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Feng
Liu1, Ji Xin Li2, Chun Mei Li2 and Xi Sheng Leng2
1Department
of General Surgery, the Fifth Affiliated Hospital, Harbin Medical
University, Harbin 150036, Heilongjiang Province, China
2Department of General Surgery, People’s Hospital,
Medical University, Beijing 100044, China
Dr. Feng Liu, graduated from Beijing Medical University as a
postgraduate in 1995, now associate professor of general surgery,
majoring hepatobilliary surgery, having 12 papers published.
Project supported by the National Natural Science Foundation and
Ministry of Public Health of China, No.37600481
Correspondence to: Dr. Feng Liu, Department of General
Surgery,the Fifth Affiliated Hospital, Harbin Medical University,
Harbin 150036, Heilongjiang Province, China
Telephone:
0086-51-5314098, Fax.
0098-51-5314088 Email.lfdlyy.163.net.
Received: 2000-07-26 Accepted: 2000-09-29
Subject
headings:
hypertension, portal; liver cirrhosis; portosystemic shunt,
surgical; endothelins; radioimmunoassay; epoprostenol; liver
cirrhosis
Liu F, Li JX, Li CM, Leng XS. Plasma endothelin in patients with
endotoxemia and dynamic comparison between vasoconstrictor and
vasodilator in cirrhotic patients. World J Gastroenterol,
2001;7(1):126-127
INTRODUCTION
Portal
hypertension is a common clinical syndrome characterized by an
abnormal increase in portal blood to the systemic circulation,
bypassing the liver. Recent studies have reported that humoral
substances play an important role in the pathogenesis of portal
hypertension, either by increasing vascular resistance at both the
intrahepatic and porto-collateral sites or affecting splanchnic
vasodilation with a concomitant increase in parto collateral blood
flow［1-6］.
Endothelin
(ET) released by endothelial cells is a 21 amino acid peptide with
potent vasoconstrictor action. Endothelin comprises a family of four
homologous isopeptides in human and animals (ET-1, ET-2, and ET-3,
VIC)［7-14］.
Most reported data are related to ET-1, which is the most powerful
vasoconstrictor. Owing to a variety of reasons, reports concerning
endothelin levels in cirrhotics are not consistent with each other.
Endothelin concentrations in plasma have been reported to be
increased in some studies and normal or reduced in others［15-20］.
Present evidence suggests that endothelin may play an important role
in modulating intrahepatic vascular resistance［21-24］.
However, the relationship between vasoconstrictor (ET, TX-) and
vasodilator (PGI2) during portosystemic shunt has not
been documented.
METHODS
We measured the concentration of endothelin in plasma using
radioimmunoassay in 121 patients with cirrhosis and compared these
values with 50 age and sex matched control subjects, and evaluated
systemic endotoxemia. At the same time, perioperative plasma
vasoconstrictor and vasodilator were clinically observed in 30
portohypertensive cirrhotic patients undergoing portosystemic shunt.
RESULTS
Plasma endothelin levels were higher in cirrhotic patients with
ascites than in those without ascites. Femoral venous plasma
endothelin levels averaged 90±23ng/L in cirrhotic patients versus
34±8ng/L in controls (P=0.000) , and that of cirrhotics with
ascites was higher than those without 106±17ng/L vs 90±23ng/L(P=0.002).
Moreover, plasma endothelin levels increased in proportion to the
severity of endotoxemia (rs=0.61,P=0.034). Both
the levels of plasma vasoconstrictors (ET, TX-) and of the
vasodilator (PGI2) were higher in portohypertensive
cirrhotic patients (ET: 107.8±25.9 ng/L vs 48.1±9.4 (P=0.000);
TX-: 349.7±198.4ng/L vs 156.3±54 (P=0.000); PGI2:
463.1±108.3 ng/L vs 227.2±46(P=0.000), and their
concentrations decreased significantly in patients after
portosystemic shunt (P=0.002).
DISCUSSION
These results suggest that endothelin has significant influence on
the portal vascular resistance of cirrhotic liver in vivo and
may play an important role in the pathogenesis of portal
hypertension［25-28］.
Endotoxin may lead to the increased synthesis and release of
endothelin. It could be that a dynamic balance between levels of
vasoconstrictor and vasodilator in plasma exists in the
pathophysiology of portohypertensive cirrhotic patients after
portosystemic shunt.
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