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Purpose Fulminant myocarditis is uncommon, but life-threatening, and some patients need mechanical circulatory support. This study was performed to evaluate how different types of mechanical circulatory support-biventricular assist device (BiVAD) or left ventricular assist device (LVAD) placement-affect intraoperative hemodynamic status. Methods From January 2013 to September 2016, the patients who underwent BiVAD or LVAD placement for fulminant myocarditis were analyzed. The mean arterial pressure (MAP), mean pulmonary arterial pressure, central venous pressure (CVP), vasoactive score, and inotropic score were recorded at five time points: after the induction of anesthesia; at weaning, 30 min after weaning, and 60 min after weaning from cardiopulmonary bypass (CPB); and at the end of surgery. The vasoactive and inotropic scores were calculated as follows: vasoactive score = norepinephrine ([micro]g/kg/min) x 100 + milrinone ([micro]g/kg/min) x 10 + olprinone ([micro]g/kg/min) x 25: inotropic score = dopamine ([micro]g/kg/min) x 1 + dobutamine ([micro]g/kg/min) x 1 + epinephrine ([micro]g/kg/min) x 100. Results We enrolled 16 patients of fulminant myocarditis. Ten of them underwent BiVAD placement, and the other underwent LVAD placement. After weaning from CPB, the BiVAD group had a significantly lower MAP but no difference in CVP. The vasoactive score was significantly higher in the BiVAD group at weaning of CPB (p = 0.015), 30 min after weaning (p = 0.004), 60 min after weaning (p = 0.005), and at the end of surgery (p < 0.016). Conclusion Patients with BiVAD placement required more vasoactive support to maintain optimal hemodynamic status compared with those with LVAD placement. This result indicates that BiVAD placement was more associated with vasoplegic syndrome., Author(s): Mariko Ezaka [sup.1] , Takuma Maeda [sup.2] [sup.3] , Yoshihiko Ohnishi [sup.2] Author Affiliations: (Aff1) 0000 0004 0436 8259, grid.459808.8, Department of Anesthesiology, New Tokyo Hospital, , 1271 Wanagaya, [...]

Byline: Pralay. Ghosh, Afzal. Azim, Sai. Saran, Arvind. Baronia, Banani. Poddar, Ratender. Singh, Mohan. Gurjar, Prabhaker. Mishra Introduction: Lung-protective ventilation strategy and prone positioning are the strategies practiced to manage [...]

Byline: Girish. Rajpal, Vikas. Naik Arterial dissection occurs when intraluminal blood penetrates into layers of the vessel wall. Cranio-cervical dissection accounts for 15-20% of causes of stroke in the young [...]

The detailed geometry of atherosclerosis-prone vascular segments may influence their susceptibility by mediating local hemodynamics. An appreciation of the role of specific geometric variables is complicated by the considerable correlation among the many parameters that can be used to describe arterial shape and size. Factor analysis is a useful tool for identifying the essential features of such an inter-related data set, as well as for predicting hemodynamic risk in terms of these features and for interpreting the role of specific geometric variables. Here, factor analysis is applied to a set of 14 geometric variables obtained from magnetic resonance images of 50 human carotid bifurcations. Two factors alone were capable of predicting 12 hemodynamic metrics related to shear and near-wall residence time with adjusted squared Pearson's correlation coefficient as high as 0.54 and P-values less than 0.0001. One factor measures cross-sectional expansion at the bifurcation; the other measures the colinearity of the common and internal carotid artery axes at the bifurcation. The factors explain the apparent lack of an effect of branch angle on hemodynamic risk. The relative risk among the 50 bifurcations, based on time-average wall shear stress, could be predicted with a sensitivity and specificity as high as 0.84. The predictability of the hemodynamic metrics and relative risk is only modestly sensitive to assumptions about flow rates and flow partitions in the bifurcation. [DOI: 10.1115/1.4002538]

High-resolution numerical simulations are carried out to systematically investigate the effect of the incoming flow waveform on the hemodynamics and wall shear stress patterns of an anatomic sidewall intracranial aneurysm model. Various wave forms are constructed by appropriately scaling a typical human waveform such that the waveform maximum and time-averaged Reynolds numbers, the Womersley number ([alpha]), and the pulsatility index (PI) are systematically varied within the human physiologic range. We show that the waveform PI is the key parameter that governs the vortex dynamics across the aneurysm neck and the flow patterns within the dome. At low PI, the flow in the dome is similar to a driven cavity flow and is characterized by a quasi-stationary shear layer that delineates the parent artery flow from the recirculating flow within the dome. At high PI, on the other hand, the flow is dominated by vortex ring formation, transport across the neck, and impingement and breakdown at the distal wall of the aneurysm dome. We further show that the spatial and temporal characteristics of the wall shear stress field on the aneurysm dome are strongly correlated with the vortex dynamics across the neck. We finally argue that the ratio between the characteristic time scale of transport by the mean flow across the neck and the time scale of vortex ring formation can be used to predict for a given sidewall aneurysm model the critical value of the waveform PI for which the hemodynamics will transition from the cavity mode to the vortex ring mode. [DOI: 10.1115/1.4002702] Keywords: aneurysm, hemodynamics, vortex formation, computational fluid dynamics, pulsatile flow

