Estimation of Hepatic Blood Flow With Indocyanine Green*

Leevy, Carroll M.; Mendenhall, Charles L.; Lesko, William; Howard, Maceo M.

doi:10.1172/jci104570

Cited by 375 publications

(171 citation statements)

References 22 publications

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“…Hepatic blood flow was estimated using the indocyanine clearance method as described by Leevy et al [14]. Uusardo et al [15] showed that hepatic blood flow can be used as an approximation for splanchnic perfusion.…”

Section: Discussionmentioning

confidence: 99%

The effect of a pre‐operative infusion of Ringer's solution on splanchnic perfusion in patients undergoing coronary artery bypass grafting

Klein¹,

Osmer

Müller

et al. 2002

Anaesthesia

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SummarySurgical patients develop a fluid deficit during pre-operative starvation. This study examines the effects of pre-operative fluid administration on haemodynamic variables, oxygenation and splanchnic perfusion in patients undergoing elective coronary artery bypass grafting. Forty-eight patients were randomised to receive either a pre-operative crystalloid infusion (crystalloid group, n ¼ 24) or no infusion (control group, n ¼ 24). Patients in the crystalloid group received a continuous infusion of Ringer's solution at 1.5 ml.kg )1 .h )1 from 22:00 h until induction of anaesthesia the next morning. Immediately before induction of anaesthesia, all patients were given a colloid infusion to increase pulmonary capillary wedge pressure and central venous pressure to similar levels in both groups. Haemodynamic and oxygenation parameters were measured using invasive cardiovascular monitoring, and splanchnic perfusion was assessed by indocyanine green clearance. Patients in the crystalloid group received a mean (SD) of 1008 (140) ml of Ringer's solution overnight. Patients in the crystalloid group had a higher splanchnic blood flow than the control group before induction of anaesthesia [mean (SD) ¼ 1782 (573) ml.min )1 vs. 1391 (333) ml.min )1 , p < 0.05]. There were no significant differences in systemic haemodynamic data and global oxygenation parameters between the two groups. Pre-operative infusion of crystalloid appears to result in an improvement in pre-operative splanchnic perfusion.

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Section: Discussionmentioning

confidence: 99%

The effect of a pre‐operative infusion of Ringer's solution on splanchnic perfusion in patients undergoing coronary artery bypass grafting

Klein¹,

Osmer

Müller

et al. 2002

Anaesthesia

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“…The median (of the reported mean HBF in the individual studies) was 1.18 L/min (range 0.93-1.90). In seven studies (with ICG and similar methodology) comprising 60 healthy controls or patients without evidence of liver disease 1,[38][39][40][41][42][43] , nϭ11), ALF (nϭ12), cirrhosis without hepatic encephalopathy (nϭ18), and AOCLD (nϭ9). NS, not significant (P ϭ .053); * P Ͻ .05; ** P Ͻ .01; *** P Ͻ .005; **** P Ͻ .001. with these studies.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Clemmesen

Gerbes²,

Gülberg³

et al. 1999

Hepatology

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Liver failure represents a major therapeutic challenge, and yet basic pathophysiological questions about hepatic perfusion and oxygenation in this condition have been poorly investigated. In this study, hepatic blood flow (HBF) and splanchnic oxygen delivery (DO 2,sp ) and oxygen consumption (VO 2,sp ) were assessed in patients with liver failure defined as hepatic encephalopathy grade II or more. Measurements were repeated after high-volume plasmapheresis (HVP) with exchange of 8 to 10 L of plasma. HBF was estimated by use of constant infusion of D-sorbitol and calculated according to Fick's principle from peripheral artery and hepatic vein concentrations. In 14 patients with acute liver failure (ALF), HBF (1.78 ؎ 0.78 L/min) and VO 2,sp (3.9 ؎ 0.9 mmol/min) were higher than in 11 patients without liver disease (1.07 ؎ 0.19 L/min, P F .01) and (2.3 ؎ 0.7 mmol/min, P F .001). In 9 patients with acute on chronic liver disease (AOCLD), HBF (1.96 ؎ 1.19 L/min) and VO 2,sp (3.9 ؎ 2.3 mmol/min) were higher than in 18 patients with stable cirrhosis (1.00 ؎ 0.36 L/min, P F .005; and 2.0 ؎ 0.6 mmol/min, P F .005). During HVP, HBF increased from 1.67 ؎ 0.72 to 2.07 ؎ 1.11 L/min (n‫)11؍‬ in ALF, and from 1.89 ؎ 1.32 to 2.34 ؎ 1.54 L/min (n‫)7؍‬ in AOCLD, P F .05 in both cases. In patients with ALF, cardiac output (thermodilution) was unchanged (6.7 ؎ 2.5 vs. 6.6 ؎ 2.2 L/min, NS) during HVP. Blood flow was redirected to the liver as the systemic vascular resistance index increased (1,587 ؎ 650 vs. 2,020 ؎ 806 Dyne · s · cm ؊5 · m 2 , P F .01) whereas splanchnic vascular resistance was unchanged. In AOCLD, neither systemic nor splanchnic vascular resistance was affected by HVP, but as cardiac output increased from 9.1 ؎ 2.8 to 10.1 ؎ 2.9 L/min (P F .01) more blood was directed to the splanchnic region. In all liver failure patients treated with HVP (n‫,)81؍‬ DO 2,sp increased by 15% (P F .05) whereas VO 2,sp was unchanged. Endothelin-1 (ET-1) and ET-3 were determined before and after HVP. Changes of ET-1 were positively correlated with changes in HBF (P F .005) and VO 2,sp (P F .05), indicating a role for ET-1 in splanchnic circulation and oxygenation. ET-3 was negatively correlated with systemic vascular resistance index before HVP (P F .05) but changes during HVP did not correlate. Our data suggest that liver failure is associated with increased HBF and VO 2,sp . HVP further increased HBF and DO 2,sp but VO 2,sp was unchanged, indicating that splanchnic hypoxia was not present.(HEPATOLOGY 1999;29: 347-355.)A basic requirement for organ function is adequate blood flow and oxygen delivery. Hepatic blood flow (HBF) and splanchnic oxygenation in patients with liver failure (in the present study, defined as having developed hepatic encephalopathy [HE] grade II or more) have not been assessed because a method to estimate HBF in such patients has not been available until recently. 1,2 Knowledge in this field, therefore, rests on indirect evidence and animal experiments. The observation that whole-body (systemic) oxygen consumpti...

