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Systemic hemodynamics and serum nitrate levels in patients undergoing endoscopic variceal ligation
Author(s) -
Yokoyama M,
Shijo H,
Ota K,
Kubara K,
Kokawa H,
Kim T,
Akiyoshi N,
Okumura M,
Inoue K
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510240110
Subject(s) - preload , hemodynamics , medicine , cardiac index , cardiology , vascular resistance , cirrhosis , cardiac output , nitric oxide , portal hypertension , portal venous pressure , venous return curve , blood volume , anesthesia
The effects of endoscopic variceal ligation (EVL) on systemic hemodynamics are unknown. This study was conducted to determine whether the obliteration of portal‐systemic collaterals by EVL affects systemic hemodynamics and serum nitrate concentrations in patients with compensated cirrhosis. We measured systemic and hepatic hemodynamics, azygos vein blood flow (AzBF), and serum nitrate concentrations before and immediately following EVL. A prompt decrease in left ventricular end‐diastolic volume (LVEDV), stroke volume, cardiac index (CI), and an increase in systemic vascular resistance index (SVRI) were observed following variceal ligation. The reduction in LVEDV was associated with a decline in CI with a rise in SVRI. There was also a prompt reduction in serum nitrate concentration following variceal ligation. AzBF also significantly decreased following variceal ligation. These findings indicate that EVL decreased cardiac output via a reduction in cardiac preload (central venous return). Blood flow through portal‐systemic collaterals has an important role in the enhanced cardiac preload of cirrhotic patients. The sudden decrease in serum nitrate concentrations suggests that endogenous nitric oxide may be involved in the regulation of systemic hemodynamics in patients with compensated cirrhosis.