Topic Highlight
Copyright ©2014 Baishideng Publishing Group Co.
World J Gastroenterol. Mar 14, 2014; 20(10): 2586-2594
Published online Mar 14, 2014. doi: 10.3748/wjg.v20.i10.2586
Figure 1
Figure 1 Possible mechanisms of hepatopulmonary syndrome. TNF-α: Tumor necrosis factor-alpha; ET-1: Endothelin-1; ETBR: Endothelin B receptors; NO: Nitric oxide; eNOS: Endothelial NO synthase; iNOS: inducible NO synthase; HO-1: Heme oxygenase-1; CO: Carbon monoxide; VEGF: Vascular endothelial growth factor.
Figure 2
Figure 2 Ventilation-perfusion mismatch; diffusion limitation of oxygen. The capillaries are known to dilate to 15-500 μm (n: 8-15 μm) in hepatopulmonary syndrome (HPS).
Figure 3
Figure 3 “Bubble” or contrast echocardiogram (apical four chamber view). A stream of microbubbles filling the left atrium following systemic venous injection is shown.
Figure 4
Figure 4 Right pulmonary artery angiogram (posteroanterior projection) showing a diffuse fine reticular pattern of multiple pulmonary telangiectasias consistent with type I hepatopulmonary syndrome.
Figure 5
Figure 5 Normal pulmonary angiography.