Effects of Caffeic Acid Phenethyl Ester (CAPE) on Hepatopulmonary Syndrome
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Effects of Caffeic Acid Phenethyl Ester (CAPE) on Hepatopulmonary Syndrome Ahmet Tekin,1,7,8 Serdar Türkyılmaz,2 Tevfik Küçükkartallar,1 Murat Çakır,1 Hüseyin Yılmaz,3 Hasan Esen,4 Burhan Ateş,5 İlhan Çiftci,6 and Adil Kartal1
Abstract—The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) on inflammatory and related histopathological changes in the lung and liver in experimental hepatopulmonary syndrome (HPS) model. Forty Sprague Dawley rats were used in this study. The animals were divided into four groups of ten rats each. Group 1 and 2 was subjected the common bile duct (CBD) but not ligated, Group 3; (cirrhosis+saline): the CBD was ligated and was given intraperitoneal saline infusion treatment during 5 weeks. Group 4; (cirrhosis+CAPE): the CBD was ligated and was given intraperitoneal CAPE infusion treatment during 5 weeks. A 5-week waiting period was observed for the development of cirrhosis and the rats' lungs and liver were taken for histopathological examination. The induction of HPS resulted in a significant increase in serum bilurubin, AST, ALT, and NO levels, and decrease PO2 and O2 saturation. The use of CAPE significant decrease these parameters. Histopathological examination revealed less congestion, portal inflammation, and nodular formations of the liver, and less congestion, emphysematous and inflammatory changes and smallest perialviolar vascular diameters, in the lung in the cirrhosis+ CAPE groups than in the other groups. CAPE treatment may be a potential approach for the treatment of hepatopulmonary syndrome in the future. KEY WORDS: cirrhosis; hepatopulmonary syndrome; rats; CAPE.
described the clinical interactions between the liver and lungs, but HPS was essentially described first by Kennedy in 1977 [3]. The most common hepatic disorder leading to HPS is liver cirrhosis, irrespective of etiology, although HPS has also been observed in many other chronic, and even acute, hepatic conditions [4]. Hypoxia in HPS occurs due to the development of intrapulmonary shunts, perfusion–diffusion defect, and discordance in ventilation–perfusion. HPS occurs in approximately 15–20% of patients with cirrhosis or portal hypertension [5, 6]. It is known that endothelium-derived vasodilators and vasoconstrictor agents play important roles in the development of HPS. Nitric oxide (NO) and endothelin-1 (ET-1) are well known among these [7, 8]. As ET-1 is secreted to the vessel lumen, endothelial nitric oxide synthase is activated and the amount of NO increases, referred to as endocrine vasodilatation [9]. In subjects with experimental cirrhosis induced by choledochus ligation, an increase in the amount of ET-1 secreted from the biliary epithelium and a related increase in pulmonary endothe-
INTRODUCTION The hepatopulmonary syndrome (HPS) is a state in which liver function impairment and pulmonary vascular dilatations develop together, and is characterized by arterial oxygen disorder [1]. In 1884, Fluckiger [2] 1
Department of General Surgery, Meram Medical Faculty, Selcuk Univers
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