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The cirrhotic liver is significantly more vulnerable to injury. This vulnerability is particularly evident after the advent of portal hypertension. In the normal liver, up to 75 percent can be resected without decompensation. By contrast, in the cirrhotic liver with portal hypertension, liver decompensation can occur even after less than 50 percent of the liver is resected. This book begins with an attempt to provide insights into this unanswered puzzle. The normal liver is soft and elastic. By contrast, the cirrhotic liver is inelastic and rigid. Flow in rigid tubes is governed by the Hagen-Poiseuille law. The law dictates that pressure gradient increases exponentially by the fourth power of the radius of the rigid sinusoid. This makes the cirrhotic liver virtually incapable of accommodating any increase in flow. The increase in pressure gradient is equivalent to the fourth power of the vessel radius. The first chapter explores the major new insight that decompensation in the cirrhotic liver is related to the loss of elasticity and the development of vessel wall rigidity, which thereafter subjects flow in the hepatic sinusoids to the Hagen-Poiseuille law. The rest of the book addresses portal hypertension in its clinical context. It invites the reader to survey multiple avenues associated with portal hypertension, including idiopathic non-cirrhotic portal hypertension, INCPH and non-alcoholic fatty liver disease, NAFLD. It also includes chapters on relationships between portal hypertension, the gastrointestinal system and the renal system. In general, the book provides several new insights into portal hypertension.
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The cirrhotic liver is significantly more vulnerable to injury. This vulnerability is particularly evident after the advent of portal hypertension. In the normal liver, up to 75 percent can be resected without decompensation. By contrast, in the cirrhotic liver with portal hypertension, liver decompensation can occur even after less than 50 percent of the liver is resected. This book begins with an attempt to provide insights into this unanswered puzzle. The normal liver is soft and elastic. By contrast, the cirrhotic liver is inelastic and rigid. Flow in rigid tubes is governed by the Hagen-Poiseuille law. The law dictates that pressure gradient increases exponentially by the fourth power of the radius of the rigid sinusoid. This makes the cirrhotic liver virtually incapable of accommodating any increase in flow. The increase in pressure gradient is equivalent to the fourth power of the vessel radius. The first chapter explores the major new insight that decompensation in the cirrhotic liver is related to the loss of elasticity and the development of vessel wall rigidity, which thereafter subjects flow in the hepatic sinusoids to the Hagen-Poiseuille law. The rest of the book addresses portal hypertension in its clinical context. It invites the reader to survey multiple avenues associated with portal hypertension, including idiopathic non-cirrhotic portal hypertension, INCPH and non-alcoholic fatty liver disease, NAFLD. It also includes chapters on relationships between portal hypertension, the gastrointestinal system and the renal system. In general, the book provides several new insights into portal hypertension.