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Poor perinatal growth impairs baboon aortic windkessel function

Published online by Cambridge University Press:  11 October 2017

A. H. Kuo*
Affiliation:
Department of Radiology and Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
J. Li
Affiliation:
Xiangya School of Medicine, Central South University, Changsha, Hunan, China Southwest National Primate Research Center, San Antonio, TX, USA
C. Li
Affiliation:
Department of Animal Science, University of Wyoming, Laramie, Wyoming Southwest National Primate Research Center, San Antonio, TX, USA
H. F. Huber
Affiliation:
Department of Animal Science, University of Wyoming, Laramie, Wyoming
P. W. Nathanielsz
Affiliation:
Department of Animal Science, University of Wyoming, Laramie, Wyoming Southwest National Primate Research Center, San Antonio, TX, USA
G. D. Clarke
Affiliation:
Department of Radiology and Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA Southwest National Primate Research Center, San Antonio, TX, USA
*
*Address for correspondence: A. H. Kuo, MD, Department of Radiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, MC 7800, San Antonio, TX 78229-3900, USA. (Email kuoa@uthscsa.edu)

Abstract

The ability of the aorta to buffer blood flow and provide diastolic perfusion (Windkessel function) is a determinant of cardiovascular health. We have reported cardiac dysfunction indicating downstream vascular abnormalities in young adult baboons who were intrauterine growth restricted (IUGR) at birth as a result of moderate maternal nutrient reduction. Using 3 T MRI, we examined IUGR offspring (eight male, eight female; 5.7 years; human equivalent 25 years) and age-matched controls (eight male, eight female; 5.6 years) to quantify distal descending aortic cross-section (AC) and distensibility (AD). ANOVA showed decreased IUGR AC/body surface area (0.9±0.05 cm2/m2v. 1.2±0.06 cm2/m2, M±s.e.m., P<0.005) and AD (1.7±0.2 v. 4.0±0.5×10−3/mmHg, P<0.005) without sex difference or group-sex interaction, suggesting intrinsic vascular pathology and impaired development persisting in adulthood. Future studies should evaluate potential consequences of these changes on coronary perfusion, afterload and blood pressure.

Type
Brief Report
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2017 

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