Changes In Aortic Flow Research Articles

Abstract 11504: Elevated Seismocardiography-Derived Chest Energy is Associated With Aortic Flow Abnormalities in Patients With Aortic Valve Disease

Introduction: Aortic valve disease (AVD) can induce abnormal flow and elevated peak velocity (Vmax), which has known association with aortopathy and implications for intervention, and thus is a key metric in AVD management. Seismocardiogram (SCG) chest acceleration measurements have been shown indicative of AVD. This study investigated relations between SCG energy and established aortic flow measures. Hypothesis: We hypothesize that standard of care clinical Vmax measurements from echocardiography or MRI correlate with SCG chest acceleration energy metrics. Methods: Healthy controls and AVD patients received standard of care echo or MRI and a same day SCG measurement (image, A). Patients had tricuspid or bicuspid aortic valve (TAV, BAV) and were presenting for routine imaging to assess valve/flow function (image, B). Controls (no known cardiovascular disease) were prospectively recruited. Subjects gave informed consent with IRB approval. MRI included 4D flow (1.5T, 1-3mm³/30-40ms); echo included 2D Doppler imaging (1.7-3.3MHz, 12-40 FPS). Standardized ascending aorta (AAo) Vmax measurements were taken from MR or echo images. SCG energy was calculated by spectral decomposition. Results: Enrolment was 76 subjects: 52 controls (48±17.4y, 23 F), 24 patients (18 BAV, 6 TAV, 31±20.9y, 5 F). Patients had elevated peak velocities (227±103cm/s vs. 106±21cm/s, p<0.01) and elevated SCG energy (10.4±2.6dB vs. 8.3±1.4dB, p<0.01). A significant relationship between elevated AAo Vmax and increased SCG energy was observed (R=0.63, p<0.01) (image, C). Conclusions: Evaluation of SCG in context of AVD shows its potential utility to screen for valve mediated aortic flow changes. Correlation observed between SCG energy and peak velocities, a key metric for management of valve disease and aortopathy, indicates the relevance of SCG measurements in this context. These results show potential for use of SCG as simple, cost-effective front-line screening tool for AVD patients.

The design and use of a simple device for the MRI assessment of changes in cardiovascular function by lower-body negative-pressure-simulated reduction of central blood volume

To use a locally designed and simple lower-body negative-pressure (LBNP) device and 1.5 T magnetic resonance imaging (MRI) to demonstrate the ability to assess changes in cardiovascular function during preload reduction. These effects were evaluated on ventricular volumes and great vessel flow in healthy volunteers, for which there are limited published data. After ethical review, 14 volunteers (mean age 33.9±7 years, mean body mass index [BMI] 23.1±2.5) underwent LBNP prospectively at 0, -5, -10, and -20 mmHg pressure, using a locally designed LBNP box. Expiratory breath-hold biventricular volumes, and free-breathing flow imaging of the ascending aorta and main pulmonary artery were acquired at each level of LBNP. At -5 mmHg, there was no change in aortic flow or left ventricular volumes versus baseline. Right ventricular output (p=0.013) and pulmonary net flow (p=0.026) decreased. At -20 mmHg, aortic and pulmonary net flow (p<0.001) decreased, as were left and right ventricular end diastolic volume (p<0.001) and left and right end systolic volumes (p=0.038 and p=0.003 respectively). Use of a MRI-compatible LBNP device is feasible to measure changes in ventricular volume and great arterial flow in the same experiment. This may enhance further research into the effects of preload reduction by MRI in a wide range of important cardiovascular pathologies.

Aortic flow changes during free breathing exercise, measured with real time MRI

Aortic flow changes during free breathing exercise, measured with real time MRI

Resynchronization improves heart-arterial coupling reducing arterial load determinants

