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Objective To observe the response of left ventricular (LV)function and structure to chronic intermittent hypoxia (CIH)early stage in New Zealand white rabbits by echocardiography.Methods The New Zealand white rabbits were placed in the CIH chamber and exposed to hypoxia for 8 weeks (6 hours/day,6 days/week).The flow of nitrogen and oxygen were regulated into the customized chambers by the gas control delivery system.The fraction of inspired oxygen was changed from 21 % to 8% for 25 s of every 1 70 s.LV structure and function was assessed by echocardiography at CIH 0,1 ,2,4,6,8 weeks and histopathology was done by HE staining simultaneously.Results ①LV structural variables:compared with 0 week,LV posterior wall and interventricular septum thickness thickened at 6 week.LV end diastolic increased at 8 week (P 1 .Isovolumic relaxation time (IVRT)decreased at 1 week and 2 week,but increased at 8 week (P < 0.05 ).④ The myocardial pathology showed that myocardial fibers disordered slightly,cardiomyocytes swelled,nuclei increased and intracellular edema when exposed to CIH for 2 week and 4 week.Vacuolar degeneration,edema and congestion were found in intercellular substance at 6 week and 8 week.Conclusions ① LV systolic and diastolic function compensation started at CIH early stage then LV structure abnormality advent later.②IVCT and IVRT are sensitive indicators of LV systolic and diastolic function compensation.
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ObjectiveTo observe right ventricle (RV) structure and function of New Zealand rabbits with chronic intermittent hypoxia (CIH) for short-term (0-8 weeks) by echocardiography. MethodsTwenty-four healthy male New Zealand rabbits were set up CIH animal model for 8 weeks. RV structure?s systolic and diastolic function were measured by conventional and tissue Doppler echocardiography at 0, 1, 2, 4, 6 and 8 week and one rabbit was sacriifced randomly for RV myocytes and pulmonary tissue pathology examination. RV structure and function parameters at 0, 1, 2, 4, 6 and 8 week were analyzed by mixed effects model analysis.ResultsRV structure variables: RV, RA at 8 week increased compared with those at 0 week, but had no signiifcant difference (P>0.05); RV systolic function variables:RVFAC at 8 week increased compared with those at 0 week (F=3.45, P<0.05), TAPSE at 4, 6, 8 week increased compared with that at 0 week (F=3.11, 3.41 and 3.86, all P<0.05), RVMPI at 4 week decreased compared with that at 0 week (F=3.46, P<0.05), recovered to baseline at 6, 8 week. Isovolumetric relaxation time (IRTc) corrected by heart rate at 1, 2, 4 week decreased compared with that at 0 week (F=3.15, 3.31 and 3.17, all P<0.05), recovered to baseline at 8 week, ET of PA at 1, 2 week decreased compared with that at 0 week (F=3.01 and 3.15, both P<0.05), recovered to baseline at 4, 6, 8 week, AT of PA at 1, 2, 4 week decreased compared with that at 0 week (F=3.13, 3.15 and 3.32, all P<0.05), recovered to baseline at 6, 8 week. RV diastolic function variables: isovolumetric contraction time (ICTc) corrected by heart rate at 2, 4 week decreased compared with that at 0 week (F=3.13 and 3.33,both P<0.05), E/E? at 1, 2 week decreased compared with that at 0 week (F=3.13 and 3.44,bothP<0.05), recovered to baseline at 4, 6, 8 week, E/A at 4, 6, 8 week increased compared with that at 0 week (F=4.01, 3.82 and 3.37, all P<0.05), E?/A? at 8 week increased compared with that at 0 week (F=3.81, P<0.05). The myocardial pathology showed that RV myocardial cell structure was normal at 4 week. Nuclei enlarged, stain darkened and some cytoplasms loosed when exposed to CIH for 8 weeks. The structure of lung tissues was normal when exposed to CIH for 4 weeks. Inflammatory cell inifltrated, capillary engorged as well as the wall of pulmonary arterioles thickened slightly at 8 week.ConclusionsRV diastolic and systolic function showed compensatory and structure was normal in early CIH (0-8 week). RV diastolic function compensated earlier than systolic function. IRT and ICT were sensitive indicators of RV systolic and diastolic function compensation.