**Meet the editor**

Prof. Dmitry V. Garbuzenko, MD was born in 1962 in Russia. In 1985 he graduated from Chelyabinsk State Medical Academy. From 1985 until 1990 he was the post-graduate student in Department of Hospital Surgery, ChSMA. Since 1990, Dr. Garbuzenko has been working in the Chelyabinsk State Medical Academy as professor in Department of Faculty Surgery. His scien-

tific interests are problems connected with portal hypertension in patients with liver cirrhosis and study of pathophysiologic basis for its treatment. Dr. Garbuzenko is a member of Russian Gastroenterological Association and of International Association of Surgeons-Hepatologists. He has authored more than 100 publications, and has 2 inventions and 1 monograph ("Gastroesophageal variceal hemorrhage in cirrhotic patients: pathogenesis, prophylactic, treatment").

Contents

**Preface IX** 

Chapter 1 **The Molecules: Abnormal** 

Yasuko Iwakiri

Chapter 3 **Extra Hepatic Portal** 

Chapter 4 **Portal Vein Thrombosis** 

Chapter 2 **Cystic Fibrosis Liver Disease 27** 

Chapter 5 **The Bacterial Endotoxins Levels** 

Chapter 6 **Traditional Chinese Medicine** 

Chapter 7 **Role of Manganese as Mediator of Central Nervous System:** 

**Vasculatures in the Splanchnic** 

Andrew Low and Nabil A. Jarad

**Venous Obstruction in Children 41**  Narendra K. Arora and Manoja K. Das

**with Cavernous Transformation** 

**Can Improve Liver Microcirculation** 

Tian Tian, Zhang Jie and Xu Hong

Juan Pablo Prestifilippo, Silvina Tallis, Amalia Delfante, Pablo Souto,

Xu Lieming, Gu Jie, Lu Xiong, Zhou Yang,

**and Systemic Circulation in Portal Hypertension 1** 

**in Myeloproliferative Disorders: Review Update 65** 

**and Reduce Portal Hypertension in Liver Cirrhosis 93** 

**Alteration in Experimental Portal Hypertension 121** 

Juan Carlos Perazzo and Gabriela Beatriz Acosta

Anca Rosu, Cristian Searpe and Mihai Popescu

**in the Blood of Cirrhotic Patients as Predictor of the Risk of Esophageal Varices Bleeding 85**  Dmitry Garbuzenko, Alexandr Mikurov and Dmitry Smirnov

### Contents

#### **Preface XI**


Juan Carlos Perazzo and Gabriela Beatriz Acosta

X Contents

Chapter 8 **Changes of Peripheral Blood Cells in Patients with Cirrhotic Portal Hypertension 133**  Lv Yunfu

## Preface

Portal hypertension is a clinical syndrome defined by a portal venous pressure gradient exceeding 5 mm Hg. It is initiated by increased outflow resistance, and can occur at a presinusoidal (intra- or extrahepatic), sinusoidal, or postsinusoidal level. As the condition progresses, there is a rise in portal blood flow, a combination that mains and worsens the portal hypertension.

Cirrhosis is the most common cause of portal hypertension in the Western world. There are more rare intrahepatic causes of portal hypertension, such as cystic fibrosis liver disease. Extra hepatic portal venous obstruction is found mainly at children, and it can also be caused by myeloproliferative diseases.

In cirrhosis, the principal site of increased resistance to outflow of portal venous blood is within the liver itself. Mesenteric arterial vasodilation is hallmark of cirrhosis and contributes to both increased portal venous inflow and a systemic hyperdinamic circulatory state. Arterial vasodilatation is regulated by a complex interplay of various vasodilator molecules and factors that influence the production of those vasodilator molecules.

Portal hypertension is associated with severe complications, including ascites, hepatic encephalopathy, hypersplenism, bleeding from gastro-esophageal varices. Despite the progress achieved over last decades, the 6-week mortality associated with variceal bleeding is still in the order of 10-20%. Endoscopic assessment of esophageal varices and the state of esophageal and stomach mucosa at the esophagogastroduodenoscopy, presents high importance for the assessment of risk of their development. However, invasiveness as well as discomfort that are tolerated by patients during the given procedure, lead to the rejection from it and therefore they can't be subjected to examination in a number of cases. Beside that, the research might be impossible to carry out in case if the state of patient is grave. The investigation of hepatic venous pressure gradient, that reflects the portal hypertension intensity best of all, haven`t been realized in the clinical practice up to now. Considering the above mentioned disadvantages of main methods, the development of additional prognostic criteria of the risk of esophageal varices bleeding remains the urgent problem of the internal medicine.

#### X Preface

Current methods of treatments in portal hypertension include farmacologic therapy by vasoactive drugs, endoscopic therapy, portosystemic shunt surgery and transjugular intrahepatic portosystemic shunts (TIPS). Expansion in the knowledge of pathophysiology of portal hypertension is need as this might provide new and useful strategies for the future. The described problems above associated mainly with portal hypertension are presented in this book.

> **Dmitry V. Garbuzenko**  Department of Surgical Diseases and Urology, Chelyabinsk State Medical Academy, Chelyabinsk, Russia

X Preface

hypertension are presented in this book.

Current methods of treatments in portal hypertension include farmacologic therapy by vasoactive drugs, endoscopic therapy, portosystemic shunt surgery and transjugular intrahepatic portosystemic shunts (TIPS). Expansion in the knowledge of pathophysiology of portal hypertension is need as this might provide new and useful strategies for the future. The described problems above associated mainly with portal

**Dmitry V. Garbuzenko** 

Russia

Department of Surgical Diseases and Urology, Chelyabinsk State Medical Academy, Chelyabinsk,

**1** 

Yasuko Iwakiri

*USA* 

*Yale University School of Medicine,* 

**The Molecules: Abnormal** 

**Vasculatures in the Splanchnic and** 

**Systemic Circulation in Portal Hypertension** 

Portal hypertension, defined as an increase in pressure within the portal vein, is a detrimental complication in liver diseases. The increased intrahepatic resistance as a consequence of cirrhosis is the primary cause of portal hypertension (Figure 1). Once it is developed, portal hypertension influences extrahepatic vascular beds in the splanchnic and systemic circulation. Two major consequences of portal hypertension in this regard are excessive arterial vasodilation/hypocontractility and the formation of portosystemic collateral vessels. Both excessive arterial vasodilation and portosystemic collateral vessel formation help to increase the blood flow through the portal vein and worsen portal hypertension. This facilitates the development of the abnormal hemodynamic condition, called the hyperdynamic circulatory syndrome, and ultimately leads to variceal bleeding and ascites (Bosch 2000; Bosch 2007;

This chapter summarizes current knowledge of molecules and factors that play critical roles in the development and maintenance of excessive arterial vasodilation and portosystemic collateral vessels in the splanchnic and systemic circulation in cirrhosis and portal

Groszmann 1993; Iwakiri 2011; Iwakiri & Groszmann 2006).

Fig. 1. Overview of portal hypertension.

**1. Introduction** 