The objective of this study was to (a) evaluate the impact of the leg press, at variable percentages of 1 repetition maximum (1RM), on heart rate variability (HRV) and blood lactate and (b) determine the relationship between HRV with blood lactate in a healthy elderly cohort. Ten healthy men (64 [+ or -] 4 years) participated in a progressive leg-press protocol to maximal exertion. Initially, 1RM for the leg press was determined for all subjects. The protocol then began at 10% of 1 RM, with subsequent increases of 10% until 30% of 1RM, followed by incremental adjustments of 5% until exhaustion. The measurement of instantaneous R-R interval variability from Poincare plots (SD1 and SD2) and time domain indexes (RMSSD and RMSM), blood pressure, and blood lactate were obtained at rest and all leg-press loads. Significant alterations of HRV and blood lactate were observed from 30% of 1RM leg press (p < 0.05). Additionally, significant correlations were found between the lactate threshold (LT) and the RMSSD threshold (r = 0.78; p < 0.01), and between the LT and SD1 threshold (r = 0.81, p < 0.01). We conclude that metabolic and cardiovascular alterations are apparent during relatively low resistance exercise (RE) loads in apparently healthy subjects. In addition, HRV indexes were associated with blood-lactate levels during RE. The practical applications is the possibility of using HRV as a noninvasive measure obtained at a relatively low cost may be used to identify neural and metabolic alterations during RE in older subjects. Key Words autonomic nervous system, anaerobic threshold, strength exercise, aging

Angiogenesis: grow with the flow During embryogenesis, blood vessels are remodelled in response to blood flow. Nicoli et al. describe a genetic pathway that explains how this mechanosensory stimulus is integrated with early developmental signals to remodel aortic arch vessels in zebrafish. The flow-induced transcription factor klf2a is required for the induction of an endothelial cell-specific microRNA, miR-126, which promotes VEGF signalling and angiogenesis through repressing Spred1, an inhibitor of VEGF signalling. This demonstrates how blood flow modulates endothelial cell-signalling pathways and implicates a microRNA as a central integration point during this process. During embryonic development, blood vessels remodel in response to blood flow. Here, a genetic pathway is described through which this mechanosensory stimulus is integrated with early developmental signals to remodel vessels of the aortic arch in zebrafish. It is found that the flow-induced transcription factor klf2a is required to induce the expression of an endothelial-specific microRNA, activating signalling through the growth factor Vegf. Within the circulatory system, blood flow regulates vascular remodelling.sup.1, stimulates blood stem cell formation.sup.2, and has a role in the pathology of vascular disease.sup.3. During vertebrate embryogenesis, vascular patterning is initially guided by conserved genetic pathways that act before circulation.sup.4. Subsequently, endothelial cells must incorporate the mechanosensory stimulus of blood flow with these early signals to shape the embryonic vascular system.sup.4. However, few details are known about how these signals are integrated during development. To investigate this process, we focused on the aortic arch (AA) blood vessels, which are known to remodel in response to blood flow.sup.1. By using two-photon imaging of live zebrafish embryos, we observe that flow is essential for angiogenesis during AA development. We further find that angiogenic sprouting of AA vessels requires a flow-induced genetic pathway in which the mechano-sensitive zinc finger transcription factor klf2a.sup.5,6,7 induces expression of an endothelial-specific microRNA, mir-126, to activate Vegf signalling. Taken together, our work describes a novel genetic mechanism in which a microRNA facilitates integration of a physiological stimulus with growth factor signalling in endothelial cells to guide angiogenesis., Author(s): Stefania Nicoli [sup.1] , Clive Standley [sup.2] , Paul Walker [sup.3] , Adam Hurlstone [sup.3] , Kevin E. Fogarty [sup.2] , Nathan D. Lawson [sup.1] Author Affiliations: (1) Program [...]

Computational fluid dynamics (CFD) modeling of blood flow from image-based patient specific models can provide useful physiologic information for guiding clinical decision making. A novel method for the generation of image-based, 3-D, multiscale vascular surface models for CFD is presented. The method generates multiscale surfaces based on either a linear triangulated or a globally smooth nonuniform rational B-spline (NURB) representation. A robust local curvature analysis is combined with a novel global feature analysis to set mesh element size. The method is particularly useful for CFD modeling of complex vascular geometries that have a wide range of vasculature size scales, in conditions where 1) initial surface mesh density is an important consideration for balancing surface accuracy with manageable size volumetric meshes, 2) adaptive mesh refinement based on flow features makes an underlying explicit smooth surface representation desirable, and 3) semi-automated detection and trimming of a large number of inlet and outlet vessels expedites model construction. Index Terms--Hemodynamics, multiscale modeling, NURB surface, surface fitting, surface mesh generation, vascular modeling.

Byline: Rudranil. Nandi, Shekhar. Basu, Susanta. Sarkar, Rakesh. Garg Background and Aims: Haemodynamic responses to laryngoscopy and endotracheal intubation and their hazards are well documented. The purpose of the study [...]

Byline: Shahed. Omar, Ahmad. Ali, Yahya. Atiya, Rudo. Mathivha, Joel. Dulhunty Context: Severe sepsis or septic shock. Aims: The aim of this study is to examine the effect of a [...]

