4.3 Article

Systemic Arterial Pressure at Maturity in Rats Following Chronic Hypoxia in Early Life

期刊

AMERICAN JOURNAL OF HYPERTENSION
卷 23, 期 11, 页码 1228-1233

出版社

OXFORD UNIV PRESS
DOI: 10.1038/ajh.2010.160

关键词

arterial stiffness; blood pressure; blood pressure variability; cyanotic congenital heart defect; hypertension; rat; telemetry

资金

  1. Canadian Institutes of Health Research
  2. Montreal Children's Hospital Research Institute

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BACKGROUND The effect of prolonged hypoxemia in early life on systemic arterial blood pressure at maturity was assessed in Sprague Dawley rats. METHODS Animals hypoxic in early life (12 males, 10 females) were raised in hypoxia (FiO(2)=0.12) for the first 10 days of life and subsequently raised in normoxia, along with age-matched controls (11 males, 9 females). At 2 months of age, arterial blood pressure was recorded intravascularly using telemetry in awake and unrestrained animals over two 12-h night-time (active) and daytime (resting) periods. Aortic pulse wave velocity was assessed in six additional hypoxic pretreated and five control anesthetized 2-month-old male rats. RESULTS Systolic, mean, and pulse pressures were significantly greater in the hypoxic pretreated group compared to the control group during resting and active periods in both sexes (P <= 0.05). Diastolic pressure and heart rate did not differ between the two groups. Hypoxic pretreated males displayed significantly increased blood pressure variability during the resting period. Aortic pulse wave velocity was also found to be elevated in the hypoxic pretreated rats. CONCLUSIONS Prolonged hypoxic stress in early life in the rat is associated with increased systolic arterial pressure at maturity very likely due to decreased arterial compliance. These findings suggest that a nutrient-independent, postnatal stress may lead to long-lasting vascular alterations predisposing to increased arterial pressure at maturity. This raises the possibility that adult survivors of congenital cyanotic cardiac disease may be at risk for secondary cardiovascular morbidity unrelated to surgical repair or residual cardiac defects.

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