P-327 Role of nitric oxide on hepatic arterial blood flow in rats with CCL4-induced liver injury

1995 ◽  
Vol 3 ◽  
pp. S118
Author(s):  
N TANAKA
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Liver Injury ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood

Nitric oxide increases hepatic arterial blood flow in rats with carbon tetrachloride–induced acute hepatic injury

1999 ◽  
Vol 117 (1) ◽  
pp. 173-180 ◽  
Author(s):  
Noriko Tanaka ◽  
Katsuaki Tanaka ◽  
Yoji Nagashima ◽  
Masaaki Kondo ◽  
Hisahiko Sekihara
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Carbon Tetrachloride ◽  
Hepatic Injury ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Acute Hepatic Injury

Importance of nitric oxide in hepatic arterial blood flow and total hepatic blood volume regulation in pigs

1997 ◽  
Vol 161 (3) ◽  
pp. 303-309 ◽  
Author(s):  
F. GRUND ◽  
H. T. SOMMERSCHILD ◽  
A. WINECOFF ◽  
M. R. UJHELYI ◽  
T. TØNNESSEN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Blood Volume ◽  
Volume Regulation ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood

scholarly journals The role of hepatic arterial blood flow on liver regeneration after partial hepatectomy.

1989 ◽  
Vol 22 (8) ◽  
pp. 2025-2031
Author(s):  
Osamu TERAMOTO ◽  
Masaru MIYAZAKI ◽  
Hisao KOSHIKAWA ◽  
Ikuo UDAGAWA ◽  
Katsuji OKUI
Keyword(s):  
Blood Flow ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood

Portal venous and hepatic arterial blood flow in hepatic diseases with marked splenomegaly

1971 ◽  
Vol 6 (1) ◽  
pp. 41-41
Author(s):  
K. Kera ◽  
S. Nakamura ◽  
T. Aikawa ◽  
K. Sasaki ◽  
T. Nakamura
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Hepatic Diseases ◽  
Arterial Blood ◽  
Marked Splenomegaly

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Venous Blood ◽  
Reference Sample ◽  
Venous Hypertension ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Systemic and hepatic hemodynamic changes in acute liver injury

1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Venous Blood ◽  
Marked Change ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Subsequent Increase ◽  
Arterial Blood

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

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