Vork M M, Glatz J F, Surtel D A, Van der Vusse G J
University of Limburg, Cardiovascular Research Institute, Maastricht (CARIM), Department of Physiology, The Netherlands.
Can J Physiol Pharmacol. 1993 Dec;71(12):952-8. doi: 10.1139/y93-144.
The present study was performed to monitor the effect of low-flow ischemia and reperfusion on changes in the protein permeability of the cardiomyocyte cell membrane and the endothelial cell layer for two cytoplasmic proteins, i.e., fatty acid binding protein (FABP) and lactate dehydrogenase (LDH), which differ appreciably with respect to physicochemical characteristics. To accomplish this, isolated rat hearts were Langendorff perfused with separate collection of vascular and interstitial effluents. Control hearts were perfused normoxically for 300 min, whereas experimental hearts were subjected to 60 min normoxia (N), 180 min low-flow ischemia (I), and finally 60 min normoxic reperfusion (R). Protein release was measured in 15 min interval fractions. During the first 240 min of perfusion 0.2% of total tissue FABP and 1.1% of total tissue LDH were detected in the effluents in both groups. Moreover, in each case 80% of released FABP and LDH was found in the interstitial effluent. During R, following I in the experimental group, appreciable amounts of both proteins were released (2.2 and 5.1% of total tissue contents for FABP and LDH, respectively). During this period the percentage of protein released in the vascular effluent increased significantly for both proteins. It is concluded that the combination of low-flow ischemia and reperfusion increases the protein permeability of both the cardiomyocyte cell membrane and the endothelial barrier. Since the release patterns of FABP and LDH with respect to time were similar during the entire perfusion protocol, it is tempting to state that protein release from tissue is a nonspecific effect of a noxious intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