Cardiac resynchronization therapy (CRT) has benefits on left ventricle (LV) performance, but its mid-term effects on LV load and LV-arterial coupling are unknown. To evaluate CRT mid-term effects on LV-arterial coupling, arterial load and its determinants, and the association between CRT-dependent aortic haemodynamic changes and the arterial biomechanics. Cardiac and aortic echographies were done in 25 patients (age: 61 ± 12 years; 14 men; New York Heart Association functional classes III-IV; LV ejection fraction = 28 ± 7%, QRS = 139 ± 20 ms) before and after (23 ± 12 days) CRT. Standard structural and functional parameters and dyssynchrony indices were evaluated. Ascending aorta flow and diameter waveforms were measured. Central pressure was derived using a transfer function and the diameter calibration method. Calculus: arterial elastance (EA); aortic impedance (Zc) and distensibility (AD); systemic resistances (SVR), total compliance (CT); global reflection coefficient; LV end-systolic elastance (EES); and LV-arterial coupling (EA/EES). After CRT EA diminished (-30%;P = 0.001), EES increased (29%; P = 0.001) and EA/EES improved (pre-CRT: 2.9 ± 0.9, post-CRT: 1.6 ± 0.7; P = 0.001). Arterial elastance changes were associated with changes in arterial properties. Cardiac resynchronization therapy was associated with pressure-independent increase in mean aortic diameter (pre-CRT: 30.0 ± 4.0 mm, post-CRT: 33.0 ± 5.1 mm; P = 0.005) and distensibility (pre-CRT: 3.8 ± 2.6 × 10(-3)mmHg(-1), post-CRT: 6.4 ± 2.5 × 10(-3) mmHg(-1); P = 0.002), and Zc reduction (pre-CRT: 3.5 ± 1.8 × 10(-2)mmHg.s/mL, post-CRT:1.9 ± 0.8 × 10(-2) mmHg.s/mL; P = 0.001) and SVR (pre-CRT:1.7 ± 0.4 mmHg.s/mL, post-CRT:1.0 ± 0.3 mmHg.s/mL; P = 0.001). Changes in EA determinants were associated with changes in aortic flow. Early after CRT central and peripheral arterial biomechanics improved, determining a pressure-independent increase in aortic diameter and a reduction in arterial load. Left ventricular systolic performance and LV-arterial coupling were enhanced. Arterial biomechanical changes were associated with aortic flow changes.

Delivery and assessment of endovascular stents to repair aortic coarctation using MR and X‐ray imaging

To investigate the utility of MR and X-ray imaging for characterizing aortic coarctation and flow, and guiding the endovascular catheter to place a stent to repair the coarctation. The descending aorta in eight dogs was looped with elastic band and tightened distal to the subclavian artery. Balanced fast field echo (bFFE) and velocity-encoded cine (VEC) MRI sequences were used for device tracking and measuring aortic flow. A T1-weighted fast-field echo sequence (T1-FFE) was used to visualize the coarctation and roadmap the aorta. Nitinol stents were guided by a nitinol guidewire and placed under MR guidance. Aortic coarctation was visible on MR and X-ray imaging. The procedure success rate was 88%. VEC MRI measured the changes in aortic flow (baseline = 1.3 +/- 0.2, coarctation = 0.2 +/- 0.02, and stent placement = 0.8 +/- 0.1 liters/minute). A significant reduction in iliac blood pressure was measured after coarctation, but it was reversed by stent placement. The stent lumen was visible on X-ray fluoroscopy, but not on MRI. Stent deployment to repair aortic coarctation is feasible under MR guidance. The combined use of MR and X-ray imaging is effective for anatomic and functional evaluation of aortic coarctation dilation, which may be crucial for optimal therapy.

The Accuracy of Aortic Valve Area Determined by Transesophageal Echocardiography using Direct Planimetry According to the Changes of Cardiac Output and Left Ventricular Ejection Fraction

