Effect of intrauterine growth restriction on the number of cardiomyocytes in rat hearts

被引:135
作者
Corstius, HB
Zimanyi, MA
Maka, N
Herath, T
Thomas, W
Van Der Laarse, A
Wreford, NG
Black, MJ
机构
[1] Monash Univ, Dept Anat & Cell Biol, Clayton, Vic 3800, Australia
[2] Leiden Univ, Med Ctr, Dept Cardiol, NL-2300 RC Leiden, Netherlands
[3] Baker Heart Res Inst, Melbourne, Vic 3004, Australia
关键词
D O I
10.1203/01.PDR.0000157726.65492.CD
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Epidentiologic studies have linked intrauterine growth restriction (IUGR) with an increased incidence of cardiovascular disease later in life; reduced cardiomyocyte number in TUGR hearts may underlie such prenatal programming. Our aim was to examine the effect of IUGR, as a result of maternal protein restriction, on the number of cardiomyocytes in the rat heart at birth. Rats were fed either a low-protein diet (LPD) or a normal-protein diet (NPD) during pregnancy. At birth, the offspring were killed and the hearts were immersion-fixed. The number of cardiomyocyte nuclei in the hearts were stereologically determined using an optical disector-fractionator approach. In some litters, cardiomyocytes were enzymatically isolated from freshly excised hearts and the proportion of binucleated cells was determined. Taking into account the number of binucleated cells, the nuclear counts were adjusted to estimate total cardiomyocyte number. Birth weight and heart weight were significantly reduced in the LPD offspring. This was accompanied by a significant reduction in the number of cardiomyocytes per heart in the LPD offspring compared with the NPD offspring (1.18 +/- 0.05 X 10(7) and 1.41 +/- 0.06 X 10(7), respectively; p = 0.001). The number of binucleated cardiomyocytes was low (similar to 3%) and equal in both groups. In conclusion, IUGR as a result of maternal protein restriction leads to a reduction in the number of cardiomyocytes per heart. As cardiomyocyte proliferation is rare after birth, it is plausible that this reduction in cardiomyocytes may lead to compromised cardiac function later in life.
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页码:796 / 800
页数:5
相关论文
共 45 条
  • [1] MYOCYTE MITOTIC DIVISION IN THE AGING MAMMALIAN RAT-HEART
    ANVERSA, P
    FITZPATRICK, D
    ARGANI, S
    CAPASSO, JM
    [J]. CIRCULATION RESEARCH, 1991, 69 (04) : 1159 - 1164
  • [2] MORPHOMETRIC STUDY OF EARLY POSTNATAL-DEVELOPMENT IN THE LEFT AND RIGHT VENTRICULAR MYOCARDIUM OF THE RAT .1. HYPERTROPHY, HYPERPLASIA, AND BINUCLEATION OF MYOCYTES
    ANVERSA, P
    OLIVETTI, G
    LOUD, AV
    [J]. CIRCULATION RESEARCH, 1980, 46 (04) : 495 - 502
  • [3] INFLUENCE OF AGE, GROWTH, AND SEX ON CARDIAC MYOCYTE SIZE AND NUMBER IN RATS
    BAI, SL
    CAMPBELL, SE
    MOORE, JA
    MORALES, MC
    GERDES, AM
    [J]. ANATOMICAL RECORD, 1990, 226 (02): : 207 - 212
  • [4] BARKER DJP, 1989, LANCET, V2, P577
  • [5] The malnourished baby and infant
    Barker, DJP
    [J]. BRITISH MEDICAL BULLETIN, 2001, 60 : 69 - 88
  • [6] Barker DJP, 1998, MOTHERS BABIES HLTH, P1
  • [7] MECHANISMS OF RAPID GROWTH IN THE NEONATAL PIG-HEART
    BEINLICH, CJ
    RISSINGER, CJ
    MORGAN, HE
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (01) : 273 - 281
  • [8] Evidence that human cardiac myocytes divide after myocardial infarction (Publication with Expression of Concern. See vol. 379, pg. 1870, 2018)
    Beltrami, AP
    Urbanek, K
    Kajstura, J
    Yan, SM
    Finato, N
    Bussani, R
    Nadal-Ginard, B
    Silvestri, F
    Leri, A
    Beltrami, CA
    Anversa, P
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (23) : 1750 - 1757
  • [9] Bertram J F, 1992, Trends Cell Biol, V2, P177, DOI 10.1016/0962-8924(92)90038-O
  • [10] The ageing spontaneously hypertensive rat as a model of the transition from stable compensated hypertrophy to heart failure
    Boluyt, MO
    Bing, OHL
    Lakatta, EG
    [J]. EUROPEAN HEART JOURNAL, 1995, 16 : 19 - 30