Determination of arterial input impedance spectra from non-invasively recorded pulses

The frequency spectra of modulus and phase of the input impedance (Zin) of large human arteries (abdominal aorta, femoral and subclavian arteries) were computed from transcutaneously recorded, uncalibrated pressure and flow pulses picked up as sphygmograms and Doppler flow velocity pulses, respectively. Since these pulses cannot be calibrated, the modulus (Zin) of the input impedance is calculated in relative units; its spectrum, however, is not influenced by this fact. A modification of the computing procedure makes it possible to determine approximately quasi-continuous frequency spectra of Zin from natural pressure and flow pulses which may be regarded as periodic functions. This is the prerequisite for a detailed analysis of the wave transmission properties of the arterial bed which manifest themselves of the input impedance. For this purpose the peripheral reflection site was moved in a proximal direction by bilateral occlusion of limb arteries. This was done by inflating cuffs placed symmetrically on both sides around the upper or lower parts of the respective limbs. When the occluding cuffs were placed around both lower legs or both thighs, the shortening of the arterial wave transmission line resulted in a marked shift of the first maximum of Zin to higher frequencies in the spectrum of Zin of the abdominal aorta and femoral artery. Bilateral occlusion of the arteries of the forearms or upper arms, however, did not have any measurable influence on Zin of the subclavian artery. Theoretical considerations show that this difference in behaviour of the several parts of the arterial system may be attributed to the varying extent of their inhomogeneity.     

Patchy fur, a mouse coat mutation associated with X-Y nondisjunction, maps to the pseudoautosomal boundary region

We have searched to define the major arterial parameters that determine aortic systolic (Ps) and diastolic (Pd) pressure in the dog. Measured aortic flows were used as input to the 2-element windkessel model of the arterial system, with peripheral resistance calculated as mean pressure divided by mean flow and total arterial compliance calculated from the decay time in diastole. The windkessel model yielded an aortic pressure wave from which we obtained the predicted systolic (Ps,wk) and diastolic (Pd,wk) pressures. These predicted pressures were compared with the measured systolic and diastolic pressures. The measurements and calculations were performed for 7 dogs under control conditions during aortic occlusion at 4 locations (the trifurcation, between the trifurcation and diaphragm, the diaphragm, and the proximal descending thoracic aorta) and during occlusion of both carotid arteries. Under all conditions studied, the predicted systolic and diastolic pressures matched the experimental ones very well: Ps,wk=(1.000+/-0.0055) Ps with r=0.958 and Pd,wk=(1.024+/-0.0035) Pd with r=0.995. Linear regression for pulse pressure (PP) resulted in PPwk=(0.99+/-0.016) PP with r=0.911. We found the accuracy of prediction equally good under control conditions and in the presence of aortic or carotid artery occlusion. Multiple regression between pulse pressure and arterial resistance and total arterial compliance yielded a poor regression constant (R2=0.19), suggesting that the 2 arterial parameters alone cannot explain pulse pressure and that flow is an important determinant as well. We conclude that for a given ejection pattern (aortic flow), 2 arterial parameters, total arterial resistance and total arterial compliance, are sufficient to accurately describe systolic and diastolic aortic pressure.     

Inhibition of neuronal nitric oxide synthase by antipsychotic drugs

Hydralazine was administered at cardiac catheterization to eight children with a ventricular septal defect (age: 2.2-8.8 years), and the extent of afterload reduction was determined using aortic input impedance and wall stress. The pulmonary to systemic blood flow ratio decreased from 2.2 +/- 0.8 to 1.8 +/- 0.4 (p < 0.05) and the pulmonary systemic resistance ratio increased from 0.11 +/- 0.08 to 0.13 +/- 0.10 (p < 0.05) after hydralazine administration. Hydralazine reduced mean aortic pressure and the amplitude of the late systolic peak of the aortic pressure wave. Peak flow velocity in the descending aorta increased from 62 +/- 14 to 81 +/- 24 cm/sec (p < 0.05). Peripheral resistance decreased significantly from 13.3 +/- 5.9 to 6.6 +/- 3.7 10(3) dyn sec/cm3 (p < 0.05). The modulus of the first harmonic, indicating pulse wave reflection, decreased from 1196 +/- 575 to 815 +/- 382 dyn sec/cm3 (p < 0.05). The characteristic impedance, indicating aortic stiffness, did not change. End-systolic wall stress decreased significantly from 54.4 +/- 16.7 to 34.8 +/- 10.2 g/cm2 (p < 0.01). Hydralazine acutely achieved afterload reduction by reducing both peripheral resistance and pulse wave reflection, and increased stroke volume.     

