Development Of Congestion Research Articles

Lipopolysaccharide Pretreatment Prevents Medullary Vascular Congestion following Renal Ischemia by Limiting Early Reperfusion of the Medullary Circulation.

Vascular congestion of the renal medulla-trapped red blood cells in the medullary microvasculature-is a hallmark finding at autopsy in patients with ischemic acute tubular necrosis. Despite this, the pathogenesis of vascular congestion is not well defined. In this study, to investigate the pathogenesis of vascular congestion and its role in promoting renal injury, we assessed renal vascular congestion and tubular injury after ischemia reperfusion in rats pretreated with low-dose LPS or saline (control). We used laser Doppler flowmetry to determine whether pretreatment with low-dose LPS prevented vascular congestion by altering renal hemodynamics during reperfusion. We found that vascular congestion originated during the ischemic period in the renal venous circulation. In control animals, the return of blood flow was followed by the development of congestion in the capillary plexus of the outer medulla and severe tubular injury early in reperfusion. Laser Doppler flowmetry indicated that blood flow returned rapidly to the medulla, several minutes before recovery of full cortical perfusion. In contrast, LPS pretreatment prevented both the formation of medullary congestion and its associated tubular injury. Laser Doppler flowmetry in LPS-pretreated rats suggested that limiting early reperfusion of the medulla facilitated this protective effect, because it allowed cortical perfusion to recover and clear congestion from the large cortical veins, which also drain the medulla. Blockage of the renal venous vessels and a mismatch in the timing of cortical and medullary reperfusion results in congestion of the outer medulla's capillary plexus and promotes early tubular injury after renal ischemia. These findings indicate that hemodynamics during reperfusion contribute to the renal medulla's susceptibility to ischemic injury.

Emergence of 4-D System Fundamental Diagram in Urban Air Mobility Traffic Flow

Urban air mobility (UAM) is an emerging mode that promises to provide relief to congested urban streets. UAM relies on airspace, however, which is an exhaustible resource considering minimum aircraft separation requirements. In light of these requirements and UAM vehicle attributes, a simulation is developed to explore UAM traffic flows and congestion development. A decentralized conflict resolution scheme is employed in the form of a non-linear program (NLP) to offer improved flexibility in detours relative to past aircraft simulations. An expansion of Edie’s definitions of density and flow rate are used in conjunction with average speed to explore the relationships between traffic flow characteristics. The results find that UAM traffic flows emulate those of other modes, by following the familiar traffic patterns of build-up and breakdown captured in the macroscopic fundamental diagram. These findings also suggest the presence of a capacity of airspace that should be carefully managed by operators to achieve optimal system performance. The relationships established in this study highlight issues that UAM operators and aviation planners may face and could be used to improve the vehicle traffic modeling of other UAM models.

Right ventricular function and its coupling with the pulmonary circulation in acute heart failure

