| Hemodynamic changes in the kidney in a pediatric rat model of sepsis-induced acute kidney injury. | |
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MedLine Citation:
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PMID: 21511700 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Sepsis is a leading cause of acute kidney injury (AKI) and mortality in children. Understanding the development of pediatric sepsis and its effects on the kidney are critical in uncovering new therapies. The goal of this study was to characterize the development of sepsis-induced AKI in the clinically relevant cecal ligation and puncture (CLP) model of peritonitis in rat pups 17-18 days old. CLP produced severe sepsis demonstrated by time-dependent increase in serum cytokines, NO, markers of multiorgan injury, and renal microcirculatory hypoperfusion. Although blood pressure and heart rate remained unchanged after CLP, renal blood flow (RBF) was decreased 61% by 6 h. Renal microcirculatory analysis showed the number of continuously flowing cortical capillaries decreased significantly from 69 to 48% by 6 h with a 66% decrease in red blood cell velocity and a 57% decline in volumetric flow. The progression of renal microcirculatory hypoperfusion was associated with peritubular capillary leakage and reactive nitrogen species generation. Sham adults had higher mean arterial pressure (118 vs. 69 mmHg), RBF (4.2 vs. 1.1 ml·min(-1)·g(-1)), and peritubular capillary velocity (78% continuous flowing capillaries vs. 69%) compared with pups. CLP produced a greater decrease in renal microcirculation in pups, supporting the notion that adult models may not be the most appropriate for studying pediatric sepsis-induced AKI. Lower RBF and reduced peritubular capillary perfusion in the pup suggest the pediatric kidney may be more susceptible to AKI than would be predicted using adults models. |
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Authors:
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Kathryn A Seely; Joseph H Holthoff; Samuel T Burns; Zhen Wang; Keshari M Thakali; Neriman Gokden; Sung W Rhee; Philip R Mayeux |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-04-20 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 301 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-07-07 Completed Date: 2011-09-08 Revised Date: 2012-01-20 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F209-17 Citation Subset: IM |
Affiliation:
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Dept. of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, 4301 West Markham St., #611, Little Rock, AR 72205, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute Kidney Injury
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etiology,
pathology,
physiopathology* Animals Animals, Newborn Biological Markers / blood Blood Flow Velocity / physiology Blood Pressure / physiology Capillary Permeability / physiology Cecum / physiology Fluid Therapy Hemodynamics / physiology* Hypothermia / etiology, physiopathology Immunohistochemistry Kidney / pathology Ligation Male Microcirculation / physiology Multiple Organ Failure / etiology, physiopathology Peritonitis / etiology Rats Rats, Sprague-Dawley Renal Circulation / physiology* Reverse Transcriptase Polymerase Chain Reaction Sepsis / complications, physiopathology* Telemetry |
| Grant Support | |
ID/Acronym/Agency:
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F30 DK-085705/DK/NIDDK NIH HHS; F30 DK085705-02/DK/NIDDK NIH HHS; R01 DK-075991/DK/NIDDK NIH HHS; R01 DK-075991-S1/DK/NIDDK NIH HHS; R01 DK075991-02S1/DK/NIDDK NIH HHS; R01 DK075991-03/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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