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Effects of fasudil on the portal and systemic hemodynamics of patients with cirrhosis
Author(s) -
Fukuda Takeshi,
Narahara Yoshiyuki,
Kanazawa Hidenori,
Matsushita Yoko,
Kidokoro Hideko,
Itokawa Norio,
Kondo Chisa,
Atsukawa Masanori,
Nakatsuka Katsuhisa,
Sakamoto Choitsu
Publication year - 2014
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12360
Subject(s) - fasudil , medicine , portal hypertension , portal venous pressure , vascular resistance , hemodynamics , cirrhosis , blood pressure , cardiology , placebo , anesthesia , rho associated protein kinase , pathology , biochemistry , signal transduction , chemistry , alternative medicine
Background and Aim Fasudil, a Rho‐kinase inhibitor, has been shown to reduce portal venous pressure in cirrhotic rats. However, its effects on portal and systemic hemodynamics have not been investigated in cirrhotic patients with portal hypertension. The aim of this study was to assess the effects of fasudil on the portal and systemic hemodynamics of cirrhotic patients with portal hypertension. Methods Twenty‐three patients with cirrhosis and portal hypertension were studied. Systemic and portal hemodynamics were measured prior to and 50 min after the initiation of intravenous administration of 30 mg fasudil ( n = 15) or placebo ( n = 8). Results After fasudil, there were significant decreases in both mean arterial pressure ( P < 0.05) and systemic vascular resistance ( P < 0.05), whereas the heart rate increased significantly ( P < 0.05). There was a significant decrease in the hepatic venous pressure gradient ( P < 0.05). Portal vascular resistance also decreased significantly ( P < 0.01). Placebo caused no significant effects. There were no symptomatic reactions caused by changes in the mean arterial pressure or heart rate after fasudil. Conclusions In cirrhotic patients with portal hypertension, fasudil lowers portal vascular resistance, resulting in decreased portal venous pressure with reducing arterial pressure.