CT Determination of Renal and Hepatic Microvascular Volumes in Experimental Acute Renal Failure

Hillman, Bruce J.; Lee, Stanley M.; Tracey, Patty; Swindell, W.; Long, David M.

doi:10.1097/00004424-198201000-00008

Cited by 22 publications

(14 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). The percentage of renal mass filled with microfil (i.e., the vascular volume fraction) varied with the regions of the kidney (Table 1) and was similar to that reported by Hillman et al (41).…”

Section: Micro-ct Images Of Rat Kidneyssupporting

confidence: 87%

“…X-ray images of thick slices of the infused tissue are exposed on high-resolution X-ray film and subsequently examined by light microscopy. This methodology has been used to examine vascular changes that occur in experimental disease conditions such as acute renal failure (21,41), diabetic nephropathy (63), papillary necrosis (25), and allograft rejection (22).…”

Section: Vascular Filling Techniquesmentioning

confidence: 99%

“…The vascular volume fractions are determined following the method used by Hillman et al (41). The determinations are made from midtransverse slices that included the cortex, the outer stripe of the outer medulla (OSOM), the inner stripe of the outer medulla (ISOM), and the inner medulla (IM).…”

Section: Analysis Of Imagesmentioning

confidence: 99%

See 2 more Smart Citations

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

View full text Add to dashboard Cite

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...

show abstract

Section: Micro-ct Images Of Rat Kidneyssupporting

confidence: 87%

Section: Vascular Filling Techniquesmentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

show abstract

“…[55][56][57][58] Briefly, animals were placed in the center of the CT scanner (Locus Ultra; GE Medical Systems, Milwaukee, Wisconsin) and a tail-vein catheter was inserted (BD Biosciences) for contrast agent injection. Single-location multisection (80 rows) cine CT scanning was begun 3 s before a bolus of 300 l of iodinated contrast medium (150 mg/ml, Omnipaque; Amersham, Princeton, New Jersey) was administered via the tail vein at a rate of 3 ml/min.…”

Section: Functional Ct and Quantification Of Perfusion Parametersmentioning

confidence: 99%

Distinct Functions of Activated Protein C Differentially Attenuate Acute Kidney Injury

Gupta

Gerlitz

Richardson

et al. 2009

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Administration of activated protein C (APC) protects from renal dysfunction, but the underlying mechanism is unknown. APC exerts both antithrombotic and cytoprotective properties, the latter via modulation of protease-activated receptor-1 (PAR-1) signaling. We generated APC variants to study the relative importance of the two functions of APC in a model of LPS-induced renal microvascular dysfunction. Compared with wild-type APC, the K193E variant exhibited impaired anticoagulant activity but retained the ability to mediate PAR-1-dependent signaling. In contrast, the L8W variant retained anticoagulant activity but lost its ability to modulate PAR-1. By administering wild-type APC or these mutants in a rat model of LPS-induced injury, we found that the PAR-1 agonism, but not the anticoagulant function of APC, reversed LPS-induced systemic hypotension. In contrast, both functions of APC played a role in reversing LPS-induced decreases in renal blood flow and volume, although the effects on PAR-1-dependent signaling were more potent. Regarding potential mechanisms for these findings, APC-mediated PAR-1 agonism suppressed LPS-induced increases in the vasoactive peptide adrenomedullin and infiltration of iNOS-positive leukocytes into renal tissue. However, the anticoagulant function of APC was responsible for suppressing LPS-induced stimulation of the proinflammatory mediators ACE-1, IL-6, and IL-18, perhaps accounting for its ability to modulate renal hemodynamics. Both variants reduced active caspase-3 and abrogated LPS-induced renal dysfunction and pathology. We conclude that although PAR-1 agonism is solely responsible for APC-mediated improvement in systemic hemodynamics, both functions of APC play distinct roles in attenuating the response to injury in the kidney. 20: 267-277, 200920: 267-277, . doi: 10.1681 Acute kidney injury (AKI) leading to renal failure is a devastating disorder, 1 with a prevalence varying from 30 to 50% in the intensive care unit. 2 AKI during sepsis results in significant morbidity, and is an independent risk factor for mortality. 3,4 In patients with severe sepsis or shock, the reported incidence ranges from 23 to 51% 5-7 with mortality as high as 70% versus 45% among patients with AKI alone. 1,8 The pathogenesis of AKI during sepsis involves hemodynamic alterations along with microvascular impairment. 4 Although many factors change during sepsis, suppression of the plasma serine protease, protein C (PC), has been shown to be predictive of early death in sepsis models, 9 and clinically has been associated with early death resulting from refractory shock and multiple organ failure in severe sepsis. 10 Moreover, low levels of PC have been J Am Soc Nephrol

show abstract

“…The tissue volume was then determined by multiplying the tissues of interest by the total scanned volume of the image. The volume fraction of vasculature in each of the renal tissues was determined following the method of Hillman et al (14). The determinations were made from midtransverse slices that included the cortex, the outer stripe of the outer medulla, the inner stripe of the outer medulla, and the inner medulla.…”

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

View full text Add to dashboard Cite

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...

show abstract

CT Determination of Renal and Hepatic Microvascular Volumes in Experimental Acute Renal Failure

Cited by 22 publications

References 0 publications

The use of microcomputed tomography to study microvasculature in small rodents

The use of microcomputed tomography to study microvasculature in small rodents

Distinct Functions of Activated Protein C Differentially Attenuate Acute Kidney Injury

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

Contact Info

Product

Resources

About