Cellular and Molecular Biology

Heart mitochondria in rats submitted to chronic hypoxia

J. Cervós Navarro1, R.Ch. Kunas2, S. Sampaolo2 and U. Mansmann2

1Instituto de Ciencias Neurológicas y Gerontológicas, Universitat Internacional de Catalunya, Barcelona, Spain, 2Department of Neuropathology and 3Department of Medical Statistic and Epidemiology, Freie Universität Berlin, Hindenburgdamm, Berlin, Germany

Offprint requests to: Prof. Dr. J. Cervós-Navarro, Instituto de Ciencias Neurológicas y Gerontológicas, Universitat Internacional de Catalunya, c/Inmaculada 22, 08017 Barcelona, Spain. Fax: +34 93 434 0608


Summary. The effect of prolonged exposure to normobaric hypoxia on the mitochondria of myocard of rats exposed for several weeks to 8 and 7% O2 has been morphometrically evaluated. Twelve male Wistar rats housed in Nalgene cages (2 per cage) with a batch of six cages placed in plexiglass chambers were maintained in air/N2 mixtures containing different concentrations of O2. Six animals kept in similar cages under normoxia served as controls. When at day 60 the FIO2 was reduced to 8%, the weight increase stagnated and after the 81st test day, on which the hypoxic animals were subdivided into 8% and 7% groups the weight curve showed a decrease in the mean body weight for both groups. The arrest and the following loss of weight beyond the 85th day may be interpreted as the expression of a limit reached in the compensation capacity. In the 8%-group the shape of the mitochondria varied more markedly often with budding and furrowing of the surface. In the 7%-group bizarre shapes and wide variations in size with a decided shift towards larger mitochondria were noteworthy. While rats kept under 8% oxygen exhibited a numerical increase in myocardial mitochondria compared to controls, the mitochondria of the 7%-group were numerically reduced. The results suggest that hypoxia of 8% oxygen is compensatable, if only to some extent, by an increasing surface of mitochondrial membranes, and that further reduction of oxygen causes compensation mechanisms to fail as seen by the severe alterations of the mitochondrial population of the cardiomyocyte in the 7%-group. Histol. Histopathol. 14, 1045-1052 (1999)

Key words: Heart, Mitochondria, Chronic hypoxia, Ultrastructural morphometry

DOI: 10.14670/HH-14.1045