Atrial conduction abnormalities in patients with systemic progressive sclerosis

BACKGROUND: Atrial abnormalities in patients with progressive systemic sclerosis have not been evaluated in terms of intra-atrial conduction. We hypothesized that a delay in atrial conduction in these patients might produce diastolic abnormalities as well as atrial arrhythmias. OBJECTIVE: To evaluate the atrial function of patients with progressive systemic sclerosis by using echocardiography to measure the intra-atrial electromechanical activation coupling interval. METHODS: Twenty patients with progressive systemic sclerosis were assessed by Doppler echocardiography. Twenty age-matched healthy controls were also evaluated. Two-dimensional guided M-modes of ventricular long axes were recorded using simultaneous phono- and electrocardiograms of the apical four chamber view at the right lateral, septal and left lateral sites of the atrioventricular rings. Transmitral and tricuspid pulsed Doppler flow velocities were also recorded. Filtered P wave duration was measured on the signal averaged ECG to determine the duration of atrial electrical activation. RESULTS: There was a delay in P on the electrocardiogram (P) at the onset of atrial contraction on long axis M-modes at all three atrioventricular ring sites in patients with progressive systemic sclerosis as compared with controls (P-right; 56 +/- 13 vs 47 +/- 10 ms, P-septal; 74 +/- 14 vs 55 +/- 10 ms, and P-lateral; 93 +/- 16 vs 72 +/- 11 ms, P < 0.01). Inter-atrial conduction time [(P-lateral)-(P-right)] was delayed in patients with progressive systemic sclerosis, compared with healthy controls (37 +/- 15 vs 25 +/- 6 ms, P < 0.01). Mitral A waves acceleration and deceleration times were also decreased in the patients. The interval was prolonged between P to the onset and the peak of the A wave in transmitral flow. Duration of the filtered P wave was significantly prolonged in progressive systemic sclerosis as compared with controls (124 +/- 12 ms vs 106 +/- 8 ms, P < 0.01). PQ intervals, E waves and acceleration and deceleration times did not differ significantly in progressive systemic sclerosis vs, controls. The A wave acceleration rate on transmitral flow (peak A wave velocity/acceleration time) showed a significant correlation with inter-atrial conduction delay (r = 0.55, P < 0.01). CONCLUSIONS: Intra-atrial electromechanical coupling intervals were delayed in patients with progressive systemic sclerosis. Thus, the mechanical late diastolic filling time due to atrial contraction in the total diastolic phase was severely limited, and this resulted in a restricted mitral A wave. We should therefore evaluate patients with progressive systemic sclerosis for significant atrial abnormalities.     

Influence of one bout of intensive running on lymphocyte micronucleus frequencies in endurance-trained and untrained men

This clinical investigation was designed to determine the effect of changes in loading patterns on left ventricular (LV) relaxation when heart rate was maintained constant. Not only were changes noted in total load or time in which load is changed, but also the contour of the ascending aortic systolic pressure wave. Twenty patients were studied. LV and ascending aortic pressure were measured by a multisensor catheter under baseline conditions (C) and after an intravenous injection of 2.5 microg angiotensin (A) and sublingual administration of 0.3 mg nitroglycerin (N). A bipolar pacing catheter was placed in the right atrium to maintain a constant heart rate throughout the protocol. The augmentation index (AI), which characterizes the contour of the ascending aortic systolic pressure wave, was defined as the ratio of the height of the late systolic shoulder/peak to that of the early systolic shoulder/peak in the pulse. The rate of isovolumic LV pressure decline was calculated as a time constant (Tau). Ascending aortic systolic pressures (mmHg) were 127+/-29 (C), 158+/-20 (A) and 109+/-15 (N). AI were 1.61+/-1.14 (C), 2.08+/-1.11 (A) and 1.27+/-1.14 (N). Tau values (msec) were 49+/-4 (C), 54+/-4 (A) and 45+/-5 (N). Tau was prolonged proportionally with increasing AI (p<0.001, r=0.64). It was concluded that late systolic pressure augmentation in the ascending aorta is one important factor that influences the rate of isovolumic left ventricular pressure decline in humans.     

Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions

This study was designed to investigate whether the left ventricular filling profile during preceding control beats significantly affects the pulse deficit caused by ventricular premature contractions (VPCs). The study group consisted of 18 patients (10 men, eight women, 15-85 years old) who underwent electrophysiological catheterization because of sinus bradycardia. Using a temporary pacing lead inserted in the right ventricular apex, isolated VPCs with various coupling intervals were produced by electrical stimulation of the right ventricle. During the production of the VPCs, the mitral filling flow velocity using pulsed wave Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The right ventricle was stimulated 800, 750, 700, 650, 600, 550, 500, 450 and 400 ms after the triggered control beat QRS complex. Pulse pressures during VPCs gradually decreased in relation to the shortening of the extrasystolic beat coupling interval. The longest coupling interval for each subject, which caused complete abolition of the pressure pulse during the VPC, was defined as the pulse deficit coupling interval. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which precede the VPC was obtained as an index expressing the left ventricular filling profile. The Ei/Ai ratio of the mitral filling flow velocity ranged from 0.7 to 4.5 (1.8 +/- 1.0). The pulse deficit coupling interval ranged from 440 to 640 ms (510 +/- 60 ms).(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term test-retest reliability of personality disorder diagnoses in opiate dependent patients

Continuous wave Doppler methods have been widely used clinically for evaluating the severity of aortic regurgitation; however, there have been no studies comparing these continuous wave Doppler methods with a strictly quantifiable reference for regurgitant severity. The purpose of this study was to test the applicability of continuous wave Doppler methods (deceleration slope and pressure half-time) for evaluation of chronic aortic regurgitation in an animal model. Eight sheep were studied 8 to 20 weeks after surgery to create chronic aortic regurgitation. Twenty-nine hemodynamically different states were obtained pharmacologically. A Vingmed 775 system was used for recording continuous wave Doppler traces with a 5 MHz annular array transducer directly placed on the heart near the apex. The aortic regurgitation was quantified as peak and mean regurgitant flow rates, regurgitant stroke volumes and regurgitant fractions determined with pulmonary and aortic electromagnetic flow probes and meters balanced against each other. Peak regurgitant flow rates varied from 1.8 to 13.6 L/min (6.3 +/- 3.2 L/min) (mean +/- SD), mean regurgitant flow rates varied from 0.7 to 4.9 L/min (2.7 +/- 1.3 L/min), regurgitant stroke volume varied from 7.0 to 48.0 ml/beat (26.9 +/- 12.2 ml/beat), and regurgitant fraction varied from 23% to 78% (53% +/- 16%). Only marginal correlations were obtained between reference indexes and continuous wave Doppler deceleration slope and pressure half-time (r = 0.55 to 0.74). A deceleration slope greater than 3 m/sec2 and pressure half-time less than 400 msec did, however, provide 100% specificity for detecting severe AR (regurgitant fraction > 50%). Our study shows that the continuous wave Doppler deceleration slope and pressure half-time methods have limited use for quantifying aortic regurgitation.     

Noninvasive detection of iliac artery disease and prediction of its severity from Doppler spectral analysis in common femoral artery

