HYPERDYNAMIC STATE IN CHRONIC LIVER-DISEASES

被引:35
作者
GROSZMANN, RJ
机构
[1] Yale University School of Medicine, New Haven, CT
关键词
HYPERDYNAMIC CIRCULATION; PORTAL HYPERTENSION; SPLANCHNIC VASODILATORS;
D O I
10.1016/S0168-8278(05)80454-4
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Reduced splanchnic arteriolar resistance and increased portal venous outflow have been associated with chronic portal hypertension. This hyperdynamic splanchnic circulatory state is accompanied by a hyperdynamic systemic circulation characterized by a high cardiac index and low systemic vascular resistance. The systemic phenomenon occurs earlier than the regional one, possibly because the increased outflow resistance induced by portal hypertension delays the effect of circulating humoral vasodilators on the splanchnic bed. Several vasoactive substances have been advanced as the vasodilator responsible for the hyperdynamic circulation. Glucagon and bile acids have been found to be potent splanchnic vasodilators in animal studies. However, neither consistently dilates other vascular beds. For example, bile acids are splanchnic - but not systemic - vasodilators. Several studies suggest a role in chronic liver disease for nitric oxide, a potent endogenous vasodilator secreted by endothelial cells. Prostaglandins have also been proposed as the responsible vasodilator. However, mixed results have been seen with experimental suppression of prostaglandin synthesis. For a hyperdynamic state to develop and persist requires not only reduced cardiac afterload, but also an increased venous return. Recently, we found an expanded plasma volume after initial vasodilation in rats with portal hypertension. This 'refill' of the circulation may be intrinsic to development of the hyperdynamic state. Furthermore, this blood volume expansion may be the link between vasodilation and the hyperdynamic circulation.
引用
收藏
页码:S38 / S40
页数:3
相关论文
共 14 条
[1]   VASODILATATION AND SODIUM RETENTION IN PREHEPATIC PORTAL-HYPERTENSION [J].
ALBILLOS, A ;
COLOMBATO, LA ;
GROSZMANN, RJ .
GASTROENTEROLOGY, 1992, 102 (03) :931-935
[2]   ROLE OF HUMORAL-FACTORS IN THE INTESTINAL HYPEREMIA ASSOCIATED WITH CHRONIC PORTAL-HYPERTENSION [J].
BENOIT, JN ;
BARROWMAN, JA ;
HARPER, SL ;
KVIETYS, PR ;
GRANGER, DN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1984, 247 (05) :G486-G493
[3]   LACK OF EFFECT OF INDOMETHACIN ON SYSTEMIC AND SPLANCHNIC HEMODYNAMICS IN PORTAL HYPERTENSIVE RATS [J].
BLANCHART, A ;
HERNANDO, N ;
FERNANDEZMUNOZ, D ;
HERNANDO, L ;
LOPEZNOVOA, JM .
CLINICAL SCIENCE, 1985, 68 (05) :605-607
[4]   EFFECTS OF PROSTAGLANDIN INHIBITION ON SYSTEMIC AND HEPATIC HEMODYNAMICS IN PATIENTS WITH CIRRHOSIS OF THE LIVER [J].
BRUIX, J ;
BOSCH, J ;
KRAVETZ, D ;
MASTAI, R ;
RODES, J .
GASTROENTEROLOGY, 1985, 88 (02) :430-435
[5]   TEMPORAL RELATIONSHIP OF PERIPHERAL VASODILATATION, PLASMA-VOLUME EXPANSION AND THE HYPERDYNAMIC CIRCULATORY STATE IN PORTAL-HYPERTENSIVE RATS [J].
COLOMBATO, LA ;
ALBILLOS, A ;
GROSZMANN, RJ .
HEPATOLOGY, 1992, 15 (02) :323-328
[6]   BILE-ACIDS DO NOT MEDIATE THE HYPERDYNAMIC CIRCULATION IN PORTAL HYPERTENSIVE RATS [J].
GENECIN, P ;
POLIO, J ;
COLOMBATO, LA ;
FERRAIOLI, G ;
REUBEN, A ;
GROSZMANN, RJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (01) :G21-G25
[7]   NA RESTRICTION BLUNTS EXPANSION OF PLASMA-VOLUME AND AMELIORATES HYPERDYNAMIC CIRCULATION IN PORTAL-HYPERTENSION [J].
GENECIN, P ;
POLIO, J ;
GROSZMANN, RJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (03) :G498-G503
[8]   HUMORAL-FACTORS MAY MEDIATE INCREASED RAT HINDQUARTER BLOOD-FLOW IN PORTAL-HYPERTENSION [J].
KORTHUIS, RJ ;
BENOIT, JN ;
KVIETYS, PR ;
TOWNSLEY, MI ;
TAYLOR, AE ;
GRANGER, DN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 249 (04) :H827-H833
[9]  
KOTELANSKI B, 1972, GASTROENTEROLOGY, V63, P102
[10]   GASTRIC-MUCOSAL BLOOD-FLOW AND ACID-SECRETION IN PORTAL HYPERTENSIVE RATS [J].
PIQUE, JM ;
LEUNG, FW ;
KITAHORA, T ;
SARFEH, IJ ;
TARNAWSKI, A ;
GUTH, PH .
GASTROENTEROLOGY, 1988, 95 (03) :727-733