Background:The accuracy of flow-related changes in aortic valve area (AVA) determined by the Gorlin formula or the continuity equation remains disputable. However, anatomic AVA can be determined by using by direct planimetry of transesophageal echocardiography (TEE). The purpose of this study was to assess the impact of changes in flow on AVA determined by TEE using direct planimetry. Method:Determination of AVA by TEE using direct planimetey was performed intraoperatively under three different hemodynamic conditions –pre-dobutamine (baseline) period, post-dobutamine period, post-CABG period– in 17 CABG patients and cardiac output (CO) with left ventricular ejection fraction (EF) were also determined by TEE simutaneously. The changes in aortic flow were induced by dobutamine infusion. Results:AVA at predobumaine period, post-dobutamine period, and post-CABG period were 2.99±0.80 cm 2, 3.01±0.79 cm, and 3.01±0.80 cm, respectively. Before dobutamin infusion, CO and EF were 2.01±0.64 L/min and 47± 10%. After dobutamine infusion, CO and EF were 3.03±1.05 L/min, 54±9% respectively and significantly increased by 54%, 18% than those measured before dobutamine infusion (p<0.01, p<0.01), respectively. After CABG, CO and EF were 3.86±1.86 L/min and 58±11% and also significantly increased by 98%, 26% than those measured before dobutamine infusion (p<0.01, p<0.01), respectively. However, despite of these significant hemodynamic changes, there were no significant changes in AVA and no significant correlations between these hemodynamic and AVA changes, neither at post-dobutamine period nor post-CABG period. Conclusion:The acute changes in CO and EF do not result in significant alterations in the anatomic AVA 논문접수일:1999년 10월 15일 심사완료일:2000년 7월 15일 교신저자:김종진, 130-022 서울 동대문구 전농동 620-56 가톨릭대학교 의과대학 내과학교실 전화:(02) 958-2388·전송:(02) 968-7250 E-mail:cjkim@sph.cuk.ac.kr

Aortic valve replacement with 'stentless' versus mechanical prosthesis: what difference in postoperative ICU course?

Aortic valve prosthesis determine a transvalvular gradient (Δp) with changes in aortic flow that can affect left ventricular geometry and function, implanted prosthesis and aortic route. In order to improve prognosis a new prosthesis has been proposed, the so called 'stentless valve' (SV), whose main characteristic is the absence of the supporting ring. Aim of our study was to evaluate if such valve could influence early postoperative course in ICU.

Exercise-related changes in aortic flow measured with spiral echo-planar MR velocity mapping.

Spiral echo-planar magnetic resonance (MR) velocity mapping was used to measure exercise-related changes in flow in the descending thoracic aorta in 10 healthy volunteers. Flow was measured at rest and immediately after dynamic exercise, with a 0.5-T imager with a surface receiving coil and electrocardiographic triggering. Supine exercise was performed with a home-built pedaling apparatus. Spiral velocity mapping was performed in a transverse plane through the descending thoracic aorta with the subject at rest. The subject was then asked to perform maximum exercise, stop, and hold his breath during a four-heartbeat acquisition time. Eight cine frames with a temporal resolution of 50 msec were acquired through systole. Each image was acquired in 40 msec during spiral acquisition of k-space data, starting at the center, 6 msec after the excitation pulse. Reproducibility of the technique was established by repeating the flow measurement in four consecutive heartbeats. At rest, the heart rate (mean +/- standard deviation), mean aortic flow, peak aortic flow, and time to peak flow were 68 beats per minute +/- 6, 41 milliliters per beat +/- 8, 107 mL/sec +/- 20, and 175 msec +/- 25, respectively. After exercise, the heart rate and mean and peak aortic flow were significantly increased (P < .001), measuring 101 beats per minute +/- 12, 57 milliliters per beat +/- 11, and 158 mL/sec +/- 29, respectively, while the time to peak flow (115 msec +/- 32) was significantly reduced (P < .001). The four sets of values obtained for the first four consecutive heartbeats measured at rest were similar, as were those obtained for the first four heartbeats after exercise.

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

Can pulsed Doppler technique measure changes in aortic blood flow in conscious rats?

To determine whether the pulsed Doppler (PD) system could be used to measure cardiac output we compared estimates of changes in aortic flow obtained from PD or electromagnetic (EM) probes on the ascending aorta in separate groups of conscious Long-Evans and Brattleboro rats under a variety of conditions. EM probes showed significant increases and decreases in aortic blood flow after administration of nitroprusside or methoxamine, respectively, but 20-MHz PD probes connected to a PD mainframe with a pulse repetition frequency (PRF) of 62.5 kHz showed no systematic changes in Doppler shift, due to "aliasing" of the Doppler signal. Aortic blood flow was significantly increased with intravenous volume expansion or isoprenaline administration, but these changes were not reliably detected by PD probes operating in a system with a PRF of 62.5 kHz. Calculation of expected peak Doppler shift signals from the phasic EM flow signal showed that these exceeded the Nyquist limit (PRF/2, i.e., 31.25 kHz) for the commercially available pulsed Doppler system. However, a modified pulsed Doppler module capable of resolving aliases and operating at a PRF of 125 kHz produced reliable results for changes in thoracic aortic Doppler shift, in good agreement with the EM probe data. In addition, placement of a cuff around the thoracic aorta did not alter cardiac baroreflex sensitivity.