Abstract Background The right ventricle (RV) is extremely sensitive to hemodynamic changes and increased impedance. In acute heart failure (AHF), the development of pulmonary venous congestion and the increase of left ventricular (LV) filling pressures favors pulmonary vascular adverse remodeling and ultimately RV dysfunction, leading to the onset of symptoms and to a further decay of cardiac dynamics. Purpose The aim of the study was to evaluate RV morphology and functional dynamics at admission and discharge in patients hospitalized for AHF, analyzing the role and the response to treatment of the RV and its coupling with pulmonary circulation (PC). Methods Eighty-one AHF patients (mean age 75.75±10.6 years, 59% males) were prospectively enrolled within 24–48 hours from admission to the emergency department (ED). In either the acute phase and at pre-discharge all patients underwent M-Mode, 2-Dimensional and Doppler transthoracic echocardiography (TTE), as well as lung ultrasonography (LUS), to detect an increase of extravascular lung water (EVLW) and development of pleural effusion. Laboratory tests were performed in the acute phase and at pre-discharge including the evaluation of NT-proBNP. Results At baseline we observed a high prevalence of RV dysfunction as documented by a reduced RV systolic longitudinal function [mean tricuspid annular plane systolic excursion (TAPSE) at admission of 16.47±3.86 mm with 50% of the patients exhibiting a TAPSE<16mm], a decreased DTI-derived tricuspid lateral annular systolic velocity (50% of the subjects showed a tricuspid s' wave<10 cm/s) and a reduced RV fractional area change (mean FAC at admission of 36.4±14.6%). Furthermore, an increased pulmonary arterial systolic pressure (PASP) and a severe impairment in terms of RV coupling to PC was detected at initial evaluation (mean PASP at admission: 38.8±10.8 mmHg; average TAPSE/PASP at admission: 0.45±0.17 mm/mmHg). At pre-discharge a significant increment of TAPSE (16.47±3.86 mm vs. 17.45±3.88; p=0.05) and a reduction of PASP (38.8±10.8 mmHg vs. 30.5±9.6mmHg, p<0.001) was observed. Furthermore, in the whole population we assisted to a significant improvement in terms of RV function and its coupling with PC as demonstrated by the significant increase of TAPSE/PASP ratio (TAPSE/PASP: 0.45±0.17 mm/mmHg vs 0.62±0.20 mm/mmHg; p<0.001). Patients significantly reduced from admission to discharge the number of B-lines and NT-proBNP (B-lines: 22.2±17.1 vs. 6.5±5 p<0.001; NT-proBNP: 8738±948 ng/l vs 4227±659 ng/l p<0.001) (Figure 1). Nonetheless, no significant changes of left atrial and left ventricular dimensions and function were noted. Conclusions In AHF, development of congestion and EVLW significantly impact on the right heart function. Decongestion therapy is effective for restoring acute reversal of RV dysfunction, but the question remains on how to impact on the biological properties of the RV. Funding Acknowledgement Type of funding source: None

Development of congestion in compressible flow with singular pressure

Development of congestion in compressible flow with singular pressure

Vascular Endothelial Growth Factor as a Prognostic Parameter in Subjects with "Plateau Red Face".

Ma, Lan, Ying Chen, Guoen Jin, Yingzhong Yang, Qin Ga, and Ri-Li Ge. Vascular endothelial growth factor as a prognostic parameter in subjects with "plateau red face." High Alt Med Biol 16:147-153, 2015.--Some individuals living at high altitude on the Qinghai Plateau in China develop a red face called " Plateau Red Face" (PRF). It is characterized by telangiectasia of the cheeks, which become a unique ruddy color. It is more common in young females than males, subjects who have polycythemia are more susceptible to PRF, and its pathogenesis is unknown. The aim of this study was to investigate associations between PRF and levels of vascular endothelial growth factor (VEGF). A total of 158 subjects (82 male and 76 female) residing at 4300 m and 140 subjects (73 male and 67 female) residing at 2260 m on the Qinghai Plateau, China, participated in this study. The determination and magnitude of PRF is evaluated by the dilation of veins on the face in the Qinghai chronic mountain sickness(CMS) score, established during the World Congress in 2004. Arterial O(2) saturation (Sao(2)), hemoglobin (Hb) concentration, pulmonary function tests, and serum concentration of VEGF (by ELISA) were measured in all participants. The occurrence of PRF was 32.9% (52/158) among subjects living at 4300 m and 15.7% (22/140) among those living at 2260 m. The levels of VEGF in PRF and non-PRF subjects were 399.9±115.6 pg/mL and 270.7±78.1 pg/mL, respectively (p<0.001) at 4300 m, and 244.4±109.0 pg/mL and 135.6±65.3 pg/mL, respectively (p<0.01) at 2260 m. However, comparing the levels of VEGF between the genders and ethnic groups at the same altitude, there were no significant differences between male and female both in Xining (p=0.12) and Maduo (p=0.18). There was also no significant difference between Tibetan and Han nationality in Xining (p=0.71), but In Maduo, the levels of VEGF in Han (351.70±122.62 pg/mL) were higher than that of Tibetan (300.20±102.89 pg/mL), and there was significant difference (p=0.01). Sao2 levels in PRF subjects (86.58±3.49) were lower than those of non-PRF subjects (88.04±3.68; p=0.018), while Hb was higher. Areas under receiver operator characteristic curve for diagnosis of PRF were 0.813, 0.679, and 0.373 for VEGF, Hb, and Sao(2), respectively. VEGF levels correlated positively with Hb levels both in Xining (r=0.367, p<0.001) and Maduo (r=0.319, p<0.001), and only negatively with Sao(2) levels in Maduo (r=-0.424, P<0.001) but not in Xining (r=0.125, p=0.141). Chronic hypoxemia may stimulate overproduction of angiogenic cytokine (VEGF), and this peptide may lead to formation of abnormal new vessels and development of congestion in mucosa and conjunctiva. Thus, VEGF may, at least in part, serve as a marker of the pathophysiologic trigger for PRF.

