Liver blood flow measurement in the rat the electromagnetic versus the microsphere and the clearance methods

Daemen, M. J. A. P.; Thijssen, H. H. W.; Essen, Helma van; Vervoort-Peters, H.T.M.; Prinzen, Frits W.; Boudier, H. A. J. Struyker; Smits, J. F. M.

doi:10.1016/0160-5402(89)90066-1

Cited by 44 publications

(12 citation statements)

References 23 publications

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“…This indicates that the H 2 gas clearance technique may be a method that assesses hepatic arterial liver perfusion rather than total hepatic blood flow (243). Moreover, ICG clearance is thought to assess only 30% of the blood flow, which was measured electromagnetically by direct placement of flow probes around the hepatic artery and portal vein (138). This may be due to a significant amount of shunting of electromagnetically measured blood flow which is not detected by the ICG method.…”

Section: B Hydrogen Xenon and Indocyanine Green Clearance Techniquementioning

confidence: 99%

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

Vollmar

Menger²

2009

Physiological Reviews

426

368

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The complex functions of the liver in biosynthesis, metabolism, clearance, and host defense are tightly dependent on an adequate microcirculation. To guarantee hepatic homeostasis, this requires not only a sufficient nutritive perfusion and oxygen supply, but also a balanced vasomotor control and an appropriate cell-cell communication. Deteriorations of the hepatic homeostasis, as observed in ischemia/reperfusion, cold preservation and transplantation, septic organ failure, and hepatic resection-induced hyperperfusion, are associated with a high morbidity and mortality. During the last two decades, experimental studies have demonstrated that microcirculatory disorders are determinants for organ failure in these disease states. Disorders include 1) a dysregulation of the vasomotor control with a deterioration of the endothelin-nitric oxide balance, an arterial and sinusoidal constriction, and a shutdown of the microcirculation as well as 2) an overwhelming inflammatory response with microvascular leukocyte accumulation, platelet adherence, and Kupffer cell activation. Within the sequelae of events, proinflammatory mediators, such as reactive oxygen species and tumor necrosis factor-alpha, are the key players, causing the microvascular dysfunction and perfusion failure. This review covers the morphological and functional characterization of the hepatic microcirculation, the mechanistic contributions in surgical disease states, and the therapeutic targets to attenuate tissue injury and organ dysfunction. It also indicates future directions to translate the knowledge achieved from experimental studies into clinical practice. By this, the use of the recently introduced techniques to monitor the hepatic microcirculation in humans, such as near-infrared spectroscopy or orthogonal polarized spectral imaging, may allow an early initiation of treatment, which should benefit the final outcome of these critically ill patients.

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Section: B Hydrogen Xenon and Indocyanine Green Clearance Techniquementioning

confidence: 99%

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

Vollmar

Menger²

2009

Physiological Reviews

426

368

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“…The liver still has an important role in ammonia clearance because the hepatic relative 13 N concentrations in PCS rats are at least as great as in normal rats even though their urea cycle capacity is not high enough to prevent hyperammonemia. In normal rats about 12% of blood flow to the liver is via the hepatic artery [50] compared with a higher proportion in dogs, sheep, and humans (about 20–35%) [51–53], and the remainder is via the portal vein. However, in PCS rats at early times after [ 13 N]ammonia injection into a femoral vein, the label is expected to arrive at the liver exclusively via the hepatic artery, which is intact in the PCS rats and which maintains a 2.7-fold increase in blood flow per gram of liver compared to that of normal liver [54], perhaps explaining the tendency for a higher-than-normal 13 N relative concentration in the livers of PCS rats in the first 5 min after the bolus injection of [ 13 N]ammonia.…”

Section: Discussionmentioning

confidence: 99%

Organ Distribution of 13N Following Intravenous Injection of [13N]Ammonia into Portacaval-Shunted Rats

et al. 2016

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Ammonia is neurotoxic, and chronic hyperammonemia is thought to be a major contributing factor to hepatic encephalopathy in patients with liver disease. Portacaval shunting of rats is used as an animal model to study the detrimental metabolic effects of elevated ammonia levels on body tissues, particularly brain and testes that are deleteriously targeted by high blood ammonia. In normal adult rats, the initial uptake of label (expressed as relative concentration) in these organs was relatively low following a bolus intravenous injection of [13N]ammonia compared with lungs, kidneys, liver, and some other organs. The objective of the present study was to determine the distribution of label following intravenous administration of [13N]ammonia among 14 organs in portacaval-shunted rats at 12 weeks after shunt construction. At an early time point (12 sec) following administration of [13N]ammonia the relative concentration of label was highest in lung with lower, but still appreciable relative concentrations in kidney and heart. Clearance of 13N from blood and kidney tended to be slower in portacaval-shunted rats versus normal rats during the 2–10 min interval after the injection. At later times post injection, brain and testes tended to have higher-than-normal 13N levels, whereas many other tissues had similar levels in both groups. Thus, reduced removal of ammonia from circulating blood by the liver diverts more ammonia to extrahepatic tissues, including brain and testes, and alters the nitrogen homeostasis in these tissues. These results emphasize the importance of treatment paradigms designed to reduce blood ammonia levels in patients with liver disease.

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“…Based on a portal blood flow of about 15 ml min -, measured by using an electromagnetical flow probe the control stimulation area which was set as 100 + 6% (*** P < 0.001, versus both control and atropinetreated rats). (Daemen et al, 1989) (Muscholl et al, 1979). Fuder et al (1985) also demonstrated an inhibition of the NA overflow using this selective muscarinic agonist at concentrations of 1 and 10 M in guinea-pig isolated atria.…”

Section: Discussionmentioning

confidence: 99%

Presynaptic muscarinic receptors inhibiting endogenous noradrenaline release in the portal vein of the freely moving rat

Remie

Coppes

Zaagsma

1989

British J Pharmacology

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1 In the portal vein of the freely moving unanaesthetized rat, the existence of presynaptically located inhibitory muscarinic receptors was investigated by use of the muscarinic agonist methacholine (MCh) 2 Infusion of MCh (0.3pgmin-1) did not significantly inhibit the endogenous noradrenaline (NA) overflow in portal plasma. However, after inducing high intra-synaptic concentrations of NA by blocking the presynaptic a2-adrenoceptors with yohimbine (lmgkg-1), MCh (0.3jpgmin-1) was able to reduce the yohimbine-induced enhanced NA overflow by 38%. 3 The MCh-induced inhibition was almost completely abolished after blockade of the presynaptic muscarinic receptors with atropine (0.6 mg kg~-). 4 During electrical stimulation of the portal vein nervous plexus the evoked NA overflow was strongly inhibited (95%) during MCh-infusion (0.3jugmin'). Again atropine (0.6 mgkg 1) was able to reverse this inhibition. 5 These results show the existence of presynaptic muscarinic receptors inhibiting endogenous NA overflow from the portal vein nervous plexus under conditions of enhanced sympathetic activity in the freely moving rat.

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Liver blood flow measurement in the rat the electromagnetic versus the microsphere and the clearance methods

Cited by 44 publications

References 23 publications

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

Organ Distribution of 13N Following Intravenous Injection of [13N]Ammonia into Portacaval-Shunted Rats

Presynaptic muscarinic receptors inhibiting endogenous noradrenaline release in the portal vein of the freely moving rat

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