached only 48.1 +/- 3.3%, a statistically significant improvement compared to HbO2 during PEEP ventilation before HES infusion (p < 0.03, Wilcoxon signed rank test), but still below baseline values (p < 0.04). Our findings demonstrate that the side effects of PEEP ventilation on cardiac output can be compensated by restoring preload, but normalizing CO did not completely normalize HbO2 of the gastric mucosa. This further emphasizes that global measurements of variables of systemic circulation and oxygenation do not necessarily reflect regional abnormalities of tissue oxygenation. Therefore, in view of the importance of tissue hypoxia especially in the splanchnic region in the pathogenesis of multiple organ failure, monitoring of HbO2 of the intestinal mucosa during PEEP ventilation may be particularly useful in the care of the critically ill patient.

Measurement of high-pressure natural gas flow using ultrasonic flowmeters

A number of analyses have been carried out on both the installation effects and the calibration problems of transit time multipath flowmeters. There is, however, only a somewhat sketchy knowledge of their field operation, their long-term performance, and their compatibility with traditional instruments and measurement techniques. In this paper, the authors, prior to analysing the principal problems regarding transit time ultrasonic flowmeters, describe the results of an experimental field investigation into the use of multi-path flowmeters for measuring large flows of high pressure natural gas. Reference is also made to the future objectives of research on this type of device.

Hepatic Denervation Induces Supersensitivity to Terbutaline of the Hepatic Arterial System in Conscious Dogs

The effects of hepatic denervation on liver blood flow and the influence of the denervation on the hemodynamic response to exogenously administered agents remain equivocal. This study examined the effects of the β2-adrenoceptor agonist, terbutaline, on liver blood flow and how these effects were influenced by surgical hepatic denervation in a conscious canine model. Two weeks after denervation, hepatic arterial flow, portal venous flow, and aortic blood flow were measured during intravenous infusion of terbutaline at 0.1, 0.2, 0.4, and 0.8 μg/kg/min, and responses were compared between the hepatic denervated and sham-operated dogs. Implantable transit-time ultrasonic flowmeter and probes were used. Hepatic arterial flow increased dose-dependently in response to terbutaline in denervated dogs, while it remained unchanged in control dogs except at the highest dose of terbutaline. The increase in hepatic arterial flow of denervated dogs was significantly greater than that of controls at all doses of terbutaline. Aortic blood flow-indexed hepatic arterial flow in response to terbutaline also differed substantially between the two groups. Terbutaline produced a marked dose-dependent increase of portal venous flow similarly in both groups. These results suggest that the β2-adrenoceptor agonist terbutaline should be effective for increasing liver blood flow and could lessen postoperative liver ischemia. We speculate that hepatic denervation induces supersensitivity of the hepatic arterial system to intravenous terbutaline.

Changes in liver blood flow after hepatectomy in conscious dogs.

Hepatic circulation after hepatectomy was investigated in conscious dogs under fasting and feeding conditions. After a 40% hepatectomy, both the hepatic arterial and portal blood flow were measured simultaneously using ultrasonic transit time flowmeters. During fasting, the total hepatic blood flow (i.e., the sum of arterial and portal blood flow) changed in a biphasic pattern after hepatectomy. The first peak (517.9 +/- 42.7 ml/min; 130.1% of preoperative flow) was seen on the 1st postoperative day (POD) and the second peak (444.8 +/- 25.6 ml/min; 112.7% of preoperative flow) occurred on the 7th POD. The portal flow demonstrated the same biphasic changes as the total hepatic flow, although the hepatic arterial flow showed only the first peak. A heart rate analysis suggested that the first peak was probably due to hyperdynamic circulatory conditions, as has been previously reported. In addition, the existence of the second peak was established by the present study. The postprandial hepatic blood flow decreased during the first 2 weeks postoperatively, but exceeded the presurgical levels on PODs 21 and 28.

The development of curved reflective surfaces for ultrasonic beam redirection in high speed gas flow measurement

Results are presented on the development of curved reflecting surfaces for use in an ultrasonic transit time flowmeter for high speed gas flow measurement. These surfaces were designed to reduce the effects of ultrasonic beam sweep which occur at high (subsonic) flowrates. They reflect the swept ultrasonic beam so as to redirect it towards the receiving transducer. Basic analysis of the effect of the flow on the reflection of beam are included and differential equations for three reflection profiles based on different assumptions about this effect are presented. Numerical techniques used in the solution of these equations are discussed. The effect of the profiles on the ultrasonic transit time is analysed. The design of a reflective ramp based on one of these profiles is presented, and experimental measurements are provided showing an increased meter range without a detectable loss of accuracy.

A new method to measure portal venous and hepatic arterial blood flow in patients intraoperatively.

