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HIGHLIGHTED TOPICS
Physiology and Pathophysiology of Sleep Apnea
1Division of Toxicology, Lovelace Respiratory Research Institute, Albuquerque, New Mexico; 2Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland; and 3University of Pittsburgh, Pittsburgh, Pennsylvania
Submitted 12 April 2005 ; accepted in final form 30 June 2005
We investigated the effects of 1) acute hypoxia and 2) 5 wk of chronic intermittent hypoxia (IH) on the systemic and pulmonary circulations of C57BL/6J mice. Mice were chronically instrumented with either femoral artery or right ventricular catheters. In response to acute hypoxia (4 min of 10% O2; n = 6), systemic arterial blood pressure fell (P < 0.005) from 107.7 ± 2.5 to 84.7 ± 6.5 mmHg, whereas right ventricular pressure increased (P < 0.005) from 11.7 ± 0.8 to 14.9 ± 1.3 mmHg. Another cohort of mice was then exposed to IH for 5 wk (O2 nadir = 5%, 60-s cycles, 12 h/day) and then implanted with catheters. In response to 5 wk of chronic IH, mice (n = 8) increased systemic blood pressure by 7.5 mmHg, left ventricle + septum weight by 32.2 ± 7.5 x 102 g/100 g body wt (P < 0.015), and right ventricle weight by 19.3 ± 3.2 x 102 g/100 g body wt (P < 0.001), resulting in a 14% increase in the right ventricle/left ventricle + septum weight (P < 0.005). We conclude that in C57BL/6J mice 1) acute hypoxia causes opposite effects on the pulmonary and systemic circulations, leading to preferential loading of the right heart; and 2) chronic IH in mice results in mild to moderate systemic and pulmonary hypertension, with resultant left- and right-sided ventricular hypertrophy.
heart rate; hypertrophy; obstructive sleep apnea; pulmonary artery pressure; right ventricular pressure; systemic arterial pressure; ventricle
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