Hepatic energy status in hypotension of different aetiologies in dogs

1991 ◽  
Vol 81 (5) ◽  
pp. 627-633 ◽  
Author(s):  
Tadashi Yokoyama ◽  
Ryoji Okamoto ◽  
Yuzo Yamamoto ◽  
Dai Manaka ◽  
Hirokazu Sasaki ◽  
...  
Keyword(s):  
Blood Flow ◽  
Energy Metabolism ◽  
Ketone Body ◽  
Venous Blood Flow ◽  
Shock Model ◽  
Arterial Ketone Body Ratio ◽  
Hepatic Energy Metabolism ◽  
Arterial Blood ◽  
Ketone Body Ratio ◽  
Significant Difference

1. The alterations in hepatic energy metabolism in hypotension induced by the administration of trimetaphan camsylate (Arfonad) were investigated in comparison with those produced by hypotension resulting from massive haemorrhage by measuring the arterial ketone body ratio, which reflects the hepatic mitochondrial redox state, and other indices of hepatic energy metabolism together with simultaneous measurement of hepatic blood flow in dogs. 2. Mean arterial blood pressure was decreased from 130 mmHg to 60 mmHg by the continuous intravenous infusion of trimetaphan camsylate or by the use of Wiggers' shock model. In hypotension induced by trimetaphan camsylate, the arterial ketone body ratio, ATP and total adenine nucleotide concentrations and energy charge were maintained at near-control values throughout the experimental period. By contrast, the arterial ketone body ratio decreased from 1.04 ±0.09 to 0.29 ±0.06 at 3 h after haemorrhage in Wiggers' shock model (P <0.01). The ATP and total adenine nucleotide concentrations and energy charge also decreased significantly in this model (P <0.05). The difference in hepatic energy status was also shown by data from 31P nuclear magnetic resonance spectroscopy. 3. During hypotension, portal venous and total hepatic blood flows diminished significantly compared with the control values in each group (P <0.01). Although there was no significant difference in total hepatic flow between the two groups, the portal venous blood flow in hypotension induced by trimetaphan camsylate was significantly higher than that in Wiggers' shock model (P <0.05). 4. During hypotension induced by trimetaphan camsylate, the hepatic energy metabolism was well maintained at the mean arterial blood pressure value of 60 mmHg, but in haemorrhagic hypotension it was severely curtailed, although there was no significant difference in total hepatic blood flow between the two groups. It is conjectured that the portal venous blood flow contributes significantly to the maintenance of hepatic energy metabolism and hepatic tissue perfusion during hypotension induced by trimetaphan camsylate.

Relationship of deranged energy metabolism in liver and kidney to arterial ketone body ratio following liver ischemia in rats

1984 ◽  
Vol 14 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Masayuki Yamamoto ◽  
Yasuyuki Shimahara ◽  
Kazue Ozawa ◽  
Takayoshi Tobe ◽  
Wolf Isselhard
Keyword(s):  
Energy Metabolism ◽  
Ketone Body ◽  
Liver Ischemia ◽  
Arterial Ketone Body Ratio ◽  
Ketone Body Ratio ◽  
Liver And Kidney ◽  
Relationship Of

Energy metabolism of the liver in brain dead dogs assessed by 31P-NMR spectroscopy and arterial ketone body ratio

Life Sciences ◽  
1991 ◽  
Vol 49 (7) ◽  
pp. 511-518 ◽  
Author(s):  
Toshiyuki Kitai ◽  
Akira Tanaka ◽  
Mitsuhiro Terasaki ◽  
Ryoji Okamoto ◽  
Kazue Ozawa ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Nmr Spectroscopy ◽  
Ketone Body ◽  
31P Nmr ◽  
31P Nmr Spectroscopy ◽  
Arterial Ketone Body Ratio ◽  
Ketone Body Ratio ◽  
Brain Dead

DEFECTIVE ENERGY METABOLISM OF LIVER MITOCHONDRIA, and ITS RELATIONSHIP WITH ARTERIAL KETONE BODY RATIO IN THE RABBIT WITH BILIARY SEPSIS

Shock ◽  
1995 ◽  
Vol 3 (6) ◽  
pp. 49
Author(s):  
Dong Jia-Hong ◽  
Han Ben-li ◽  
Huang Zhi-qiang ◽  
Wang Ao-chuan ◽  
Sun Wen-bin ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Ketone Body ◽  
Liver Mitochondria ◽  
Arterial Ketone Body Ratio ◽  
Ketone Body Ratio ◽  
Biliary Sepsis

CHANGES OF KETONE BODY RATIO REFLECTING HEPATIC ENERGY METABOLISM IN CARDIOVASCULAR PROCEDURES

ASAIO Journal ◽  
1996 ◽  
Vol 42 (2) ◽  
pp. 36
Author(s):  
G. Liu ◽  
M. Q. Wang ◽  
S. Fukunaga ◽  
T. Sueda ◽  
Y. Matsuura ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Ketone Body ◽  
Hepatic Energy Metabolism ◽  
Ketone Body Ratio

DEFECTIVE ENERGY METABOLISM OF LIVER MITOCHONDRIA AND ITS RELATIONSHIP WITH ARTERIAL KETONE BODY RATIO IN THE RABBIT WITH BILIARY SEPSIS.

