Lung capillary changes in hepatic cirrhosis in rats

Schraufnagel, Dean E.; Malik, Renuka; Goel, Vinay; Ohara, Narihiro; Chang, Sunghoe

doi:10.1152/ajplung.1997.272.1.l139

Cited by 37 publications

(41 citation statements)

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“…The capillary width ranged from 7.82 ± 0.29 mm in CBDL animals to 6.95 ± 0.25 mm in PPVL animals, compared with 6.20±0.51 mm in sham mice, confirming the significant microvascular dilatation after CBDL (Po0.05 vs sham). These findings confirm earlier work from Fallon et al 26 and Schraufnagel et al 27 showing pulmonary vasodilation in CBDL, but not in PPVL and sham animals.…”

Section: Pulmonary Architecturesupporting

confidence: 92%

Vascular corrosion casting: analyzing wall shear stress in the portal vein and vascular abnormalities in portal hypertensive and cirrhotic rodents

Steenkiste

Trachet

Casteleyn

et al. 2010

Laboratory Investigation

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Vascular corrosion casting is an established method of anatomical preparation that has recently been revived and has proven to be an excellent tool for detailed three-dimensional (3D) morphological examination of normal and pathological microcirculation. In addition, the geometry provided by vascular casts can be further used to calculate wall shear stress (WSS) in a vascular bed using computational techniques. In the first part of this study, the microvascular morphological changes associated with portal hypertension (PHT) and cirrhosis in vascular casts are described. The second part of this study consists of a quantitative analysis of the WSS in the portal vein in casts of different animal models of PHT and cirrhosis using computational fluid dynamics (CFD). Microvascular changes in the splanchnic, hepatic and pulmonary territory of portal hypertensive and cirrhotic mice are described in detail with stereomicroscopic examination and scanning electron microscopy. To our knowledge, our results are the first to report the vascular changes in the common bile duct ligation cirrhotic model. Calculating WSS using CFD methods is a feasible technique in PHT and cirrhosis, enabling the differentiation between different animal models. First, a dimensional analysis was performed, followed by a CFD calculation describing the spatial and temporal WSS distributions in the portal vein. WSS was significantly different between sham/cirrhotic/pure PHT animals with the highest values in the latter. Up till now, no techniques have been developed to quantify WSS in the portal vein in laboratory animals. This study showed for the first time that vascular casting has an important role not only in the morphological evaluation of animal models of PHT and cirrhosis, but also in defining the biological response of the portal vein wall to hemodynamic changes. CFD in 3D geometries can be used to describe the spatial and temporal variations in WSS in the portal vein and to better understand the forces affecting mechanotransduction in the endothelium.

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Section: Pulmonary Architecturesupporting

confidence: 92%

Vascular corrosion casting: analyzing wall shear stress in the portal vein and vascular abnormalities in portal hypertensive and cirrhotic rodents

Steenkiste

Trachet

Casteleyn

et al. 2010

Laboratory Investigation

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“…However, the few detailed pathological studies were carried out before the standardisation of a universal definition of HPS and prior to the availability of imaging modalities used to detect IPVD. Nonetheless, dilatation of capillary vessels in alveolar regions [1,45] is a central prerequisite and the principal pathophysiological hallmark of arterial deoxygenation in both human and experimental HPS [46,47]. In addition, in animal models, intravascular accumulation of macrophages in the pulmonary microcirculation and increased numbers of pulmonary capillaries have been shown, suggesting a vasculogenic response [47,48].…”

Section: Pathologymentioning

confidence: 99%

Pulmonary-Hepatic vascular Disorders (PHD)

Rodríguez-Roisín

Krowka

Hervé

et al. 2004

European Respiratory Journal

706

600

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“…SCHRAUFNAGEL et al [71] recently measured pulmonary capillary size, density, and branching frequency in the rat after chronic bile duct ligation. All three parameters were increased, suggesting that the pathogenesis of HPS may result from both vascular dilatation and increased angiogenesis.…”

Section: Pulmonary Haemodynamics and Mechanisms Of Pulmonary Intravasmentioning

confidence: 99%

Pulmonary vascular disorders in portal hypertension

Hervé

Lebrec²,

Brénot³

et al. 1998

Eur Respir J

328

239

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aaThis review focuses on the pulmonary vascular complications of chronic liver failure and portal hypertension. The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome (HPS), which is characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance (PVR) is elevated. The exact pathophysiological mechanisms of these pulmonary vascular disorders are unknown. However, since HPS and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the factor that determines their development must be portal hypertension.A brief review of the haemodynamic changes observed in cirrhosis with portal hypertension is summarized, and the clinical and experimental evidence suggesting that the liver exerts a critical influence on the regulation of pulmonary vascular tone and angiogenesis is described. Portopulmonary hypertension is then discussed, focusing in turn on its clinical presentations, management and potential mechanisms, and referring to our findings in 39 patients with portopulmonary hypertension and 140 patients with primary pulmonary hypertension (PPH) admitted between 1986 and 1996 at Antoine Béclère Hospital. Finally, HPS will be examined, with a discussion of the mechanisms of hypoxaemia and intrapulmonary vascular dilatation, as well as its clinical presentation, diagnosis and treatment, with special attention to liver transplantation. Haemodynamics in cirrhosis with portal hypertensionAn understanding of pulmonary haemodynamics in liver disease with portal hypertension is important to a study of the pulmonary vascular disorders seen in this setting. A hyperdynamic circulatory state with high cardiac output, low systemic vascular resistance and low PVR is present in 30-50% of patients with cirrhosis and also in animal models of portal hypertension [1][2][3][4]. Compared with healthy subjects ( fig. 1) The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathoph...

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Lung capillary changes in hepatic cirrhosis in rats

Cited by 37 publications

References 0 publications

Vascular corrosion casting: analyzing wall shear stress in the portal vein and vascular abnormalities in portal hypertensive and cirrhotic rodents

Vascular corrosion casting: analyzing wall shear stress in the portal vein and vascular abnormalities in portal hypertensive and cirrhotic rodents

Pulmonary-Hepatic vascular Disorders (PHD)

Pulmonary vascular disorders in portal hypertension

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