The intraoperative measurement of the afferent circulation of the liver, namely the hepatic artery flow and portal venous flow was carried out upon 14 anesthetized patients having carcinoma in the splanchnic area, mainly in the head of the pancreas by means of transit time ultrasonic volume flowmeter. The hepatic artery flow, portal venous flow and total hepatic flow were 0.377±0.10; 0.614±0.21; 0.992±0.276 l/min respectively. The ratio of hepatic arterical flow to portal venous flow was 0.66±0.259 There was a sharp, significant increase in hepatic arterial flow (29.8±6.1%, p<0,01) after the temporary occlusion of the portal vein, while the temporary occlusion of hepatic artery did not have any significant effect on portal venous circulation. The interaction between hepatic arterial flow and portal venous flow is a much disputed question, but according to the presented data here, it is unquestionable, that the decrease of portal venous flow immediately results a significant increase in hepatic artery circulation.

In vivo validation of magnetic resonance blood volume flow measurements with limited spatial resolution in small vessels.

The accuracy of magnetic resonance phase contrast volume flow measurements in small blood vessels is expected to be smaller than in large vessels, because of partial volume effects at the vessel boundary. Accuracy was validated in the dog femoral artery, diameter 3.5 +/- 0.7 mm, using an ultrasonic transit-time flowmeter (TT). The number of pixels per vessel diameter (ND) ranged from 1.6 to 4.8. The vessel cross-section was determined using a threshold in the magnitude image. Between the two methods the correlation coefficient was 0.95 (range 10-200 ml/min). The proportional difference (PD), (QTT-QMR)/1/2(QTT+QMR), was 0.8%, showing no systematic difference between the methods. The PDs standard deviation was 27%, and 19% for flow rates above 30 ml/min. Only a significant decrease of the PDs variance was found at the highest ND values, suggesting other sources of error than partial volume effects. It is concluded that with an ND value of about 3, accurate blood volume flow rates can be determined.

Effects of volume loading on pulmonary venous flow pattern in dogs with normal left ventricular function.

The effects of altered loading conditions on the pattern of pulmonary venous flow are poorly understood. The authors investigated such effects, therefore, by using volume loading in 6 open-chest dogs. The pulmonary venous flow volume rate curve was obtained with a transit-time ultrasonic flowmeter at a fixed heart rate. Measurements were performed in the control and several states during the intravenous infusion of dextran. The influences of volume loading on hemodynamic and pulmonary venous flow variables were compared between the control state and three interventional states in which mean left atrial pressure was approximately 1, 2, and 3 mm Hg above the control value. The systolic flow volume (SI), which corresponds to left atrial reservoir volume, significantly increased, but the early diastolic flow volume (DI), which corresponds to left atrial conduit volume, did not show significant change with volume loading. The flow volume during left atrial contraction significantly increased with volume loading. The flow volume during one cardiac cycle (PVF) significantly increased with volume loading. Approximately 73% of increased PVF was distributed to the systolic flow. The rest was distributed to the early diastolic flow (14%) and to the flow during left atrial contraction (12%). The change in the ratio of SI/DI significantly and positively correlated with the change in mean left atrial pressure (r = 0.87, P < 0.001). These findings indicate that increased pulmonary venous flow induced by volume loading in dogs with normal left ventricular function is mainly distributed to the left atrial reservoir volume.

Validation of miniature ultrasonic transit-time flow probes for measurement of renal blood flow in rats

This study validates the accuracy of miniature ultrasonic transit-time flow probes for measuring renal blood flow (RBF) in the rat. Probes for 1-mm and 2-mm vessels were calibrated ex vivo using excised arteries at varying flow rates and hematocrit (Hct). Correlation between measured and true flow rates for the 2-mm probe were identical (r = 1.0) at both normal and subnormal Hct values. Correlation for the 1-mm probe was high (r = 0.994) at normal Hct, but varied at both high flow rates and subnormal Hct values. In vivo correlation of RBF measurements using the 1-mm probe with the clearance and extraction of p-aminohippuric acid showed a high correlation (r = 0.84; n = 72, P < 0.0001) over a wide range of flow rates (0.5-21 ml/min) and Hct (36-74%). Zero flow levels remained steady, averaging -0.2 +/- 0.2 ml/min during occlusion in the living animal and -0.1 +/- 0.3 ml/min after exsanguination. This study shows that the ultrasonic transit-time flowmeter (1-mm and 2-mm probes) is a reasonably accurate and reliable method with which to measure RBF in the anesthetized, acute-instrumented rat.

