Increased accumulation of plasma albumin in the extracellular space of the heart during hypoxia.

The question which was investigated in this study is whether an augmented capillary protein permeability occurs during hypoxia, an effect which might worsen the supply conditions of the tissue during O2 deficiency. Anaesthetized and thoracotomized rats and mice received an i.v. injection of lissamine-rhodamine B200 (RB200)-conjugated albumin and were then ventilated with a gas mixture of 11 vol % O2 for 3 min. At the end of this period the heart was rapidly frozen and histological sections were subsequently scanned for changes in the distribution of labelled albumin. In the control hearts 4.6% (rats) and 4.5% (mice) of the microscopic fields showed penetration of labelled albumin into the extracellular space of the heart. Hypoxia, however, proved to induce an increased shift of plasma albumin into this space in localized areas with signs of increases in the extracellular volume in these areas. The changes in distribution were observed in 26.0 and 35.8% of fields scanned in the histological preparations of the hearts of rats and mice, respectively. Affected areas were found to be randomly distributed through all layers of the heart. The results show that localized accumulation of plasma albumin and edema formation is induced in the extracellular space of the myocardium by even moderate degrees of respiratory hypoxia.