Effects of increasing blood hemoglobin levels on systemic hemodynamics of acutely anemic cirrhotic patients

被引:36
作者
Elizalde, JI
Moitinho, E
García-Pagán, JC
Cirera, I
Escorsell, A
Bandi, JC
Jiménez, W
Bosch, J
Piqué, JM
Rodés, J
机构
[1] Univ Barcelona, Dept Gastroenterol, Hosp Clin, E-08036 Barcelona, Spain
[2] Univ Barcelona, Hosp Clin, Inst Clin Malalties Digest, Liver Unit, Barcelona, Spain
[3] Univ Barcelona, Hosp Clin, Inst Invest Biomed August Pi & Sunyer, Hormonal Lab, Barcelona, Spain
关键词
blood viscosity; portal hypertension; portal pressure; systemic vascular resistance; vascular hindrance;
D O I
10.1016/S0168-8278(98)80260-2
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background/Aims: In experimental portal hypertension, blood hemoglobin levels have been shown to influence the hyperdynamic circulatory state. The aim of this study was to assess the hemodynamic effects of increasing hemoglobin concentration in human portal hypertension. Methods: Sixteen cirrhotic patients recovering from a variceal bleeding episode were randomly assigned to receive two units of packed red cells or 500 ml of a protein solution, Systemic and portal hemodynamics, and rheological and hormonal parameters were measured at baseline and after expansion. Results: Both groups were similar with respect to the degree of liver failure, severity of the bleeding episode, activation of the endogenous vasopressor systems, and hemodynamic parameters. The administration of either erythrocytes or a protein solution prompted a similar increase in total blood volume and suppression of vasopressor systems, Both groups of patients experienced similar increases in wedged hepatic venous pressure. Hepatic venous pressure gradient was not significantly modified but tended to increase in erythrocyte-transfused patients. Cardiopulmonary pressures increased, but this increment was significant in the non-blood-trans-fused patients only Cardiac output decreased in erythrocyte-transfused patients, while it increased in the group receiving a protein solution. Red blood cell transfusion resulted in an increase in systemic vascular hindrance (resistance/blood viscosity), whereas the administration of a protein solution prompted a decrease in this parameter, thus reflecting true vasoconstriction and vasodilation, respectively. Conclusions: An increase in blood hemoglobin in acutely anemic cirrhotic patients attenuates their hyperdynamic circulation beyond viscosity-dependent changes, an effect which might be counteracted by the effects on portal venous pressure gradient.
引用
收藏
页码:789 / 795
页数:7
相关论文
共 31 条
[1]   ENDOTHELIUM-DERIVED RELAXING FACTOR IS IMPORTANT IN MEDIATING THE HIGH-OUTPUT STATE IN CHRONIC SEVERE ANEMIA [J].
ANAND, IS ;
CHANDRASHEKHAR, Y ;
WANDER, GS ;
CHAWLA, LS .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1995, 25 (06) :1402-1407
[2]   ASSESSMENT OF THE RENIN-ANGIOTENSIN SYSTEM IN CIRRHOTIC-PATIENTS - COMPARISON BETWEEN PLASMA-RENIN ACTIVITY AND DIRECT MEASUREMENT OF IMMUNOREACTIVE RENIN [J].
ASBERT, M ;
JIMENEZ, W ;
GAYA, J ;
GINES, P ;
ARROYO, V ;
RIVERA, F ;
RODES, J .
JOURNAL OF HEPATOLOGY, 1992, 15 (1-2) :179-183
[3]   Hyperdynamic circulation in patients with cirrhosis: Direct measurement of nitric oxide levels in hepatic and portal veins [J].
Battista, S ;
Bar, F ;
Mengozzi, G ;
Zanon, E ;
Grosso, M ;
Molino, G .
JOURNAL OF HEPATOLOGY, 1997, 26 (01) :75-80
[4]   HEMODYNAMIC EVALUATION OF THE PATIENT WITH PORTAL-HYPERTENSION [J].
BOSCH, J ;
MASTAI, R ;
KRAVETZ, D ;
NAVASA, M ;
RODES, J .
SEMINARS IN LIVER DISEASE, 1986, 6 (04) :309-317
[5]   EFFECT OF PLASMA-VOLUME EXPANSION ON PORTAL HYPERTENSION [J].
BOYER, JL ;
CHATTERJEE, C ;
IBER, FL ;
BASU, AK .
NEW ENGLAND JOURNAL OF MEDICINE, 1966, 275 (14) :750-+
[6]   Increased blood hemoglobin attenuates splanchnic vasodilation in portal-hypertensive rats by nitric oxide inactivation [J].
Casadevall, M ;
Pique, JM ;
Cirera, I ;
Goldin, E ;
Elizalde, I ;
Panes, J ;
MartinezCuesta, MA ;
Bosch, J ;
Teres, J ;
Rodes, J .
GASTROENTEROLOGY, 1996, 110 (04) :1156-1165
[7]  
CASADEVALL M, 1993, GASTROENTEROLOGY, V106, pA60
[8]   IMPAIRED RESPONSIVENESS TO ANGIOTENSIN-II IN EXPERIMENTAL CIRRHOSIS - ROLE OF NITRIC-OXIDE [J].
CASTRO, A ;
JIMENEZ, W ;
CLARIA, J ;
ROS, J ;
MARTINEZ, JM ;
BOSCH, M ;
ARROYO, V ;
PIULATS, J ;
RIVERA, F ;
RODES, J .
HEPATOLOGY, 1993, 18 (02) :367-372
[9]   ANEMIA INCREASES GASTRIC BLOOD-FLOW IN NONCIRRHOTIC AND CIRRHOTIC-PATIENTS [J].
CIRERA, I ;
PANES, J ;
BORDAS, JM ;
LLACH, J ;
BOSCH, J ;
PIQUE, JM ;
TERES, J ;
RODES, J .
GASTROINTESTINAL ENDOSCOPY, 1995, 42 (05) :403-407
[10]   Anemia worsens hyperdynamic circulation of patients with cirrhosis and portal hypertension [J].
Cirera, I ;
Elizalde, JI ;
Pique, JM ;
Feu, F ;
Casadevall, M ;
Goldin, E ;
Teres, J ;
Bosch, J ;
Rodes, J .
DIGESTIVE DISEASES AND SCIENCES, 1997, 42 (08) :1697-1702