Functional magnetic resonance imaging (fMRI) is an important technique for neuroimaging. The conventional system identification methods used in fMRI data analysis assume a linear time-invariant system with the impulse response described by the hemodynamic responses (HDR). However, the measured blood oxygenation level-dependent (BOLD) signals to a particular processing task (for example, rapid event-related fMRI design) show nonlinear properties and vary with different brain regions and subjects. In this paper, radial basis function (RBF) neural network (a powerful technique for modelling nonlinearities) is proposed to model the dynamics underlying the fMRI data. The equivalence of the proposed method to the existing Volterra series method has been demonstrated. It is shown that the first- and second-order Volterra kernels could be deduced from the parameters of the RBF neural network. Studies on both simulated (using Balloon model) as well as real event-related fMRI data show that the proposed method can accurately estimate the HDR of the brain and capture the variations of the HDRs as a function of the brain regions and subjects. Index Terms--Event-related design, functional magnetic resonance imaging (fMRI), hemodynamic response (HDR), neural network, radial basis functions (RBF), Volterra kernels.

The left atrium (LA) acts as a booster pump during late diastole, generating the Doppler transmittal A wave and contributing incrementally to left ventricular (LV) filling. However, after volume loading and in certain disease states, LA contraction fills the LV less effectively, and retrograde flow (i.e., the Doppler Ar wave) into the pulmonary veins increases. The purpose of this study was to provide an energetic analysis of LA contraction to clarify the mechanisms responsible for changes in forward and backward flow. Wave intensity analysis was performed at the mitral valve and a pulmonary vein orifice. As operative LV stiffness increased with progressive volume loading, the reflection coefficient (i.e., energy of reflected wave/ energy of incident wave) also increased. This reflected wave decelerated the forward movement of blood through the mitral valve and was transmitted through the LA, accelerating retrograde blood flow in the pulmonary veins. Although total LA work increased with volume loading, the forward hydraulic work decreased and backward hydraulic work increased. Thus wave reflection due to increased LV stiffness accounts for the decrease in the A wave and the increase in the Ar wave measured by Doppler. hemodynamics; left atrium; A wave; Ar wave; Doppler echocardiography

Autoregulation of rena; blood flow (RBF) is caused by the myogenic response (MR), tubuloglomerular feedback (TGF), and a third regulatory mechanism that is independent of TGF but slower than MR. The underlying cause of the third regulatory mechanism remains unclear; possibilities include ATP, ANG II, or a slow component of MR. Other mechanisms, which, however, exert their action through modulation of MR and TGF are pressure-dependent change of proximal tubular reabsorption, resetting of RBF and TGF, as well as modulating influences of ANG II and nitric oxide (NO). MR requires < 10 s for completion in the kidney and normally follows first-order kinetics without rate-sensitive components. TGF takes 30-60 s and shows spontaneous oscillations at 0.025-0.033 Hz. The third regulatory component requires 30-60 s; changes in proximal tubular reabsorption develop over 5 min and more slowly for up to 30 min, while RBF and TGF resetting stretch out over 20-60 min. Due to these kinetic differences, the relative contribution of the autoregulatory mechanisms determines the amount and spectrum of pressure fluctuations reaching glomerular and postglomerular capillaries and thereby potentially impinge on filtration, reabsorption, medullary perfusion, and hypertensive renal damage. Under resting conditions, MR contributes ~50% to overall RBF autoregulation, TGF 35-50%, and the third mechanism < 15%. NO attenuates the strength, speed, and contribution of MR, whereas ANG II does not modify the balance of the autoregulatory mechanisms. tubuloglomerular feedback; myogenic response; renal hemodynamics; time factors

The present study examined the hypothesis that hypertonic saline dextran (HSD), given after an initial instill, attenuates exaggerated inflammation that occurs with a second insult. Adult rats (n = 15 per group) were divided into groups 1 (sham burn), 2 [40% total body surface area burn + 4 ml/kg isotonic saline (IS) + 4 ml * [kg.sup.-1] * % [burn.sup.-1] lactated Ringer solution (LR)], and 3 (burn + 4 ml/kg HSD + LR), all studied 24 h after burns. Groups 4 (sham burn), 5 (burn + IS + LR), and 6 (burns + HSD + LR) received intratracheal (IT) vehicle 7 days after burns; groups 7 (burn + IS + LR) and 8 (burn + HSD + LR) received IT Streptococcus pneumoniae (4 x [10.sup.6] colony-forming units) 7 days after burn. Groups 4-8 were studied 8 days after burn and 24 h after IT septic challenge. When compared with sham burn, contractile defects occurred 24 h after burn in IS-treated but not HSD-treated burns. Cardiac inflammatory responses (pg/ml TNF-[alpha]) were evident with IS (170 [+ or -] 10) but not HSD (45 [+ or -] 5) treatment vs. sham treatment (80 [+ or -] 15). Pneumonia-related sepsis 8 days after IS-treated burns (group 7) exacerbated TNF-[alpha] responses/contractile dysfunction vs. IS-treated burns in the absence of sepsis (P < 0.05). Sepsis that occurred after HSD-treated burns (group 8) had less myocyte TNF-[alpha] secretion/better contractile function than IS-treated burns given septic challenge (group 7, P < 0.05). We conclude that an initial burn injury exacerbates myocardial inflammation/dysfunction occurring with a second insult: giving HSD after the initial insult attenuates myocardial inflammation/dysfunction associated with a second hit. suggesting that HSD reduces postinjury risk for infectious complications. rat model; Langendorff perfusion; burn complicated by sepsis; cardiac myocytes, tumor necrosis factor-[alpha]; interleukin-1[beta]; interleukin-6

