Redistribution of renal blood flow in patients with liver cirrhosis

Sacerdoti, David; Merlo, A.; Merkel, Carlo; Zuin, R; Gatta, Angelo

doi:10.1016/s0168-8278(86)80084-8

Cited by 21 publications

(15 citation statements)

References 40 publications

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“…Indeed, although overall peripheral vascular resistance is clearly decreased, a decrease in resistance is not seen in every vascular bed (Newby and Hayes, 2002). In cirrhosis, splanchnic arterial vessels are markedly dilated and splanchnic blood flow is markedly increased, but blood flow is reduced in the kidney (Epstein et al, 1970;Merkel et al, 1981;Gatta et al, 1982;Sacerdoti et al, 1993), even though the juxtamedullary blood flow is relatively maintained, due to the paracrine action of substances such as prostaglandin PGE 2 (Sacerdoti et al, 1986), and is probably also reduced in the brain (Almdal et al, 1989;Dillon et al, 1995;Guevara et al, 1998a;Dam et al, 1998) and muscles (Maroto et al, 1993). In advanced disease, the imbalance between splanchnic vasodilatation and the reduction of blood flow to other organs worsens (Newby and Hayes, 2002).…”

Section: The Splanchnic Vasodilatationmentioning

confidence: 99%

Vasoactive factors and hemodynamic mechanisms in the pathophysiology of portal hypertension in cirrhosis

Gatta

Bolognesi

Merkel

2008

Molecular Aspects of Medicine

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Section: The Splanchnic Vasodilatationmentioning

confidence: 99%

Vasoactive factors and hemodynamic mechanisms in the pathophysiology of portal hypertension in cirrhosis

Gatta

Bolognesi

Merkel

2008

Molecular Aspects of Medicine

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“…Despite this hyperdynamic circulation, there is increased renal vascular resistance, renal hypoperfusion (35), and retention of water and salt, which precede the development of ascites (30,67). The increase in renal vascular resistance in patients with cirrhosis appears to mainly affect the superficial cortex, sparing medullary blood flow, as suggested by studies using either ultrasound (83,84) or xenon-washout techniques (52). Thus, because more of the RBF is shunted toward the deeper nephrons, which have an enhanced sodium reabsorbing capability, it is possible that this redistribution is contributing to the enhanced sodium and water retention that is typically seen in cirrhosis (104).…”

Section: Use Of Micro-ct To Investigate Disease Conditions In the Kidneymentioning

confidence: 99%

“…Because there is a transcortical gradient of renin, with greater quantities present in the superficial glomeruli than in the juxtamedullary glomeruli (81), it is possible that the increased levels of renin (and angiotensin II) present in the cortex cause a predominant local cortical vasoconstriction in CBDL, thus contributing to the vasoconstriction. Furthermore, the medullary circulation might be preserved due to specific activation of medullary vasodilators such as PGE 2 and/or nitric oxide (35,84).…”

Section: Use Of Micro-ct To Investigate Disease Conditions In the Kidneymentioning

confidence: 99%

The use of microcomputed tomography to study microvasculature in small rodents

Bentley

Ortiz

Ritman

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

135

109

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The use of microcomputed tomography to study microvasculature in small rodents. Am J Physiol Regulatory Integrative Comp Physiol 282: R1267-R1279, 2002 10.1152/ajpregu.00560.2001.-Appropriate nephron function is dependent on the intrarenal arrangement of blood vessels. The preferred and primary means to study the architecture of intrarenal circulation has been by filling it with opaque substances such as india ink, radio-opaque contrast material, or various polymers for study by light or scanning electron microscopy. With such methodologies, superficial vessels may obscure deep vessels and little quantitative information may be obtained. Serial-section microtomy has not been practical because of problems relating to alignment and registration of adjacent sections, lost sections, and preparation time and effort. Microcomputed tomography (micro-CT) overcomes such limitations and provides a means to study the three-dimensional architecture of filled vessels within an intact rodent kidney and to obtain more quantitative information. As an example of micro-CT's capabilities, we review the use of micro-CT to study the alterations in renal microvasculature caused by the development of liver cirrhosis after chronic bile duct ligation. In this example, micro-CT evidence shows a selective decrease in cortical vascular filling in the kidney, with a maintenance of medullary vascular filling. These changes may contribute to the salt and water retention that accompanies cirrhosis. These results indicate that micro-CT is a promising method to evaluate renal vascular architecture in the intact rodent kidney relative to physiological and pathological function. kidney; imaging; microcirculation; vasculature APPROPRIATE NEPHRON FUNCTION appears to be dependent on the detailed three-dimensional interrelationship of blood vessels with the tubular components. Many techniques and/or methods have been developed to examine the microanatomic arrangement of pre-and postglomerular vasculature (4,29,36,40,54,55,59,71,98). In this respect, such efforts were prompted by early studies showing that urinary excretion varied in relation to the intrarenal environment and was dependent on the coupling of renal microcirculation and tubular components. In 1947, Trueta and colleagues (96), studying the crush syndrome in rabbits, observed that there was a shift of blood flow from the renal cortex to the medulla during hemorrhage. They suggested this shift to be the major explanation for the lack of urine flow, despite a preservation of renal blood flow (RBF). The shift of blood flow within the renal cortex from superficial short nephrons to deep long nephrons was later observed in sodium-retaining states such as cardiac insufficiency, hepatic cirrhosis, or hypovolemia (1,18,53,104). showed that changes in renal perfusion pressure, within a range (75-130 mmHg) in which RBF remains unchanged (RBF autoregulation), were followed by dramatic changes in sodium excretion. This situation is comparable to that seen in the early stages Address for reprint requ...

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“…Functional renal impairment in compensated cirrhosis is subclinical, the alterations being a reduction of renal blood flow (RBF), 1 (2,3,4), in particular the cortical component (5,6), usually without depression of GFR (3,4), a blunted response to a sodium load (7), and increased proximal tubular sodium reabsorption (8). When ascites develops, sodium and water excretion are demonstrably impaired, and RBF is decreased further (3,4), effects that may be associated with reduced GFR.…”

Section: Introductionmentioning

confidence: 99%

Eicosanoid excretion in hepatic cirrhosis. Predominance of 20-HETE.

Sacerdoti¹,

Balazy²,

Angeli³

et al. 1997

J. Clin. Invest.

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The cytochrome P450 system transforms AA to hydroxyeicosatetraenoic acid (HETE) metabolites that are vasoactive and affect transport in several nephron segments. A principal product of this system, 20-HETE, participates in key mechanisms that regulate the renal circulation and extracellular fluid volume. We hypothesized that excess production of 20-HETE, which constricts the renal vasculature, contributes to the renal functional disturbances in patients with hepatic cirrhosis, particularly the depression of renal hemodynamics. The development of a precise and sensitive gas chromatographic/mass spectrometric method makes it possible to measure 20-HETE and the subterminal HETEs

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Redistribution of renal blood flow in patients with liver cirrhosis

Cited by 21 publications

References 40 publications

Vasoactive factors and hemodynamic mechanisms in the pathophysiology of portal hypertension in cirrhosis

Vasoactive factors and hemodynamic mechanisms in the pathophysiology of portal hypertension in cirrhosis

The use of microcomputed tomography to study microvasculature in small rodents

Eicosanoid excretion in hepatic cirrhosis. Predominance of 20-HETE.

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