Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure*

Lieberman, Fred L.; Reynolds, Telfer B.

doi:10.1172/jci105622

Cited by 217 publications

(71 citation statements)

References 38 publications

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“…However, there were increases in the plasma concentration of albumin in six patients. The proportion of the injected dose of '4C incorporated into albumin was higher (Fa/Fb greater than unity, Table II) ing to be increased in patients with liver disease (12)(13)(14)(15). Only one of our patients had an unequivocally elevated plasma volume, but the mean plasma volume for the group was higher than that for the controls.…”

Section: Resultsmentioning

confidence: 99%

Augmentation of albumin but not fibrinogen synthesis by corticosteroids in patients with hepatocellular disease

Cain¹,

Mayer²,

Jones³

1970

J. Clin. Invest.

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A B S T R A C T Simultaneous studies of albumin and fibrinogen metabolism have been conducted using the carbonate-14C method before and after a 13 day course of prednisolone in eight patients with hepatocellular disease. Initially six patients were hypoalbuminemic. The mean plasma albumin and fibrinogen concentrations and albumin and fibrinogen synthetic rates were all lower than the corresponding values in a group of control subjects. Prednisolone therapy was associated with significant increases in the plasma concentration and synthetic rate of albumin but changes in the intravascular albumin pools were not significant. It is inferred that a low synthetic rate of albumin in a patient with liver disease does not necessarily represent the maximum capacity of the diseased liver to synthesize this protein.Changes in the plasma concentration, intravascular pool, and synthetic rate of fibrinogen were small and inconsistent. The data are compatible with a selective action of corticosteroids on hepatic protein metabolism and with the existence of different mechanisms for the control of albumin and fibrinogen synthesis.

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Section: Resultsmentioning

confidence: 99%

Augmentation of albumin but not fibrinogen synthesis by corticosteroids in patients with hepatocellular disease

Cain¹,

Mayer²,

Jones³

1970

J. Clin. Invest.

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“…Cirrhotic patients have a cardiovascular disturbance characterized by low arterial pressure, high cardiac output, and increased plasma volume (1)(2)(3)(4). Besides arteriolar vasodilation and arteriovenous shunting, these patients exhibit a diminished sensitivity to pressor hormones and impaired hypoxic vasoconstriction (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Liver cirrhosis induces renal and liver phospholipase A2 activity in rats.

Vishwanath¹,

Frey²,

Escher³

et al. 1996

J. Clin. Invest.

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Maintenance of renal function in liver cirrhosis requires increased synthesis of arachidonic acid derived prostaglandin metabolites. Arachidonate metabolites have been reported to be involved in modulation of liver damage. The purpose of the present study was to establish whether the first enzyme of the prostaglandin cascade synthesis, the phospholipase A 2 (PLA 2 ) is altered in liver cirrhosis induced by bile duct excision. the mRNA of PLA 2 (group I and II) and annexin-I a presumptive inhibitor of PLA 2 enzyme was measured by PCR using glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as an internal standard. The mean mRNA ratio of group II PLA 2 /GAPDH was increased in liver tissue by 126% ( P Ͻ 0.001) and in kidney tissue by 263% ( P Ͻ 0.006) following induction of liver cirrhosis. The increase in group II PLA 2 mRNA in cirrhotic animals was reflected by an increase in PLA 2 protein and enzyme activity in both liver and kidney tissues. Since the mRNA of group I PLA 2 was not detectable and Group IV PLA 2 activity measured in liver and kidney tissue samples was very low and not changed following induction of cirrhosis, it is likely that the major PLA 2 activity measured in liver and kidney corresponds to group II PLA 2 enzyme. The mean mRNA ratio of annexin-I/GAPDH was increased in liver tissue by 115% ( P Ͻ 0.05) but unchanged in kidney tissue following induction of cirrhosis. The protein content of annexin-I and -V were not affected by bile duct excision in liver and kidney tissue indicating that upregulation of group II PLA 2 activity was not due to downregulation of annexin-I or -V. Group II PLA 2 activity of glomerular mesangial cells stimulated by interleukin-1 ␤ was enhanced by bile juice and various bile salts. In conclusion, activity of group II PLA 2 is upregulated partly due to enhanced transcription and translation in cirrhosis and is furthermore augmented by elevated levels of bile salts. ( J. Clin. Invest. 1996. 98:365-371.)

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“…They are renal sodium retention and a reduction in glomerular filtration rate occurring spontaneously or during drug-induced natriuresis. Measurements of total plasma volume during exhibition of these phenomena, however, indicate increases above normal (1)(2)(3)(4)(5)(6)(7)(8)(9)(10), and these increases cannot be accounted for by leakage of the measuring substance from the plasma during mixing (8). The presence of a reduced effective or nonportal plasma volume has been inferred as an alternative explanation (11,12).…”

Section: Introductionmentioning

confidence: 99%

Effective plasma volume in cirrhosis with ascites. Evidence that a decreased value does not account for renal sodium retention, a spontaneous reduction in glomerular filtration rate (GFR), and a fall in GFR during drug-induced diuresis

Lieberman¹,

Ito²,

Reynolds³

1969

J. Clin. Invest.

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Plasma Volume in Cirrhosis of the Liver: Its Relation of Portal Hypertension, Ascites, and Renal Failure*

Cited by 217 publications

References 38 publications

Augmentation of albumin but not fibrinogen synthesis by corticosteroids in patients with hepatocellular disease

Augmentation of albumin but not fibrinogen synthesis by corticosteroids in patients with hepatocellular disease

Liver cirrhosis induces renal and liver phospholipase A2 activity in rats.

Effective plasma volume in cirrhosis with ascites. Evidence that a decreased value does not account for renal sodium retention, a spontaneous reduction in glomerular filtration rate (GFR), and a fall in GFR during drug-induced diuresis

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