Shock ◽  
1995 ◽  
Vol 3 ◽  
pp. 49-50
Author(s):  
Jia-Hong Dong ◽  
Ben-Ii Han ◽  
Zhi-qiang Huang ◽  
Ao-chuan Wang ◽  
Wen-bin Sun ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Ketone Body ◽  
Liver Mitochondria ◽  
Arterial Ketone Body Ratio ◽  
Ketone Body Ratio ◽  
Biliary Sepsis

Effect of dobutamine on the arterial ketone body ratio and portal blood flow velocity in cirrhosis

2008 ◽  
Vol 13 (4) ◽  
pp. 209-216 ◽  
Author(s):  
Kozo Kajlmura ◽  
Fuminori Morlyasu ◽  
Tohru Kimura ◽  
Minora Okuma ◽  
Keiichiro Mori ◽  
...  
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Ketone Body ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Arterial Ketone Body Ratio ◽  
Ketone Body Ratio

The fundamental factor determining the clinical prognosis of prolonged jaundice—Relation to the arterial ketone body ratio

1985 ◽  
Vol 15 (1) ◽  
pp. 18-22 ◽  
Author(s):  
Masayuki Yamamoto ◽  
Hideki Fujii ◽  
Katsuhiko Sugahara ◽  
Sadao Kawashima ◽  
Kazue Ozawa ◽  
...  
Keyword(s):  
Ketone Body ◽  
Clinical Prognosis ◽  
Arterial Ketone Body Ratio ◽  
Fundamental Factor ◽  
Ketone Body Ratio ◽  
Prolonged Jaundice

HEMOSTATIC EVALUATION OF PATIENTS UNDERGOING LIVER TRANSPLANTATION

1987 ◽  
Author(s):  
S R Rettke ◽  
C A Owen ◽  
E J W Bowie ◽  
T L Cole ◽  
R H Wiesner ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Blood Flow ◽  
Coagulation Factors ◽  
Stage Ii ◽  
Skin Closure ◽  
Donor Liver ◽  
Ischemia Time ◽  
Arterial Blood ◽  
Significant Difference ◽  
Diseased Liver

Significant hemostatic abnormalities can occur during orthotopic liver transplantation (OLT). This study addressed three goals: 1)evaluation of the hemostatic mechanism at each stage of the OLT; 2) the relationship of the coagulation process with the thrombelastograph (TEG); and 3) comparison of results in patients requiring retransplantation or who died, with the overall pattern. To evaluate hemostasis during 50 consecutive OLTs, a detailed coagulation and TEG study was done. The surgical procedure was divided into the following stages: Stage I--induction of anesthesia to occlusion of blood flow to the patient’ s diseased liver; Stage II—occlusion of blood flow to the patient’ s diseased liver to reperfusion of the patient’ s new liver; and Stage III—reperfusion of the new liver until skin closure. 28 ml of arterial blood were sampled at the beginning and end of each stage and up to five days posttransplantation for the following: platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, prothrombin, factors V, VII, IX, and X, plasminogen, antiplasmin, antithrombin III (functional and immunologic), fibrinolytic split products, and TEG. The patient’ s core temperature and amount of blood products transfused were obtained intraoperatively during each of the six data times. The ischemia time of the donor liver was recorded. Significant hemostatic abnormalities developed during each of the 50 OLTs, especially during reperfusion of the donor liver. In some instances, this was corrected within one hour, but platelet counts continued to fall, and a number of coagulation factors rebounded only partially. The TEG values correlated with laboratory data and blood loss, but the correlations were not strong. The patient’ s requirement for red cells varied with the operative drop in temperature; however, the donor liver ischemia time and length of Stage II made no significant difference. It is concluded that 1) significant deterioration of coagulation factors occurs during OLT, 2) the TEG is an effective screening test that affords prompt information, 3) aggressive measures should be taken to maintain the patient’ s body temperature at 37°C, 4) patient outcome was not predicted by intraoperative hemostatic evaluation.

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.

Sign in / Sign up

Export Citation Format

Share Document