Effect of Monitoring System Structure on Short-term Prediction of Highway Travel Time

This article discusses how the structure of the measurement system affects the short-term forecasts of travel time based on it. The effects of section length and location of different measurement stations were investigated. The study used empirical data. The research was carried out on a 28-km long interurban two-lane highway section. The prediction models were made as feedforward multilayer perceptron neural networks. The main results showed that the division of long road sections into shorter sub-links in the travel time measurement system was important. Furthermore, it would be crucial to obtain information about traffic flow rates entering the section in order to time the start of congestion correctly. In conclusion, the structure of the monitoring system should be based on the analysis of a typical location and the development of congestion along the section.

Venular thrombosis is the key event in the pathogenesis of antibody-mediated cardiac rejection.

A review of the histopathologic features of serial biopsies and excised grafts of 117 experimental and clinical cardiac allografts and xenografts revealed a common sequence in the development of histopathologic changes in grafts showing antibody-mediated (hyperacute and acute vascular) rejection. Based on these observations, we propose the new concept that thrombosis of cardiac veins and venules is the initial key event in antibody-mediated rejection. This is followed by the development of congestion in the subtended venules and capillaries accompanied by interfascicular and, later, intermyocyte edema. Subsequently, focal or diffuse interstitial hemorrhage affecting the subendocardium, extending sometimes to involve the inner half of the ventricular myocardium, is observed. Antibody-mediated rejection therefore appears to be analogous to incomplete venous infarction of the heart. The observed histopathology (in which venular thrombosis plays a key role) favors a thrombogenic basis for the classical features of antibody-mediated rejection, namely edema, vascular thrombi and interstitial hemorrhage. A key role for venular thrombosis would explain the non-uniform distribution of the changes and may suggest new ways of preventing antibody-mediated xenograft rejection.

The Future For Intelligent Transport Systems: Keynote Opening Speech

Intelligent transport systems are essential if the objective of integrated transport systems in the UK is to be achieved. The historic reasons for the development of congestion in the UK are described. Before road pricing can be introduced, the importance of adequate research and appropriate decision making is stressed. This paper was presented at the Future of Intelligent Transport Systems Conference, Newcastle-upon-Tyne, November 5 1999, and for the covering abstract see ITRD E111197.

Furosemide induced hepatotoxicity.

Furosemide-induced (400mg/kg ip) hepatotoxicity progressing to centrilobular necrosis was studied by light and electron microscopy in Swiss white mice. Centrilobular glycogen depletion and cytoplasmic foaminess, usually accompanied by extensive vacuolation, were detectable by light microscopy 1 1/2 hr after furosemide. Centrilobular congestion and hydropic single cell necrosis developed after 3 hr. Electron microscopy revealed disaggregation of polyribosomes, vesiculation of endoplasmic reticulum, an endocytic origin for the vacuolation, and a definite sequence in the development of congestion. Vacuolation coincided with loss of microvilli and resulted in detachment of sinusoidal lining cells from hepatocytes. Small vacuoles apparently formed at the sinusoidal margin of hepatocytes by fusion of microvilli. Congestion and occlusion of sinusoidal lumens developed as a consequence of erythrocytes entering the enlarged Disse space, possibly through pores in the lining cells, and thence entering endocytic vacuoles. The vacuolation, loss of microvilli and terminal hydropic degeneration suggest an important role for the plasma membrane in the development of furosemide-induced hepatotoxicity. Comparisons with known membrane toxins support this concept.