A closed-loop control scheme for intraaortic balloon pumping

The beneficial hemodynamic effects of IABP are critically dependent on balloon timing relative to the diastolic phase of the cardiac cycle. A microprocessor-based controller has been developed to implement real-time automation of IABP using P-R intervals to regulate balloon deflation and systolic time intervals to trigger balloon inflation in a semi-automatic fashion. Experiments were performed on anesthetized open-chest dogs. Simultaneous measurement of aortic pressure and flow, coronary flow, and left ventricular pressure were recorded. Muscle segment lengths in normal and ischemic border zones were also measured from implanted pairs of endocardial ultrasonic dimension gages. P-waves were obtained from atrial cardiograms, and heart sounds were detected using a special filtering circuit. Both signals were input together with ECG to automate IABP timing. Systolic time intervals were calculated in real-time. IABP efficacy was assessed from changes in aortic flow, coronary flow, tension time index, end diastolic pressure, and the endocardial viability ratio. Comparisons were made between automated and manual timing set by a certified technician. Results indicate that automated timing yielded equivalent hemodynamic enhancement with greater ease of adjustment. A closed-loop control scheme is proposed which allows complete automatic device operation and the capability to rapidly achieve the optimum of any directly measurable hemodynamic variable.

Temporal relationship between early systolic closure of the aortic valve and aortic flow: Experimental study with and without systolic anterior motion of the mitral valve

To investigate the causative factors of typical early systolic closure (ESC) of the aortic valve (AoV), the temporal relationships of ESC with changes in blood pressures and aortic flow (AoF) were examined in dogs with experimentally induced ESC with and without systolic anterior motion (SAM) of the mitral valve. SAM was induced by dobutamine administration. Typical ESC was observed, but no SAM or left ventricular outflow obstruction, in five of the eight dogs treated with isoproterenol. Regardless of the presence or absence of SAM, the onset of ESC occurred before and the end of ESC immediately after the peak of AoF. A similar time relationship was noted between partial closure of the AoV, and pressure and flow changes before administration of isoproterenol, as well as after its termination. These results exclude a rapid decrease in flow velocity as the cause of ESC in our experimental preparation. The nearly uniform temporal relationship between ESC and changes in AoF observed under various conditions is considered to have important implications in the cause of ESC.

Change in pulmonary and systemic circulation in acute ventricular septal defect.

The correlation between left to right ventricular (L-R) shunt flow and other hemodynamic changes was studied in 16 dogs with an acute ventricular septal defect (VSD) and normal pulmonary vascular bed. The interventricular shunt flow was measured directly with a specially designed electromagnetic flowmeter probe, where the area of the VSD was constant. The sudden presentation of VSD increased pulmonary arterial pressure, pulmonary flow and left ventricular end-diastolic pressure. L-R shunt flow was not changed significantly by atrial pacing except when the rate was increased to over 200/min. Dogs with a VSD were treated with isoproterenol and dextran to vary the shunt flow and hemodynamic parameters. L-R shunt flow was decreased by isoproterenol and increased by dextran loading. The percentage changes of L-R shunt flow from pre-drug values correlated well with the change in left ventricular end-diastolic pressure (r = 0.75) and the ratio of pulmonary to systemic vascular resistance (r = -0.73). Change in total pulmonary vascular resistance had a greater effect on L-R shunt flow than did a change in systemic vascular resistance, whereas a change in aortic flow had less effect (r = 0.35) on L-R shunt flow than did a change in preload and afterload. The time to peak LV dP/dt, as an index of cardiac contractility, and heart rate were not correlated with the relative change in L-R shunt flow. These results indicate that L-R shunt flow induced by the sudden presentation of a VSD varied with changes in the pulmonary and systemic circulation.

Effects of right ventricular ischemia on left ventricular geometry and the end-diastolic pressure-volume relationship in the dog.