The direct interrogation of iliac artery disease (IAD) with color-coded duplex scanning is limited by the presence of intestinal gas or obesity. The purposes of this study were to examine the diagnostic accuracy of duplex ultrasound (DUS) analysis of spectral waves in common femoral artery (CFA) for detection of IAD and to predict its severity. DUS and arteriography were performed in 107 lower extremities in this study. The following were calculated from the CFA spectral waves obtained by DUS: peak systolic velocity (PSV), acceleration (PSV/pulse rise time), and deceleration (PSV/pulse decay time). In patients with isolated IAD, the treadmill exercise test was also performed to evaluate the ischemic severity expressed as recovery rate of ankle pressure index five minutes after exercise (RR-API). Forty-six lower extremities with IAD and 61 without IAD were diagnosed by arteriography. PSV was significantly reduced in lower extremities with IAD (109.5 +/- 32.7 vs 59.8 +/- 32.9 cm/s, P < 0.05). The deceleration detected IAD with a greater specificity and sensitivity vs acceleration (100.0 vs 82.0% and 97.8 vs 82.6%, respectively). Moreover, the acceleration and deceleration significantly correlated with the RR-API (r = 0.589, P < 0.05 and r = 0.779, P < 0.01, n = 14, respectively). The present evaluation is a simple and accurate technique to augment other examinations for detection of IAD and to assess its ischemic severity.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Echocardiographic hemodynamic and morphometric predictors of survival after two-ventricle repair in infants with critical aortic stenosis

OBJECTIVES: The purpose of this study was to identify echocardiographic hemodynamic and morphometric factors that would predict which infants with critical aortic stenosis could undergo relief of left ventricular outflow obstruction as opposed to the Norwood procedure. BACKGROUND: Echocardiographic predictors of survival in infants with critical aortic stenosis after two-ventricle repair have been mainly limited to morphometric factors, which have limitations. Echocardiographic hemodynamic predictors of survival in these patients have not previously been studied. METHODS: Doppler color flow mapping and pulsed Doppler techniques were used to obtain hemodynamic measurements of flow in the ascending, transverse and descending aorta, the ductus arteriosus, and across the aortic and mitral valves in infants with critical aortic stenosis. Morphometric measurements of the left heart structures were obtained, and comparisons were made between survivors and nonsurvivors for the hemodynamic and morphometric factors. RESULTS: Twenty-eight infants (mean age 1 +/- .6 days, mean weight 3.6 +/- .6 kg) with critical aortic stenosis were evaluated. Nineteen had a two-ventricle repair initially attempted, and nine had a Norwood operation. Among the patients with a two-ventricle repair, the hemodynamic factors associated with survival after two-ventricle repair included predominant or total antegrade flow in the ascending (p < 0.01) and transverse aorta (p < 0.05). Aortic valve gradient, mitral valve inflow and direction of flow in the ductus arteriosus and descending aorta were unrelated to outcome. The morphometric factors associated with survival after two-ventricle repair included the indexed aortic annulus (p < 0.0002), aortic root (p < 0.003), ascending aorta (p < 0.008) and left ventricular long-axis length (p < 0.01). Left ventricular volume, mass, ejection fraction and mitral valve area were not related to outcome after two-ventricle repair. CONCLUSIONS: In infants with critical aortic stenosis, predominant or total antegrade flow in the ascending and transverse aorta was associated with survival after two-ventricle repair. Determination of a one- versus two-ventricle repair remains a complex issue in infants with critical aortic stenosis. In addition to established morphometric predictors, hemodynamic information on the direction of flow in the aorta may help to define candidates for the Norwood operation.     

Towards optimization of wave reflection: therapeutic goal for tomorrow?

1. The conventional approach to drug therapy of hypertension and heart failure considers only effects of such drugs on peripheral resistance, cardiac output and heart rate. 2. A more complete approach needs to consider the pulsatile nature of cardiac ejection and so the influence of arterial stiffness and wave reflection properties and the effects of drugs on these. 3. Wave reflection normally aids cardiac function when full body height is achieved and arterial distensibility is high. However, with ageing or in hypertension the arteries stiffen and wave reflection returns early, augmenting systolic pressure, increasing pulse pressure and reducing the capacity for coronary perfusion. 4. In mature or older adults, delay of or reduction in wave reflection is an important therapeutic strategy for management of hypertension, angina pectoris and cardiac failure. 5. Beneficial effects of such therapy cannot always be gauged from conventional recordings of blood pressure, but can be inferred from analysis of pulse waveform.     