The rodent model of myocardial infarction (MI) is extensively used in heart failure studies. However, long-term follow-up of echocardiographic left ventricular (LV) function parameters such as the myocardial performance index (MPI) and its ratio with the fractional shortening (LVFS/MPI) has not been validated in conjunction with invasive indexes, such as those derived from the conductance catheter (CC). Sprague-Dawley rats with left anterior descending coronary artery ligation (MI group, n = 9) were compared with a sham-operated control group (n = 10) without MI. Transthoracic echocardiography (TTE) was performed every 2 wk over an 8-wk period, after which classic TTE parameters, especially MPI and LVFS/MPI, were compared with invasive indexes obtained by using a CC. Serial TTE data showed significant alterations in the majority of the noninvasive functional and structural parameters (classic and novel) studied in the presence of MI. Both MPI and LVFS/MPI significantly (P < 0.05 for all reported values) correlated with body weight (r = -0.58 and 0.76 for MPI and LVFS/MPI, respectively), preload recruitable stroke work (r = -0.61 and 0.63), LV end-diastolic pressure (LVEDP) (r = 0.82 and -0.80), end-diastolic volume (r = 0.61 and -0.58), and end-systolic volume (r = 0.46 and -0.48). Forward stepwise linear regression analysis revealed that, of all variables tested, LVEDP was the only independent determinant of MPI (r = 0.84) and LVFS/MPI (r = 0.83). We conclude that MPI and LVFS/MPI correlate strongly and better than the classic noninvasive TTE parameters with established, invasively assessed indexes of contractility, preload, and volumetry. These findings support the use of these two new noninvasive indexes for long-term analysis of the post-MI LV remodeling. echocardiography; heart failure; hemodynamics; ventricular function

A clinical method for monitoring cardiac output (CO) should be continuous, minimally invasive, and accurate. However, none of the conventional CO measurement methods possess all of these characteristics. On the other hand, peripheral arterial blood pressure (ABP) may be measured reliably and continuously with little or no invasiveness. We have developed a novel technique for continuously monitoring changes in CO by mathematical analysis of a peripheral ABP waveform. In contrast to the previous techniques, our technique analyzes the ABP waveform over time scales greater than a cardiac cycle in which the confounding effects of complex wave reflections are attenuated. The technique specifically analyzes 6-min intervals of ABP to estimate the pure exponential pressure decay that would eventually result if pulsatile activity abruptly ceased (i.e., after the high frequency wave reflections vanish). The technique then determines the time constant of this exponential decay, which equals the product of the total peripheral resistance and the nearly constant arterial compliance, and computes proportional CO via Ohm's law. To validate the technique, we performed six acute swine experiments in which peripheral ABP waveforms and aortic flow probe CO were simultaneously measured over a wide physiologic range. We report an overall CO error of 14.6%. Index Terms--Arterial blood pressure, arterial tree, cardiac output, distributed effects, hemodynamics, mathematical modeling, pulse contour analysis, system identification, wave reflections, Windkessel.

The 'hemodynamic inverse problem' is the determination of arterial system properties from pressures and flows measured at the entrance of an arterial system. Conventionally, investigators fit reduced arterial system models to data, and the resulting model parameters represent putative arterial properties. However, no unique solution to the inverse problem exists--an infinite number of arterial system topologies result in the same input impedance ([Z.sub.in]) and, therefore, the same pressure and flow. Nevertheless, there are exceptions to this theoretical limitation; total peripheral resistance ([R.sub.tot]), total arterial compliance ([C.sub.tot]), and characteristic impedance ([Z.sub.o]) can be uniquely determined from input pressure and flow. [Z.sub.in] is determined completely by [C.sub.tot] and [R.sub.tot] at low frequencies, [Z.sub.o] at high frequencies, and arterial topology and reflection effects at intermediate frequencies. We present a novel method to determine the relative contribution of [Z.sub.o], [C.sub.tot], [R.sub.tot] and arterial topology/reflection to [Z.sub.in] without assuming a particular reduced model. This method is tested with a large-scale distributed model of the arterial system, and is applied to illustrative cases of measured pressure and flow. This work, thus, lays the theoretical foundation for determining the arterial properties responsible for increased pulse pressure with age and various arterial system pathologies. Index Terms--Apparent arterial compliance, hemodynamics, mathematical modeling, pulse wave reflection.

