© 2002 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Cardiovascular response to acute hypoxemia in adult rats hypoxemic neonatally
Department of Pediatrics McGill University & Division of Cardiology Montréal Children's Hospital, 2300 Tupper Street, Montréal, Québec, Canada H3H 1P3
* Corresponding author. Tel.: +1-514-934-4423; fax: +1-514-934-4391 charles.rohlicek{at}mcgill.ca
Objective: To determine the effects of chronic hypoxemia neonatally on the cardiovascular response to acute hypoxemia in adulthood. Methods: Experiments were conducted on adult rats (82±2 days) which had been made chronically hypoxemic (hypobaric hypoxia equivalent to FiO2=0.14) during the first ten days of life but raised in room air (Neonatally Hypoxemia) as well as on adult rats never previously hypoxemic (Control). The animals were instrumented with catheters in the right common carotid artery and superior vena cava for measurements of mean systemic arterial pressure (MAP), central venous pressure, heart rate (HR), arterial blood gases, and arterial as well as mixed venous O2 saturation. Oxygen consumption (
O2) was measured allowing calculation of cardiac index (CI), stroke volume index (SVI) and systemic vascular resistance index (SVRI). The rats were made acutely hypoxemic by exposure to FiO2=0.10 for 20 min. Results: HR increased and MAP decreased to similar extents in both groups during acute hypoxemia. However, SVI and CI increased significantly (P<0.05) during acute hypoxemia in the Neonatally Hypoxemic group (24±6%, 41±8%) but respectively decreased and did not change in the Control animals (–13±6%, 2±6%). SVRI fell significantly more during hypoxemia in the Neonatally Hypoxemic animals than in the Control group (36±4% vs. 14±5%). Conclusions: Hypoxemia experienced in early life has long-term effects on the cardiovascular response to acute hypoxemia at maturity. This may have important implications for individuals hypoxemic in early life due to congenital cyanotic heart defects or pulmonary disease secondary to prematurity.
KEYWORDS Hypoxia/anoxia; Developmental biology; Hemodynamics; Ventricular function; Vasoconstriction/dilation
2 Present address: Department of Physiology, Nippon Dental University, 1-9-20 Fujimi, Chiyoda-ku, Tokyo, 102-8158, Japan.
1 Present address: Department of Nursing, Shinshu University School of Allied Medical Sciences, 3-1-1 Asahi, Matsumoto, Nagano 390-8261, Japan.
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