Effects of BQ-123 on systemic and renal hemodynamic responses to endothelin-1 in the rat split hydronephrotic kidney

OBJECTIVE: To assess the site of action of endothelin-1 in vessels of different sizes in the kidney in vivo and investigate the function of endothelin A (ET(A)) receptors in mediating renal and systemic vasoconstriction. DESIGN: The luminal diameters of different vessels were measured and glomerular blood flow in cortical glomeruli was determined by intravital videomicroscopy in the split hydronephrotic kidney of anesthetized female Wistar rats. METHODS: The rats were infused with endothelin-1 (40 pmol/kg per min) with or without pretreatment with the selective ET(A)-receptor antagonist BQ-123 (0.5 mg/kg). Aortic clamping was used to control renal blood pressure during the endothelin-1 infusion. RESULTS: Exogenous endothelin-1 induced a significant rise (30+/-3%) in mean arterial pressure and a marked, long-lasting fall in glomerular blood flow (53+/-3%) related to reduction of the inner diameter of arcuate (-30%), interlobular arteries (-33%) and afferent arterioles (-17%). Aortic clamping to normalize renal blood pressure did not attenuate the vasoconstriction and reduction in glomerular blood flow. Pretreatment with BQ-123 significantly reduced both the endothelin-1-induced rise in mean arterial pressure (12+/-1%) and the fall in glomerular blood flow (-23+/-11%). BQ-123 blunted the response to endothelin-1 in arcuate (-12%), interlobular (-11%) and afferent vessels (-5%). Acetylcholine and nitroprusside completely reversed the vasoconstriction in BQ-123-pretreated animals. CONCLUSIONS: BQ-123 largely prevented the hemodynamic effects of exogenously administered endothelin-1. Our direct in-vivo techniques showed that ET(A) receptors are, at least in part, involved in endothelin-1 -mediated vasoconstriction in the rat kidney, and support the hypothesis that ET(A) receptors may help to control arterial pressure in anesthetized rats.     

Damping Effect on Waves Propagating Past a Submerged Horizontal Plate and a Vertical Porous Wall

A set of analytical solutions for waves propagating past a combined submerged horizontal plate and vertical porous wall breakwater system is presented. The wave damping effect caused by the horizontal plate induced flow constriction is considered in the analysis. The velocity potentials in each fluid domain are derived based on the linear wave theory and the unknown coefficients are determined from the matching conditions using three sets of orthogonal eigenfunctions. Reflection and transmission coefficients are presented to evaluate the performance of the breakwater system. The analytical solutions in terms of the reflection and transmission coefficients as well as the hydrodynamic force on the vertical porous wall are found in good agreement with published laboratory measurements. In comparison with the solutions without taking into account the wave damping effect, the present analytical solutions significantly improve the accuracy of the wave predictions, especially for the reflected waves.     

Effects of spinal cord ischemia on evoked potential recovery and postischemic regional spinal cord blood flow

The effects of spinal cord ischemia on spinal cord blood flow (SCBF) and somatosensory (SSEP) and motor (MEP) evoked potentials were investigated in a rabbit model of reversible spinal cord ischemia. Spinal cord ischemia was produced by balloon occlusion of the infrarenal aorta for 30, 60, and 90 min. SCBF, SSEPs, and MEPs were measured before, during, and 1 h after aortic occlusion. Aortic occlusion produced absolute ischemia of the caudal cord followed by hyperemia upon reperfusion. SSEP's and MEP's were obliterated during ischemia but demonstrated gradual albeit incomplete recovery following reperfusion with amplitude recovery inversely proportional to the duration of ischemia. Later peaks were more severely affected by a given period of ischemia than were early waves. In general, SSEP's were more resistant to ischemia than were MEP's although the differences were not significant.     