Coronary artery disease (CAD) is characterized by the progression of atherosclerosis, a complex pathological process involving the initiation, deposition, development, and breakdown of the plaque. The blood flow mechanics in arteries play a critical role in the targeted locations and progression of atherosclerotic plaque. In coronary arteries with motion during the cardiac contraction and relaxation, the hemodynamic flow field is substantially different from the other arterial sites with predilection of atherosclerosis. In this study, our efforts focused on the effects of arterial motion and local geometry on the hemodynamics of a left arterior descending (LAD) coronary artery before and after clinical intervention to treat the disease. Three-dimensional (3D) arterial segments were reconstructed at 10 phases of the cardiac cycle for both pre- and postintervention based on the fusion of intravascular ultrasound (IVUS) and biplane angiographic images. An arbitrary Lagrangian-Eulerian formulation was used for the computational fluid dynamic analysis. The measured arterial translation was observed to be larger during systole after intervention and more out-of-plane motion was observed before intervention, indicating substantial alterations in the cardiac contraction after angioplasty. The time averaged axial wall shear stress ranged from -0.2 to 9.5 Pa before intervention compared to -0.02 to 3.53 Pa after intervention. Substantial oscillatory shear stress was present in the preintervention flow dynamics compared to that in the postintervention case.

The study of wave propagation at different points in the arterial circulation may provide useful information regarding ventriculoarterial interactions. We describe a number of hemodynamic parameters in the carotid, brachial, and radial arteries of normal subjects by using noninvasive techniques and wave-intensity analysis (WIA). Twenty-one normal adult subjects (14 men and 7 women, mean age 44 [+ or -] 6 yr) underwent applanation tonometry and pulsed-wave Doppler studies of the right common carotid, brachial, and radial arteries. After ensemble averaging of the pressure and flow-velocity data, local hydraulic work was determined and a pressure-flow velocity loop was used to determine local wave speed. WIA was then applied to determine the magnitude, timings, and energies of individual waves. At all sites, forward-traveling (S) and backward-traveling (R) compression waves were observed in early systole. In mid- and late systole, forward-traveling expansion waves (X and D) were also seen. Wave speed was significantly higher in the brachial (6.97 [+ or -] 0.58 m/s) and radial (6.78 [+ or -] 0.62 m/s) arteries compared with the carotid artery (5.40 [+ or -] 0.34 m/s; P < 0.05). S-wave energy was greatest in the brachial artery (993.5 [+ or -] 87.8 mJ/[m.sup.2]), but R-wave energy was greatest in the radial artery (176.9 [+ or -] 19.9 mJ/[m.sup.2]). X-wave energy was significantly higher in the brachial and radial arteries (176.4 [+ or -] 32.7 and 163.2 [+ or -] 30.5 mJ/[m.sup.2], respectively) compared with the carotid artery (41.0 [+ or -] 9.4 mJ/[m.sup.2]; P < 0.001). WIA illustrates important differences in wave patterns between peripheral arteries and may provide a method for understanding ventriculo-arterial interactions in the time domain. hemodynamics; wave transmission; ultrasound; tonometry

A functional microcirculation is vital to the survival of mammalian tissues. In vivo video microscopy is often used in animal models to assess microvascular function, providing real-time observation of blood flow in normal and diseased tissues. To extend the capabilities of in vivo video microscopy, we have developed a contrast-enhanced system with postprocessing video analysis tools that permit quantitative assessment of microvascular geometry and function in vital organs and tissues. FITC-labeled dextran (250 kDa) was injected intravenously into anesthetized mice to provide intravascular fluorescence contrast with darker red blood cell (RBC) motion. Digitized video images of microcirculation in a variety of internal organs (e.g., lung, liver, ovary, and kidney) were processed using computer-based motion correction to remove background respiratory and cardiac movement. Stabilized videos were analyzed to generate a series of functional images revealing microhemodynamic parameters, such as plasma perfusion, RBC perfusion, and RBC supply rate. Fluorescence contrast revealed characteristic microvascular arrangements within different organs, and images generated from video sequences of liver metastases showed a marked reduction in the proportion of tumor vessels that were functional. Analysis of processed video sequences showed large reductions in vessel volume, length, and branch-point density, with a near doubling in vessel segment length. This study demonstrates that postprocessing of fluorescence contrast video sequences of the microcirculation can provide quantitative images useful for studies in a wide range of model systems. microhemodynamics; fluorescence microscopy; video analysis

Byline: Maria-del-Mar Fernandez (1,1), Enrique Piacentini (1), Lluis Blanch (1), Rafael Fernandez (1) Keywords: Endotracheal suctioning; Mechanical ventilation; Acute respiratory failure; Health technology assessment Abstract: Objective To compare changes in lung volume, oxygenation, airway pressure, and hemodynamic effects induced by suctioning with three systems in critically ill patients with mild-to-moderate lung disease, and also to evaluate the effects of hyperoxygenation applied prior to the maneuver as suggested by some guidelines. Design Prospective crossover study. Setting General intensive care department of a university-affiliated hospital. Patients Ten mechanically ventilated patients with mild-to-moderate acute respiratory failure. Interventions Patients were ventilated in volume control mode with a mean tidal volume of 490+-88 ml, PEEP 7+-4 cmH2O and FiO.sub.2 0.36+-0.05. Suctioning was performed sequentially with a quasi-closed system, with an open system 10 min later, and finally with a closed system. Thereafter, pure oxygen was applied for 2 min and the whole suctioning sequence was repeated in reverse order. Measurements and main results Patients' mean PaO.sub.2/FiO.sub.2 ratio was 273+-28 mmHg. The reductions in lung volume during suctioning were similar with the quasi-closed (386+-124 ml) and closed system (497+-338 ml), but significantly higher with the open system (1281+-656 ml, P=0.022). We found no significant hemodynamic adverse effects, and no significant SpO.sub.2 reductions with all the studied suctioning techniques. Pre-oxygenation with pure oxygen did not induce additive effects in lung volume changes. With and without pre-oxygenation, lung volume returned to baseline in every patient within 10 min. Conclusions Suctioning with closed and quasi-closed systems reduces the substantial losses in lung volume observed with the open system. Nevertheless, in patients without severe lung disease these changes were transient and rapidly reversible. Author Affiliation: (1) Critical Care Center, Hospital de Sabadell, Parc Tauli s/n, 08208 , Sabadell, Spain Article History: Registration Date: 03/09/2004 Received Date: 04/12/2003 Accepted Date: 03/09/2004 Online Date: 12/10/2004 Article note: Financial support: 'Red GIRA' Network for Research in Respiratory Failure. Presented in part at the 14th Annual Congress ESICM. Geneva 30 Sept--3 Oct 2001.

