A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Myocardial LDH isoenzyme patterns in rats exposed to cold and/or hypobaric hypoxia
Tekijät: Kaaja R, Are K
Julkaisuvuosi: 1982
Journal: Acta medica Scandinavica. Supplementum
Tietokannassa oleva lehden nimi: Acta medica Scandinavica. Supplementum
Lehden akronyymi: Acta Med Scand Suppl
Vuosikerta: 668
Aloitussivu: 136
Lopetussivu: 42
Sivujen määrä: 7
ISSN: 0365-463X
Tiivistelmä
Exposure of rats to hypobaric hypoxia (9.5% O2) for 40 days produced cardiac hypertrophy, increases in the total LDH activity and subunit M percentage of LDH and a significant decrease (50%) in H/M ratio when compared to control rats. An equally long exposure to cold (+6 degrees C) did not affect heart weight or total LDH activity, but a significant increase (17.6%) in the H/M ratio developed. Simultaneous exposure to cold (+6 degrees C) and hypoxia (9.5% O2) caused a significant decrease in the H/M ratio, but there was no change in the total LDH-activity when compared to the control group. The poor hypoxic tolerance of the cold-exposed rats could partly be explained by disadvantageous distribution of LDH isoenzymes leading to impaired glycolytic capacity of such an aerobic organ as the heart.
Exposure of rats to hypobaric hypoxia (9.5% O2) for 40 days produced cardiac hypertrophy, increases in the total LDH activity and subunit M percentage of LDH and a significant decrease (50%) in H/M ratio when compared to control rats. An equally long exposure to cold (+6 degrees C) did not affect heart weight or total LDH activity, but a significant increase (17.6%) in the H/M ratio developed. Simultaneous exposure to cold (+6 degrees C) and hypoxia (9.5% O2) caused a significant decrease in the H/M ratio, but there was no change in the total LDH-activity when compared to the control group. The poor hypoxic tolerance of the cold-exposed rats could partly be explained by disadvantageous distribution of LDH isoenzymes leading to impaired glycolytic capacity of such an aerobic organ as the heart.