Experimental study of cerebral autoregulation during cardiopulmonary bypass with or without pulsatile perfusion

Twenty-four adult mongrel dogs were divided into four equal groups according to the following method of cardiopulmonary bypass: normothermic continuous (so-called nonpulsatile) perfusion, normothermic pulsatile perfusion, hypothermic continuous perfusion, and hypothermic pulsatile perfusion. Cerebral blood flow was determined by measuring the volume of sagittal sinus venous blood outflow with a transit-time ultrasonic flowmeter. Cardiopulmonary bypass was initiated at a flow rate of 80 ml/kg per minute. Cerebral temperature was maintained at 37 degrees C in the normothermic groups and at 25 degrees C in the hypothermic groups. Arterial pH and carbon dioxide were maintained within the physiologic range by alpha-stat acid-base regulation. Mean cerebral perfusion pressure and blood flow were not affected during 90 minutes of the bypass. The respective values were 67.1 mm Hg and 37.1 ml/100 gm brain per minute with normothermic continuous perfusion, 72.8 mm Hg and 39.0 ml/100 gm per minute with nonpulsatile perfusion, 98.0 mm Hg and 23.0 ml/gm per minute with hypothermic continuous perfusion, and 86.8 mm Hg and 22.3 ml/100 gm per minute with hypothermic pulsatile perfusion. Pump flow rates were altered from 10 to 120 ml/kg per minute in a stepwise fashion to obtain graded changes of perfusion pressure. Cerebral blood flow, however, was not changed significantly by cerebral perfusion pressure so long as perfusion pressure was greater than 50 mm Hg. Conversely, cerebral blood flow changed proportionally with cerebral perfusion pressure at a pressure less than 50 mm Hg. The correlation between cerebral blood flow and perfusion pressure was described as two separate lines determined by linear regression. The slope of the regression line relating cerebral blood flow to perfusion pressure was 0.16 +/- 0.08 for a cerebral perfusion pressure above 50 mm Hg and 0.68 +/- 0.11 below 50 mm Hg in the normothermic continuous perfusion group; 0.14 +/- 0.09 and 0.32 +/- 0.09 with normothermic pulsatile perfusion; 0.10 +/- 0.04 and 0.62 +/- 0.18 with hypothermic continuous perfusion; 0.09 +/- 0.08 and 0.39 +/- 0.04 in the hypothermic pulsatile perfusion group. The slope above 50 mm Hg was significantly smaller and closer to zero in all groups than it was at a perfusion pressure below 50 mm Hg (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Weight vector for thermal diffusion flowmeters, Part 1: General theory

A linear theory of thermal diffusion flowmeters is developed. These are flowmeters in which the flow interferes with heat conduction in the fluid and causes a change in the temperature distribution. At low flows the change in the temperature measured at one or more points is proportional to the flow rate. In this linear regime, velocity profile effects can be calculated using the weight vector approach already well known in electromagnetic flowmeter theory and becoming useful also in transit-time ultrasonic and Coriolis mass flowmeters. In Part 1 of this paper the general expression for the weight vector for the thermal diffusion flowmeter is derived and the condition for ‘ideal’ thermal diffusion flowmeters is worked out. In Part 2 of the paper the axisymmetric weight function for a particular flowmeter configuration is calculated and used to predict its sensitivity to a fully developed laminar flow profile. The requirements for validity of the weight vector theory and for the neglect of free convection are worked out under general conditions in Part 1 and under particular circumtances in Part 2.

Pressor and endocrine responses to lesions of canine rostral ventrolateral medulla.

To understand the mechanism(s) of reduction in arterial pressure (AP) after kainic acid cytotoxic lesions in the rostral ventrolateral medulla (RVLM), recordings of AP, cardiac output (CO), heart rate (HR), plasma catecholamines, and cortisol were obtained from awake relaxed dogs. Mongrels (n = 12) were instrumented with a solid-state pressure transducer in the descending aorta and a pulse transit-time ultrasonic flowmeter on the aortic arch. After the dogs recovered from thoracotomy, AP, CO, HR, and plasma levels of epinephrine, norepinephrine, and cortisol were recorded periodically or measured at rest over 2-3 wk followed by unilateral, cytotoxic lesion placement in the rostral C1 area of the RVLM. After the dogs recovered from lesion surgery, the measurements were repeated, and, compared with prelesion control values, they showed significantly decreased AP (-23.1 mmHg) and total peripheral resistance (-0.014 peripheral resistance units) but no significant changes in CO or HR. The reduction in AP may be caused partially by significant reductions in plasma epinephrine (-47%), norepinephrine (-34%), and cortisol (-66%) levels. Lesion sites corresponded to the rostral C1 area, immunocytochemically positive for phenylethanolamine-N-methyltransferase (PNMT). These observations support the concept that a discrete site in the RVLM, demarcated by a rostral subgroup of PNMT-immunoreactive cell bodies, contributes to direct sympathoexcitatory support of resting AP. The neurotransmitter responsible for vasomotor tone, however, remains unknown. This study also provides new information suggesting a role for catecholamine and cortisol regulation from this putative vasomotor center.