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“…Blood gluconeogenic amino acids were determined using high-performance liquid chromatography (11). Indocyanine green was measured spectrophotometrically at 810 nm to estimate hepatic blood flow, according to the method of Leevy et al (12). Hepatic glycogen content was measured as previously described (13).…”

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confidence: 99%

Small Increases in Insulin Inhibit Hepatic Glucose Production Solely Caused by an Effect on Glycogen Metabolism

et al. 2001

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Based on our earlier work, a 2.5-fold increase in insulin secretion should completely inhibit hepatic glucose production through the hormone's direct effect on hepatic glycogen metabolism. The aim of the present study was to test the accuracy of this prediction and to confirm that gluconeogenic flux, as measured by three independent techniques, was unaffected by the increase in insulin. A 40-min basal period was followed by a 180-min experimental period in which an increase in insulin was induced, with euglycemia maintained by peripheral glucose infusion. Arterial and hepatic sinusoidal insulin levels increased from 10 ؎ 2 to 19 ؎ 3 and 20 ؎ 4 to 45 ؎ 5 U/ml, respectively. Net hepatic glucose output decreased rapidly from 1.90 ؎ 0.13 to 0.23 ؎ 0.16 mg ⅐ kg ؊1 ⅐ min ؊1 . Three methods of measuring gluconeogenesis and glycogenolysis were used: 1) the hepatic arteriovenous difference technique (n ‫؍‬ 8), 2) the [ (1) showed that hepatic glucose production (HGP) can be inhibited by selective increases in the arterial or portal vein insulin concentration. In response to a 14-U/ml increase in arterial insulin (no change in portal insulin), a Ͼ50% reduction in net hepatic glucose output (NHGO) was observed. Likewise, a 14-U/ml increase in portal insulin (no change in arterial insulin) also resulted in a Ͼ50% reduction in NHGO. In addition, the above studies showed that insulin acted directly on the liver, with a rise in hepatic sinusoidal insulin quickly inhibiting HGP by reducing net hepatic glycogenolysis. The indirect effect of insulin on HGP, on the other hand, resulted from a decrease in gluconeogenic flux rate caused by a reduction in the flow of gluconeogenic amino acids and glycerol to the liver and diversion of carbon derived from glycogenolysis to lactate rather than glucose. The reduction in HGP in this group was also, in part, the result of a decrease in net hepatic glycogenolysis, which occurred as a result of a slight rise in the hepatic sinusoidal insulin level, which, in turn, occurred as a result of the rise in hepatic artery insulin. It took 1 h to detect a significant indirect effect of insulin on HGP.Sindelar et al.(1) created selective changes in the arterial or portal insulin level by infusing somatostatin to inhibit insulin secretion and replacing insulin by infusion through a peripheral and/or portal catheter. Stimulation of pancreatic insulin secretion, on the other hand, results in an increase in both portal and arterial levels of the hormone. Therefore, in the present study, our aim was to determine if a two-to threefold increase in insulin, occurring simultaneously in portal and peripheral blood, would inhibit HGP primarily through an effect on glycogen metabolism. Although Sindelar et al. (1) reported that portally delivered insulin did not affect gluconeogenic flux, their estimate of the latter relied solely on the measurement of the net hepatic uptake (arteriovenous [AV] difference) of gluconeogenic precursors. In the present study, we combined the hepatic AV difference technique, along...

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Estimation of Hepatic Blood Flow With Indocyanine Green*

Cited by 375 publications

References 22 publications

The effect of a pre‐operative infusion of Ringer's solution on splanchnic perfusion in patients undergoing coronary artery bypass grafting

The effect of a pre‐operative infusion of Ringer's solution on splanchnic perfusion in patients undergoing coronary artery bypass grafting

Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Small Increases in Insulin Inhibit Hepatic Glucose Production Solely Caused by an Effect on Glycogen Metabolism

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