A method for studying the biomechanical load response of the (in vitro) lumbar spine under dynamic flexion-shear loads

A method was developed to study the biomechanical response of the lumbar motion segment (Functional Spinal Unit, FSU) under a dynamic (transient) load in flexion. In order to inflict flexion-distraction types of injuries (lap seat-belt injuries) different load pulses were transferred to the specimen by means of a padded pendulum. The load response of the specimen was measured with a force and moment transducer. The flexion angulation and displacements were determined by means of high-speed photography. Two series of tests were made with ten specimens in each and with two different load pulses: one moderate load pulse (peak acceleration 5 g, rise time 30 ms, duration 150 ms) and one severe load pulse (peak acceleration 12 g, rise time 15 ms, duration 250 ms). The results showed that the moderate load pulse caused residual permanent deformations at a mean bending moment of 140 Nm and a mean shear force of 430 N at a mean flexion angulation of 14 degrees. The severe load pulse caused evident signs of failure of the segments at a mean bending moment of 185 Nm and a mean shear force of 600 N at a mean flexion angulation of 19 degrees. Significant correlations were found between the load response and the size of the specimen, as well as between the load response and the bone mineral content (BMC) in the two adjacent vertebrae. Comparisons with lumbar spine response to static flexion-shear loading indicated that the specimens could withstand higher bending moments before injury occurred during dynamic loading, but the deformations at injury tended to be smaller for dynamic loading.     

Influence of polarity reversal on defibrillation success with biphasic shocks and a transvenous/subcutaneous defibrillator system in a porcine animal model

Clinical studies show that polarity reversal affects defibrillation success in transvenous monophasic defibrillators. Current devices use biphasic shocks for defibrillation. We investigated in a porcine animal model whether polarity reversal influences defibrillation success with biphasic shocks. In nine anesthetized, ventilated pigs, the defibrillation efficacy of biphasic shocks (14.3 ms and 10.8 ms pulse duration) with "initial polarity" (IP, distal electrode = cathode) and "reversed polarity" (RP, distal electrode = anode) delivered via a transvenous/subcutaneous lead system was compared. Voltage and current of each defibrillating pulse were recorded on an oscilloscope and impedance calculated as voltage divided by current. Cumulative defibrillation success was significantly higher for RP than for IP for both pulse durations (55% vs 44%, P = 0.019) for 14.3 ms (57% vs 45%, P < 0.05) and insignificantly higher for 10.8 ms (52% vs 42%, P = ns). Impedance was significantly lower with RP at the trailing edge of pulse 1 (IP: 44 +/- 8.4 vs RP: 37 +/- 9.3 with 14.3 ms, P < 0.001 and IP: 44 +/- 6.2 vs RP: 41 +/- 7.6 omega with 10.8 ms, P < 0.001) and the leading edge of pulse 2 (IP: 37 +/- 5 vs RP: 35 +/- 4.2 omega with 14.3 ms, P = 0.05 and IP: 37.5 +/- 3.7 vs RP: 36 +/- 5 omega with 10.8 ms, P = 0.02). In conclusion, in this animal model, internal defibrillation using the distal coil as anode results in higher defibrillation efficacy than using the distal coil as cathode. Calculated impedances show different courses throughout the shock pulses suggesting differences in current flow during the shock.     

Direct in vivo measurement of flow-dependent nitric oxide production in mesenteric resistance arteries

PURPOSE: To determine whether the concentration of nitric oxide (NO) at the arterial wall is increased subsequent to the abrupt elevation of blood flow in resistance arteries. METHODS: Eight dogs underwent laparotomy with anesthesia, and their small bowels were exteriorized. NO concentration was measured with NO-specific electrodes (200-micro-tip diameter) at the outer wall of the mesenteric arteries. Flow was increased by occlusion of the adjacent mesenteric arteries. In four animals, flow and NO concentration were measured after the administration of Nomega-nitro-L-arginine-methyl ester (L-NAME) to inhibit NO production. RESULTS: As arterial flow was increased from a baseline of 5.4 +/- 1.3 ml/min to 10.9 +/- 1.8 ml/min (p = 0.001), NO electrode current was elevated in every animal. With repetition of the flow stimulus, the response tended to be attenuated. In the first experimental trial, NO electrode current measured at the arterial wall increased from 2.86 +/- 0.56 to 3.00 +/- 0.60 nA (p = 0.02). L-NAME (10 mg/kg intravenous) effectively inhibited NO synthase as indicated by the elevation of mean arterial pressure (11 +/- 1.7 mm Hg; p = 0.04). After administration of L-NAME, NO electrode current measured at the outer arterial wall fell 0.23 +/- 0.05 nA (p = 0.02). CONCLUSIONS: The data indicate that a doubling of blood flow in the canine mesenteric resistance arteries is associated with an increase in NO concentration of at least 100 nm at the outer arterial wall. This association is probably a substantial underestimation of the actual concentration because of the geometry of the electrode tip. To our knowledge, ours is the first report of direct in vivo measurement of flow-dependent NO release in resistance arteries.     

