A plasma membrane fatty acid-binding protein (h-FABPpm) has been isolated from rat hepatocytes. Analogous proteins have also been identified in adipocytes, jejunal enterocytes and cardiac myocytes, all cells with high transmembrane fluxes of fatty acids. These 43 kDa, highly basic (pI = 9.1) FABPpm's appear unrelated to the smaller, cytosolic FABP's (designated FABP's) identified previously in the same tissues. h-FABPpm appears closely related to the mitochondrial isoform of glutamic-oxaloacetic transaminase (mGOT), and both the purified protein and liver cell plasma membranes (LPM) possess GOT enzymatic activity. From their relative GOT specific activities it is estimated that h-FABPpm constitutes approximately 2% of LPM protein, or about 0.7 x 10(7) sites per cell. A monoclonal antibody-based competitive inhibition enzyme immunoassay (CIEIA) for h-FABPpm is described; it yields an estimate of 3.4 x 10(7) h-FABPpm sites per hepatocyte. Quantitated by either method, h-FABPpm appears to be a highly abundant protein constituent of LPM.

Animals↗

PubMedDate not supplied

Thermodamage, thermosensitivity and thermotolerance of normal swine oesophagus.

The normal swine oesophagus was heated using an intracavity microwave radiator for 30 min at 45, 46, 47, 48 and 49 degrees C. The animals were sacrificed 48 h or 30 days later. The degree of heat injury was evaluated on an histological score system with a maximum possible damage score of 100 per cent. The acute heat injury (48 h after heating) at these temperatures was 2, 17, 40, 50 and 67 per cent respectively. The main feature of acute heat damage was degenerative necrosis or thrombosis of blood vessels at the oesophageal wall. This occurred only in one out of nine cases at 45 and 46 degrees C heating, but in seven out of nine cases at 48 and 49 degrees C. The main feature of late heat damage was fibrosis. The score of chronic damage for the above groups was 12, 23, 30, 34 and 51 per cent, respectively. When animals were preheated at 44 degrees C for 30 min and then reheated at 45-49 degrees C 4 h later, we found that preheating could provide about 2 degrees C protection. From the above data, we suggest that 45 degrees C and 30 min heating is a safe dose for normal oesophageal tissue.

Adaptation, Physiological↗

PubMedDate not supplied

Acute heat injury to the normal swine rectum.

Intracavitary hyperthermia was applied to the rectum of normal pigs at 43 degrees, 44 degrees, 45 degrees, 46 degrees, 47 degrees and 48 degrees C for 30 min. A score of temperature-induced histological changes of each specimen was made 48 h after heating. The scores from each specimen and temperature were used for regression analysis. Judging from the regression lines of the scores obtained for rectum and oesophagus, we conclude that the thermosensitivity of the rectum is about 1 degree C higher than that of the oesophagus. It suggested that 43 degrees C/30 min could be a safe dose for normal rectum. The thermosensitivity of swine rectum is discussed.

Animals↗

PubMedDate not supplied

Late heat damage in normal swine rectum: a comparison of thermosensitivity of rectum and oesophagus.

The normal swine rectum was heated using an intracavitary microwave radiator for 30 min at 43, 44, 45, 46, 47, and 48 degrees C. The animals were sacrificed 30 days later. The degree of heat injury was evaluated on a histological score system with a maximum possible damage score of 36 (100%). The scores for late damage were 8, 21, 23, 54, 58, and 74%, respectively. The 50% maximum damage was 45.8 +/- 0.5 degrees C/30 min. With the same score system, the heat damage to the oesophagus, which we have calculated previously, was evaluated and compared with that of the present data. The heat damage at the same temperature applied to the lumen was more severe in the rectum than that of the oesophagus. There was a roughly 2-3 degrees C difference in thermosensitivity between these two organs.

Animals↗