Microcomputed tomography of kidneys following chronic bile duct ligation

Ortiz, Mariela; Garcia-Sanz, A.; Bentley, Michael D.; Fortepiani, Lourdes A.; Garcı́a-Estañ, Joaquı́n; Ritman, Erik L.; Romero, J. Carlos; Juncos, Luis A.

doi:10.1111/j.1523-1755.2000.00324.x

Cited by 48 publications

(35 citation statements)

References 34 publications

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“…[25][26][27][28] In addition, the implementation of quantitative analyses of 3D vascular networks revealed a previously unrecognized reduction of vessel branches during disease progression paralleled by increased tortuosity of the remaining vessels. Extending previous studies, [51][52][53] we found that not only post-glomerular vessels, i.e., capillaries, but all large-to-small-sized blood vessels in the kidney exhibited substantially reduced luminal diameters during disease progression.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported on Microfil perfusion of the renal vasculature in mice and rats. [25][26][27][28] Here, we used this highresolution ex vivo mCT method to analyze vessel morphometrics that can be derived from perfused renal vasculature, such as branching, size and tortuosity, in progressive kidney fibrosis.…”

Section: Peritubular Capillary Rarefaction Correlates With Fibrosis Imentioning

confidence: 99%

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Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Ehling¹,

Bábíčková

Gremse

et al. 2016

Journal of the American Society of Nephrology

124

131

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Progressive kidney diseases and renal fibrosis are associated with endothelial injury and capillary rarefaction. However, our understanding of these processes has been hampered by the lack of tools enabling the quantitative and noninvasive monitoring of vessel functionality. Here, we used micro-computed tomography (mCT) for anatomical and functional imaging of vascular alterations in three murine models with distinct mechanisms of progressive kidney injury: ischemia-reperfusion (I/R, days 1-56), unilateral ureteral obstruction (UUO, days 1-10), and Alport mice (6-8 weeks old). Contrast-enhanced in vivo mCT enabled robust, noninvasive, and longitudinal monitoring of vessel functionality and revealed a progressive decline of the renal relative blood volume in all models. This reduction ranged from 220% in early disease stages to 261% in late disease stages and preceded fibrosis. Upon Microfil perfusion, high-resolution ex vivo mCT allowed quantitative analyses of three-dimensional vascular networks in all three models. These analyses revealed significant and previously unrecognized alterations of preglomerular arteries: a reduction in vessel diameter, a prominent reduction in vessel branching, and increased vessel tortuosity. In summary, using mCT methodology, we revealed insights into macro-to-microvascular alterations in progressive renal disease and provide a platform that may serve as the basis to evaluate vascular therapeutics in renal disease.

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Section: Discussionmentioning

confidence: 99%

Section: Peritubular Capillary Rarefaction Correlates With Fibrosis Imentioning

confidence: 99%

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Ehling¹,

Bábíčková

Gremse

et al. 2016

Journal of the American Society of Nephrology

124

131

View full text Add to dashboard Cite

show abstract

“…To prepare rat kidneys for micro-CT, the blood is flushed from renal vasculature at physiological pressure with an infusion of heparinized 0.9% saline (37,69). The infusion is continued with a formalin solution to fix the tissue, and the free formalin is flushed from the kidneys with a saline solution.…”

Section: Preparation Of Tissue For Micro-ctmentioning

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

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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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“…However, previous information has not been available in regards to microvessel density in renal tissue during the hypertension. To measure the changes in microvasculature, we used micro-CT, which provides a means to obtain quantitative volumetric information (6,15,22). NO is an important physiological antagonist of vasoconstrictors such as ANG II.…”

Section: Discussionmentioning

confidence: 99%

“…Losartan was used to determine the role of AT 1 receptors. To examine and measure the changes in renal vasculature, we used a three-dimensional X-ray microcomputed tomography (micro-CT) system (6,15,22). These changes were further evaluated by histological examination.…”

mentioning

confidence: 99%

Effect of losartan on renal microvasculature during chronic inhibition of nitric oxide visualized by micro-CT

Fortepiani

Ruiz

Passardi

et al. 2003

American Journal of Physiology-Renal Physiology

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G -nitro-Larginine methyl ester (L-NAME) leads to an elevated systemic blood pressure and reduction in renal blood flow without significant changes in urinary sodium and water excretion. Simultaneous administration of ANG II AT 1 receptor antagonist losartan and L-NAME prevents the alterations in blood pressure and renal hemodynamics. Microcomputed tomography (micro-CT) was used to investigate the role of ANG II in the changes of renal microvasculature during chronic NO inhibition. Sprague-Dawley rats were given L-NAME with or without AT 1 receptor antagonist losartan (40 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 each) in their drinking water for 19 days. Kidneys from each group (control, L-NAME-, and L-NAME ϩ losartan-treated rats) were perfusion-fixed in situ, infused with a silicon-based polymer containing lead chromate, and scanned by micro-CT. The microvasculature in the reconstructed three-dimensional renal images was studied using computerized analytic techniques. Kidneys of L-NAMEtreated rats had significantly fewer normal glomeruli (28,824 Ϯ 838) than those of control rats (36,266 Ϯ 3,572). Losartan normalized the number to control values (34,094 Ϯ 1,536). The amount of vasculature in the cortex, outer medulla, and inner medulla of L-NAME-treated rats was about two-thirds that of control rats; losartan normalized the values to control levels. These data indicate that chronic treatment with the NO synthase inhibitor L-NAME produces a generalized rarefaction of renal capillaries. Because simultaneous AT1 receptor blockade abolished those changes, the data suggest that the reduction in vasculature is mediated by ANG II through AT 1 receptors. NG -nitro-L-arginine methyl ester; angiotensin II NITRIC OXIDE (NO) is a physiologically important vasodilator, which plays a major role in the regulation of systemic and renal hemodynamics (16). Chronic inhibition of NO synthesis produces a general vasoconstriction that leads to an increased blood pressure and impairment of renal function including decreased renal blood flow (RBF) and glomerular filtration rate (GFR) without significant changes in urinary sodium and water excretion (3,11,30). Besides the functional changes, the inhibition of NO synthesis produces renal vascular damage including glomerulosclerosis, ischemia, necrosis, and increased interstitium (12, 24). The mechanism underlying the effect of NO synthesis inhibition is not completely understood, but it is likely that the renin-angiotensin system is responsible for the renal and systemic alterations induced by the chronically reduced NO bioavailability. For instance, the simultaneous blockade of NO synthesis and ANG II AT 1 receptor prevents the hypertension, renal functional and morphological consequences of the inhibition of NO synthesis alone (35). Ohishi et al. (20) found that the blockade of ANG II AT 1 receptors attenuated the vasoconstriction elicited by the inhibition of NO synthesis in juxtamedullary afferent and efferent arterioles perfused in vitro. In vivo experiments (23) showed that NO modulated the ANG II re...

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Microcomputed tomography of kidneys following chronic bile duct ligation

Abstract: The results indicate that after CBDL, there is a selective decrease in cortical vascular filling, which may contribute to the salt and water retention that accompanies cirrhosis.

Cited by 48 publications

References 34 publications

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

Quantitative Micro-Computed Tomography Imaging of Vascular Dysfunction in Progressive Kidney Diseases

The use of microcomputed tomography to study microvasculature in small rodents

Effect of losartan on renal microvasculature during chronic inhibition of nitric oxide visualized by micro-CT

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