We studied the effects of right ventricular ischemia on left ventricular three-dimensional geometry and the end-diastolic pressure-volume relationship in 16 open-chest dogs before and after pericardiectomy. Left ventricular volume was calculated from three internal dimensions measured with ultrasonic crystals. In one group of eight dogs, right coronary artery (RCA) occlusion for 2 min with the pericardium intact reduced aortic flow by 24 +/- 9% (p less than .001) and septal-lateral dimension by 8 +/- 5% (p less than .01), without changing anterior-posterior and apical-basal dimensions. However, parameters of left ventricular systolic function (aortic flow, left ventricular systolic pressure, peak dP/dt, and mean percent systolic shortening) were similar to those observed at a comparable level of left ventricular end-diastolic volume during inferior vena caval occlusion. In the other group of eight dogs, during RCA occlusion before pericardiectomy the left ventricular end-diastolic pressure-volume relationship determined during rapid blood transfusion shifted leftward and upward significantly from the preocclusion relationship. After pericardiectomy, RCA occlusion caused less significant changes in aortic flow and septal-lateral dimension as well as in the left ventricular end-diastolic pressure-volume relationship. We concluded that right ventricular ischemia causes a leftward shift of the interventricular septum in end-diastole and an alteration of the left ventricular end-diastolic pressure-volume relationship without changing left ventricular myocardial performance. These changes are enhanced by the intact pericardium.

131 PHASIC MITRAL FLOW DURING SPONTANEOUS RESPIRATION

We have previously demonstrated that changes in preload will influence mitral flow (QM) prior to changes in aortic flow (QA), while a change in afterload will influence QA first. During spontaneous unobstructed inspiration and Mueller maneuvers, QA is minimum during inspiration and reaches a maximum in early expiration. We tested whether primary changes in QM or QA were dominantly responsible for the observed respiratory variation in QA. In 7 acutely instrumented dogs, we placed both mitral and ascending aortic flow probes, closed the pericardium and chest and allowed spontaneous respiration to resume. We evaluated preload (QM) or afterload (QA) dominance by measuring which integrated flow reached its' inspiratory minimum or expiratory maximum first during a single respiratory cycle.These data suggest that while an afterload influence does exist, preload changes dominate over afterload changes in determining changes in LV stroke volume during respiration under our experimental conditions with small changes in pleural pressure with or without a change in lung volume.

Responses of aortic baroreceptors to changes of aortic blood flow and pressure in rat

To test the hypothesis that aortic baroreceptors may respond not only to changes of aortic pressure but also to changes of aortic flow, sinusoidal flow waves were applied at 1 Hz to the aorta of urethan-anesthetized rats by infusion and withdrawal of 90 microliters blood with a pump while aortic blood pressure and single baroreceptor fiber activity were monitored. Averages from 20 to 30 pressure wave forms and nerve impulse histograms were established by computer for each single fiber during control (no pump), pump instroke (I), and outstroke (O). Fiber activity increased 20 +/- 3% (mean +/- SEM, n = 28 fibers) and decreased 23 +/- 4% with respect to control during I and O, respectively, whereas estimated changes of aortic flow were +/- 21%. The number of nerve impulses increased (I) and decreased (O) mainly during late systolic pressure rise did not change significantly, but the rate of late systolic pressure fall decreased 42 +/- 7 mmHg/s (I) and increased 39 +/- 11 mmHg/s (O). These results suggest that, because of the rate sensitivity of aortic baroreceptors, changes in aortic flow are reflected in changes of nerve impulse firing patterns during the blood pressure decrease in late systole, even in the absence of significant changes in systolic, diastolic, and pulse pressure.

Mechanical performance of the working rat heart: Response to calcium

Although calcium is generally considered a substance that can enhance cardiac pump performance, few data exist to demonstrate such effect when plasma ionized calcium is varied in the clinical concentration range. We have studied the relationship between perfusate ionized calcium concentration ([Ca 2+]) and myocardial mechanical performance in the isolated, blood perfused, ejecting rat heart. With pre- and afterload near constant, observations were made before and after steadystate increases in [Ca 2+] from low (mean ± SEM: 0.74 ± 0.01 m M) to normal (1.01 ± 0.04 m M); from low (1.01 ± 0.02 m M) to higher than normal (1.45 ± 0.04 m M, i.e., within the clinical hypercalcemia range); and to an excessive value (1.94 ± 0.03 m M). When [Ca 2+] was increased from low to normal levels, aortic blood flow and stroke volume increased by approximately 25% of control ( P < 0.025); heart rate did not change significantly. In contrast, when [Ca 2+] was raised from 1.03 m M (normal value) to 1.45 m M (within the clinical hypercalcemia range) or to 1.94 m M (above the clinical hypercalcemia range), the changes in aortic flow and stroke volume were less ( P < 0.05) as compared to those observed when ionized calcium was adjusted from a level below normal. We conclude that the isolated, blood-perfused heart with pre- and afterload near constant, responds to sustained increases in perfusate ionized calcium with increased aortic flow and stroke volume, but that these changes are disproportionally small when ionized calcium is elevated to above normal from a normal baseline value.