Lectin histochemistry of astrocytic tumors and in vitro characterization of lectin-induced modifications on the proliferation of the SW1088, U373 and U87 human astrocytic cell lines

The availability of a simple-to-use, automatic measurement system for noninvasive flow estimation is imperative, given the clinical demand for an acceptable noninvasive procedure rather than the standard invasive procedure of thermodilution. A method for calculating cardiac output from noninvasively derived pressure pulses has been developed, and the results of a preliminary evaluation study on post-cardiac surgery patients for whom invasive flow measures were readily available for comparison are provided in this report. The proposed method relies on fast Fourier transform (FFT) analysis of pulses measured externally at the carotid and femoral pressure points. A transfer function of the aorta is computed from digitally filtered pulse measurements, and a tapered model of the aorta is parametrically adapted using a simplex optimization algorithm so that its transfer function matches that derived experimentally. An aortic input impedance term is obtained from the optimized model and utilized along with the carotid pulse (analogous to input voltage) to compute aortic flow. In addition to its automation, attractive features of this method include the requirement for relatively few pulses for analysis as well as considerable resistance to noise artifact. For 59 data records collected from 54 post-cardiac surgery patients, the average flow measurements computed over several pulses compare well with the standard, invasive method of thermodilution. Preliminary results also indicate a strong potential for tracking changes in cardiac output over time, and invite further use of the method in monitoring hemodynamically unstable patients.     

Left ventricular function in children with the Marfan syndrome

Aortic dilatation and heart valve lesions are common in the Marfan syndrome but whether primary alterations occur in left ventricular (LV) function has not been studied hitherto. LV size, mass and systolic as well as diastolic function were studied by M-mode and Doppler echocardiography and cine magnetic resonance imaging in 22 Marfan children aged 3.0-15.4 years and in 22 age-matched healthy children. No child had significant valve disease. Heart rate and systolic blood pressure were comparable in the groups but diastolic blood pressure was higher in the controls (67 +/- 7 mmHg vs 62 +/- 8 mmHg, P = 0.030). No statistically significant differences were found in LV size, mass or systolic function. The Marfan children had slower LV peak diameter lengthening rates (106 +/- 27 mm.s-1 vs 132 +/- 29 mm.s-1, P = 0.004), prolonged relaxation times (155 +/- 22 ms vs 140 +/- 19 ms, P = 0.023), slower deceleration of the early transmitral velocity (580 +/- 144 cm.s-1 vs 720 +/- 160 cm.s-2, P = 0.006), and smaller early-to-late peak velocity ratios (1.99 +/- 0.40 vs 2.29 +/- 0.46, P = 0.031). These data indicate that LV early diastolic function (relaxation) is impaired in the Marfan syndrome. Weakened elastic recoil due to the underlying connective tissue abnormality may best explain this novel observation.     

Dependence of aortic pulse wave assessments on behavioural state in normal term fetus

To investigate any influence of behavioural states on the pulse waves in the descending aorta, 21 human fetuses were studied in utero in uncomplicated gestation at the age of 36-41 weeks. The fetal behavioural states were identified using two real-time scanners and one cardiotocograph. The aortic waveform data and pulse wave velocity (PWV) were recorded by means of two double phase-locking echo-trackers. The PWV of the fetal aorta was significantly lower in fetal behavioural state (FBS) 2F than in FBS 1F, when the fetus was apnoeic, and was also reduced in both states during fetal breathing. The calculated pulse pressure showed the same trend as the PWV. The fetal aortic end diastolic diameter and the pulse amplitude did not alter, when the two states changed. Our data suggest that the central haemodynamics in term fetuses are independently influenced by their behavioural state as well as by fetal breathing. The study of pulse waves in the fetal aorta should preferably be performed during apnoea in state 1F, when neither gross body movements nor breathing movements disturb the recording.