Byline: H. Kato (), T. Katori (), Y. Nakamura (), H. Kawarasaki () Abstract: We examined the effect of continuous intravenous infusion of epoprostenol (35 ng/kg/min) on severe portopulmonary hypertension caused by biliary atresia. Pulmonary hemodynamics improved and brain natriuretic peptide and human atrial natriureic peptide decreased to normal values during epoprostenol therapy. However, the improvement in pulmonary hemodynamics was not sufficient to permit liver transplantation. Our patient was obliged to stop epoprostenol therapy because of financial problems and epoprostenol was tapered off safely over 6 weeks. Author Affiliation: () Department of Pediatrics, University of Tokyo Hospital, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan 113-8655, JP () Department of Pediatric Surgery, Jichi Medical School, 3311-1, Yakushiji, Minamikawachi-machi, Kawachi-gun, Tochigi, Japan 329-0431, JP

Pressure-based fractional flow reserve (FFR) is used clinically to evaluate the functional severity of a coronary stenosis, by predicting relative maximal coronary flow ([Q.sub.s]/[Q.sub.n]). It is considered to be independent of hemodynamic conditions, which seems unlikely because stenosis resistance is flow dependent. Using a resistive model of an epicardial stenosis (0-80% diameter reduction) in series with the coronary microcirculation at maximal vasodilation, we evaluated FFR for changes in coronary microvascular resistance ([R.sub.cor] = 0.2-0.6 mmHg*[ml.sup.-1]*min), aortic pressure ([P.sub.a] = 70-130 mmHg), and coronary outflow pressure ([P.sub.b] = 0-15 mmHg). For a given stenosis, FFR increased with decreasing [P.sub.a] or increasing [R.sub.cor]. The sensitivity of FFR to these hemodynamic changes was highest for stenoses of intermediate severity. For [P.sub.b] > 0, FFR progressively exceeded [Q.sub.s/[Q.sub.n] with increasing stenosis severity unless [P.sub.b] was included in the calculation of FFR. Although the [P.sub.b]-corrected FFR equaled [Q.sub.s]/[Q.sub.n] for a given stenosis, both parameters remained equally dependent on hemodynamic conditions, through their direct relationship to both stenosis and coronary resistance. coronary artery stenosis; coronary circulation; coronary stenosis evaluation; coronary flow reserve

Renal function was studied in mice of different ages. In metabolic cage experiments, the renal electrolyte excretion was similar in young (n = 8; 5-to 7-wk-old) and adult (n = 6; 20- to 22-wk-old) CD-1 (ICR) BR mice, whereas spontaneous drinking volume and urinary flow rate were significantly higher in the adult compared with the young mice. Subsequently, the renal functional reserve was investigated by amino acid (AA) infusion (10%) in anesthetized young (n = 8) and adult (n = 6) mice. Because the body weight of adult mice was significantly higher than that of young animals, one group of adult mice (n = 8) received 12.5% AA to ensure that the dose of AA related to body weight was similar in both groups. Young animals constantly infused with Ringer solution served as time controls (n = 8). Glomerular filtration rate (GFR) at baseline was similar in each group. Because of AA, GFR significantly increased in young mice but not in both groups of adult animals, whereas in time controls GFR remained constant. Urinary flow rate and sodium excretion were elevated by AA in young and adult mice. We conclude that in CD-1 mice the first signs of age-related changes in kidney function concern alterations in renal hemodynamics, whereas renal tubular function appears to be preserved. kidney; amino acids; glomerular filtration rate; physiological aging

We investigated the interplay of neural and hemodynamic mechanisms in postexercise hypotension (PEH) in hypertension. In 15 middle-aged patients with mild essential hypertension, we evaluated blood pressure (BP), cardiac output (CO), total peripheral resistance (TPR), forearm (FVR) and calf vascular resistance (CVR), and autonomic function [by spectral analysis of R-R interval and BP variabilities and spontaneous barorefiex sensitivity (BRS)] before and after maximal exercise. Systolic and diastolic BP, TPR, and CVR were significantly reduced from baseline 60-90 min after exercise. CO, FVR, and HR were unchanged. The low-frequency (LF) component of BP variability increased significantly after exercise, whereas the LF component of R-R interval variability was unchanged. The overall change in BRS was not significant after exercise vs. baseline, although a significant, albeit small, BRS increase occurred in response to hypotensive stimuli. These findings indicate that in hypertensive patients, PEH is mediated mainly by a peripheral vasodilation, which may involve metabolic factors linked to postexercise hyperemia in the active limbs. The vasodilator effect appears to override a concomitant, reflex sympathetic activation selectively directed to the vasculature, possibly aimed to counter excessive BP decreases. The cardiac component of arterial baroreflex is reset during PEH, although the baroreflex mechanisms controlling heart period appear to retain the potential for greater opposition to hypotensive stimuli. autonomic nervous system; baroreflex; heart rate variability; hemodynamics