Myocardial oxygen consumption and blood flow during nicotine infusion: effect of combined alpha- and beta-adrenergic blockade.

The effect of combined alpha- and beta-adrenergic blockade with phenoxybenzamine and propranolol, respectively, on changes in left ventricular myocardial oxygen consumption and blood flow during nicotine administrations (36 micrograms/kg/min, i.v.) was evaluated in anesthetized, open-chest dogs. Myocardial blood flow was estimated by injection of 8 to 10 micrometers diameter radioactive microspheres into the left atrium, and myocardial oxygen consumption was computed from the Fick principle. Before adrenergic blockade, nicotine caused a market (+151%) elevation in myocardial oxygen consumption and a parallel increase in myocardial blood flow. The increase in myocardial blood flow was uniform transmurally. These cardiac changes were accompanied by elevations in systemic arterial and left atrial pressures, peripheral vascular resistance, and heart rate, but by no change in aortic flow or in myocardial contractility. After adrenergic blockade, nicotine caused somewhat lesser, though still marked, elevations in myocardial oxygen consumption (+60%) and blood flow (+43%). Again, myocardial blood flow increases were uniform transmurally. Also, nicotine-induced increases in systemic arterial and left atrial pressure and in peripheral vascular resistance persisted after adrenergic blockade, whereas heart rate remained constant and aortic flow and myocardial contractility declined. The results indicate that nonadrenergic mechanisms contribute significantly to the increase in myocardial oxygen demand during nicotine infusion.

Instantaneous blood flow responses to positive end-expiratory pressure with spontaneous ventilation.

Variable hemodynamic responses to positive end-expiratory pressure (PEEP) with spontaneous ventilation have been reported. To clarify these responses, 15 awake patients were studied using a catheter-tip velocity transducer to record phasic aortic root blood flow continuously before, during and after PEEP (10 cm H2O) applied with a face mask. Central blood volume and effective ventricular filling pressures were measured. Phasic pulmonary artery blood flow was also simultaneously recorded in three of these patients. PEEP produced an acute aortic blood flow reduction, detected within one respiratory cycle. Stroke volume decreased 12%, and since heart rate was unchanged, cardiac output also declined (p less than 0.05). Inspiratory-to-expiratory aortic flow changes were less during PEEP. In contrast, inspiratory-to-expiratory pulmonary artery flow alterations were exaggerated due to a marked flow decline during expiration. Central blood volume and effective left ventricular filling pressure decreased 9% and 19%, respectively (p less than 0.05 in all patients). The decrease in pulmonary artery flow was associated with a decrease in central blood volume in the three patients in whom pulmonary flow was measured. PEEP promptly reduces cardiac output during spontaneous ventilation, related to a decrease in pulmonary flow in expiration.

Effect of unilateral nephrectomy on the localization of aortic sudanophilic lesions in cholesterol-fed rabbits

The method of polar coordinate mapping of lesions on the aortic wall around orifices was used to study the effect of unilateral nephrectomy on sudanophilic lesions in rabbits. Four groups of six rabbits each were studied. Group I had a right nephrectomy with a short renal artery stump. Group II had a sham right nephrectomy. Group III had a left nephrectomy with a short renal artery stump and Group IV a sham left nephrectomy. All groups were allowed to recover for one week and were then fed rabbit chow enriched with 2% cholesterol and 6% corn oil for a four-week period. Groups I and III showed a marked alteration in lesions around the stump with both proximal and distal peaks. Group I also showed the development of skewing of the left renal lesion to the left, presumably because of a change in aortic flow due to removal of the proximal right renal flow. The right renal artery had a lesion skewed to the right; this was not altered by left nephrectomy and was probably due to coeliac flow. The data provides strong evidence that sudanophilic lesions in rabbit aortas are altered by local flow disturbances.