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[Hyperdynamic circulation in patients with liver cirrhosis and portal hypertension].
Korean J Gastroenterol. 2009 Sep; 54(3):143-8.KJ

Abstract

Hyperdynamic circulation in patients with liver cirrhosis is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure and currently focused on understanding the pathogenesis because of possibility of developing novel treatment modality. Basically, these hemodynamic alternations arise from portal hypertension. Portosystemic collaterals develop to counterbalance the increased intrahepatic vascular resistance to portal blood flow and induce an increase in venous return to heart. Increased shear stress in vascular endothelial cell related high blood flow by portosystemic shunting contributes to this upregulation of eNOS resulting in NO overproduction. Additionally, bypassing through portosystemic collaterals and escaping degradation of over-produced circulating vasodilators in the diseased liver can promote the peripheral arterial vasodilation. Vasodilation of the systemic and splanchnic circulations lead to a reduced systemic vascular resistance, and increased cardiac output and splanchnic blood flow. Furthermore, neurohumoral vasoconstrictive systems including systemic nervous system, rennin angiotensin aldosterone system, and vasopressin are intensively activated secondary to vasodilation. However, hyperdynamic circulation would be more aggravated by the activated vasoconstrictive systems. With the progression of the cirrhotic process, hyperdynamic alternations can be more profound due to hyporesponsiveness to vasoconstrictors and increased shunt formation in conjunction with autonomic neuropathy. Eventually, splanchnic arterial vasodilation results in an increase portal venous inflow, maintaining the elevated portal venous pressure. Hyperdynamic circulation is intimately involved in portal hypertension with liver cirrhosis, therefore it is reasonable to have an interest in complete understanding of the pathogenesis of hyperdynamic circulation to develop novel treatment modality.

Authors+Show Affiliations

Department of Internal Medicine, Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, Korea.No affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

kor

PubMed ID

19844149

Citation

Kim, Moon Young, and Soon Koo Baik. "[Hyperdynamic Circulation in Patients With Liver Cirrhosis and Portal Hypertension]." The Korean Journal of Gastroenterology = Taehan Sohwagi Hakhoe Chi, vol. 54, no. 3, 2009, pp. 143-8.
Kim MY, Baik SK. [Hyperdynamic circulation in patients with liver cirrhosis and portal hypertension]. Korean J Gastroenterol. 2009;54(3):143-8.
Kim, M. Y., & Baik, S. K. (2009). [Hyperdynamic circulation in patients with liver cirrhosis and portal hypertension]. The Korean Journal of Gastroenterology = Taehan Sohwagi Hakhoe Chi, 54(3), 143-8.
Kim MY, Baik SK. [Hyperdynamic Circulation in Patients With Liver Cirrhosis and Portal Hypertension]. Korean J Gastroenterol. 2009;54(3):143-8. PubMed PMID: 19844149.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Hyperdynamic circulation in patients with liver cirrhosis and portal hypertension]. AU - Kim,Moon Young, AU - Baik,Soon Koo, PY - 2009/10/22/entrez PY - 2009/10/22/pubmed PY - 2009/11/13/medline SP - 143 EP - 8 JF - The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi JO - Korean J Gastroenterol VL - 54 IS - 3 N2 - Hyperdynamic circulation in patients with liver cirrhosis is characterized by increased cardiac output and heart rate, and decreased systemic vascular resistance with low arterial blood pressure and currently focused on understanding the pathogenesis because of possibility of developing novel treatment modality. Basically, these hemodynamic alternations arise from portal hypertension. Portosystemic collaterals develop to counterbalance the increased intrahepatic vascular resistance to portal blood flow and induce an increase in venous return to heart. Increased shear stress in vascular endothelial cell related high blood flow by portosystemic shunting contributes to this upregulation of eNOS resulting in NO overproduction. Additionally, bypassing through portosystemic collaterals and escaping degradation of over-produced circulating vasodilators in the diseased liver can promote the peripheral arterial vasodilation. Vasodilation of the systemic and splanchnic circulations lead to a reduced systemic vascular resistance, and increased cardiac output and splanchnic blood flow. Furthermore, neurohumoral vasoconstrictive systems including systemic nervous system, rennin angiotensin aldosterone system, and vasopressin are intensively activated secondary to vasodilation. However, hyperdynamic circulation would be more aggravated by the activated vasoconstrictive systems. With the progression of the cirrhotic process, hyperdynamic alternations can be more profound due to hyporesponsiveness to vasoconstrictors and increased shunt formation in conjunction with autonomic neuropathy. Eventually, splanchnic arterial vasodilation results in an increase portal venous inflow, maintaining the elevated portal venous pressure. Hyperdynamic circulation is intimately involved in portal hypertension with liver cirrhosis, therefore it is reasonable to have an interest in complete understanding of the pathogenesis of hyperdynamic circulation to develop novel treatment modality. SN - 1598-9992 UR - https://www.unboundmedicine.com/medline/citation/19844149/[Hyperdynamic_circulation_in_patients_with_liver_cirrhosis_and_portal_hypertension]_ L2 - http://www.kjg.or.kr/journal/view.html?doi=10.4166/kjg.2009.54.3.143 DB - PRIME DP - Unbound Medicine ER -