Influence of estrogen on aortic stiffness and endothelial function in female rats. Am J Physiol Heart Circ Physiol 282: H491-H498, 2002; 10.1152/ajpheart.00589.2001.--Mechanisms underlying cardioprotective properties of estrogens are not fully understood. We evaluated effects of ovariectomy and estrogen replacement on arterial distensibility and endothelial function in rats. Sprague-Dawley rats were sham operated (Sham) or ovariectomized and treated with 17[beta]-estradiol (OVX-[E.sub.2]) or vehicle (OVX) for 3 wk. Anesthetized rats were instrumented for measurement of central and peripheral arterial blood pressures and carotid and hindquarters blood flows. Arterial distensibility was evaluated in anesthetized rats on the basis of changes in thoracoabdominal pressure pulse wave velocity (PWV). PWV was calculated as the distance between the two central and peripheral cannula tips divided by transit time. Ovariectomy significantly reduced PWV (390 [+ or -] 19 and 472 [+ or -] 42 cm/s in OVX and Sham, respectively). Estrogen treatment completely normalized PWV (490 [+ or -] 37 cm/s). Estrogen-treated rats were associated with left ventricular hypertrophy and increased pulse pressure. Resting hemodynamic parameters were similar in all groups. Estrogen replacement significantly potentiated bradykinin vasodilatory responses in the hindlimb, but not in the carotid vascular bed. Hemodynamic responses to sodium nitroprusside and ANG II were similar in all groups. In conclusion, our results demonstrate for the first time that aortic stiffness determined by PWV is decreased in estrogen-deficient rats. Estrogen treatment increases aortic stiffness and potentiates endothelial vasodilator function in the hindquarters, but not in the carotid vascular bed, suggesting a regional heterogeneity in the modulatory influence of estrogen on vasomotor function. aortic elasticity; regional hemodynamics

Three clinical models of the clinical syndrome of heart failure, a cardiorenal, a hemodynamic, and a neurohormonal model, are discussed. Clinical research investigations indicate that therapeutic strategies based on the cardiorenal and cardiocirculatory models provide symptom relief, while therapeutic strategies from neurohormonal models prevent disease progression.

Schuijt, Martin P., Munesh Basdew, Richard van Veghel, Rene de Vries, Pramod R. Saxena, Regien G. Schoemaker, and A. H. Jan Danser. A[T.sub.2] receptor-mediated vasodilation in the heart: effect of myocardial infarction. Am J Physiol Heart Circ Physiol 281: H2590-H2596, 2001.--To investigate the functional consequences of postinfarct cardiac angiotensin (ANG) type 2 (A[T.sub.2]) receptor upregulation, rats underwent coronary artery ligation or sham operation and were infused with ANG II 3-4 wk later, when scar formation is complete. ANG II increased mean arterial pressure (MAP) more modestly in infarcted animals than in sham animals. The A[T.sub.1] receptor antagonist irbesartan, but not the A[T.sub.2] receptor antagonist PD123319, decreased MAP and antagonized the ANG II-mediated systemic hemodynamic effects. Myocardial (MVC) but not renal vascular conductance (RVC) was diminished in infarcted versus sham rats. ANG II did not affect MVC and reduced RVC in all rats. MVC was unaffected by irbesartan and PD123319 in all animals. However, with PD123319, ANG II reduced MVC in sham but not infarcted animals, and, with irbesartan, ANG II increased MVC in infarcted but not sham animals. Irbesartan increased RVC and antagonized the ANG II-mediated renal effects in all animals. RVC, at baseline or with ANG II, was not affected by PD123319 in infarcted and sham animals. In conclusion, coronary but not renal A[T.sub.2] receptor stimulation results in vasodilation, and this effect is enhanced in infarcted rats. angiotensin; heart failure; receptors; vasoconstriction/dilation Received 27 April 2001; accepted in final form 21 August 2001

Yu, Ming, Venkat Gopalakrishnan, Thomas W. Wilson, and J. Robert McNeill. Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension. Am J Physiol Heart Circ Physiol 281:H2511-H2517, 2001.--The contribution ofendothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension. angiotensin II; bosentan; blood pressure; cardiac output; total peripheral resistance; deoxycorticosterone acetate Received 25 April 2001; accepted in final form 17 August 2001

Byline: Ankur. Khandelwal, Rudrashish. Haldar, Arun. Srivastava, Prabhat. Singh The existence of neural connection between the limbic system (hypothalamus, hippocampus, amygdala, and other adjacent areas) and the autonomic nervous system [...]

Byline: A. Ricard-Hibon (1), M.-R. Losser (1), R. Kong (1), S. Beloucif (1), B. Teisseire (1), D. Payen (1) Keywords: Key words Endotoxin; Fluid loading; Doppler; Vascular reactivity; Vasoplegia; Norepinephrine Abstract: Objective: This study aimed to evaluate the impact of fluid loading on hemodynamics and vascular hypocontractility to norepinephrine (NE) in an endotoxic shock model. Design: Mean arterial pressure (MAP), aortic blood flow velocity (AoV, 20 MHz Doppler) and aortic conductance (AoC = AoV/MAP) were studied during 180 min (T0--T180) in 41 anesthetized and ventilated rabbits. Interventions: Shock was induced by a 600 ug/kg bolus injection of endotoxin. Fluid loading (20 ml/kg colloids) was infused from T90 to T120. Dose-response curves to NE were performed at T0, T60 and T120 in endotoxic and non-endotoxic animals with or without fluid loading. Measurements and results: Endotoxin decreased pressure (-23 %, p &lt 0.05) and flow (-42 %, p &lt 0.05) corresponding to a decrease in conductance (-19 %, p &lt 0.05). Fluid loading did not improve hypotension but markedly increased systemic flow (+51 %, p &lt 0.01), corresponding to a hyperkinetic syndrome. Vascular reactivity to NE was impaired after endotoxin at T60 since the pressure response to NE was depressed (p &lt 0.01) and flow did not decrease. In non-fluid-loaded groups, the pressure response to NE recovered at T120, with no reduction in flow. In fluid-loaded endotoxic animals, however, the pressure response to NE was still impaired at T120 (p &lt 0.05), but with a decrease in flow. Conclusions: Fluid loading transformed the hypodynamic profile of endotoxic shock into a hyperdynamic state without improving blood pressure. Depressed vascular reactivity to NE was observed in both hyperdynamic and hypodynamic states, suggesting that a reduced vascular reactivity does not necessarily imply systemic vasodilation. Author Affiliation: (1) Laboratoire de Recherche, Departement d'Anesthesie-Reanimation, Centre Hospitalier Universitaire Lariboisiere, Assistance Publique -- Hopitaux de Paris, 2, rue Ambroise Pare, F-75475 Paris Cedex 10, France Tel.: +(33) -1-49-95-80-85 Fax: +(33) -1-49-95-85-43 email: dpayen.lariboisiere@invivo.edu, FR Article note: Received: 25 August 1997 Accepted: 9 June 1998

Byline: J. R. Masclans (1), R. Iglesia (1), B. Bermejo (1), M. Pico (1), R. Rodriguez-Roisin (2), M. Planas (1) Keywords: Key words Acute lung injury; Cardiopulmonary interactions; Eicosanoids; Lipid emulsions; Nutritional support; Prostaglandins Abstract: Objective: To investigate the gas exchange and pulmonary haemodynamic responses to two different intravenous fat emulsions in patients with acute respiratory distress syndrome (ARDS). Design: Prospective, randomized, double-blind, placebo-controlled study. Setting: Intensive care unit in a university-affiliated hospital. Patients: 21 patients with ARDS [mean age, 57 +- 3 (SEM) years Acute Physiology and Chronic Health Evaluation II, 20 +- 3 Murray's score, 2.85 +- 0.12] consecutively admitted. Interventions: Patients were assigned to three groups (n = 7 each): group A (LCT) received long-chain triglycerides (20 % LCT), group B (MCT/LCT), medium-chain triglycerides/long-chain triglycerides (20 % MCT/LCT: 50/50) and group C placebo (0.9 % sodium chloride, NaCl). The infusion was always given at the rate of 2 mg/kg min over a total period of 12 h, with a volume infusion of 500 ml in each group. Measurements: Data were collected before, immediately after and 12 h after infusion ceased. Pulmonary and systemic haemodynamic and gas exchange variables were measured at each time point. Serum triglyceride cholesterol, and non-esterified fatty acids levels were measured. Results: During LCT infusion, cardiac output, oxygen consumption and oxygen delivery increased (all p &lt 0.05), whereas pulmonary haemodynamics, arterial oxygen tension, mixed venous partial pressure of oxygen and venous admixture ratio remained essentially unaltered. No changes were observed following MCT/LCT infusion. Conclusions: The administration of LCT emulsion given at a slow rate did not alter arterial oxygenation because of the beneficial effect of a high cardiac output, hence offsetting the detrimental effect of increased O.sub.2 consumption. Author Affiliation: (1) Serveis de Medicina Intensiva, Medicina Preventiva, and Hematologia, Hospital General Universitari Vall d'Hebron, Universitat AutA2noma de Barcelona, Barcelona, Spain, ES (2) Servei de Pneumologia i Allergia RespiratA2ria, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Departament de Medicina, Hospital Clinic, Universitat de Barcelona, Barcelona, Spain, ES Article note: Received: 1 December 1997 Accepted: 3 June 1998

Sixteen women were studied to investigate the renal and systemic hemodynamic changes in the midluteal and midfollicular phases of the menstrual cycle. The decrease in mean arterial pressure, which was caused by the primary vasolidation during the midluteal phase of the menstrual cycle, was found to be similar to the increase in cardiac output experienced during early pregnancy. Both the peripheral vasodilation during the luteal phase of the menstrual cycle and the early part of pregnancy were related to the rise in renal plasma flow and renal vascular resistance.