低体温下の心臓活動 : 冬眠哺乳動物の心筋Caイオン調節機構に学ぶ  [in Japanese] Heart Function under Hypothermia : Study on Mechanism of Ca Ion Regulation in Hearts of Mammalian Hibernators  [in Japanese]

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Abstract

Most mammals are not capable of surviving at low body temperature for extended periods. Although some degree of hypothermia provides an advantage in medical treatment, such as organ plantation and open heart surgery, through depression of the energy consumption and prevention of accumulation of harmful metabolites, the lowering of body temperature causes serious cold-damage to cells, probably by overloading Ca<SUP>2+</SUP>, resulting from a perturbation of membrane ion regulation. Mammalian hibernators undergo extreme hypothermia (near 0°C) during hibernation without any damage to their bodies, indicating the existence of an effective strategy for the protection of cells and tissues against cold. Recent studies on excitation-contraction coupling of cardiac muscles of hibernators found dramatic changes in Ca<SUP>2+</SUP> regulatory systems, Ca channels and sarcoplasmic reticulum (SR), during hibernation. The contraction usually depends on Ca<SUP>2+</SUP> influx through Ca channels, whereas during hibernation, Ca<SUP>2+</SUP> for contraction is derived mainly from intracellular Ca stores, SR. Further electrophysiological and biochemical studies in hibernating animals revealed that these are attributed to both the marked enhancement of the Ca<SUP>2+</SUP> uptake ability of SR and much less activation of Ca channels. These changes greatly contribute to the reduction of cytoplasmic Ca<SUP>2+</SUP> after contraction. Thus, during hibernation, hearts are kept functioning normally at low body temperature through avoiding Ca<SUP>2+</SUP> overload. The present mechanism of adaptation to cold provides a useful model for studying a strategy for overcoming cold injury.

Journal

  • Advances in Animal Cardiology

    Advances in Animal Cardiology 28(2), 71-76, 1995-12-01

    Japanese Society of Veterinary Cardiology

References:  24

Codes

  • NII Article ID (NAID)
    10008286822
  • NII NACSIS-CAT ID (NCID)
    AN10192925
  • Text Lang
    JPN
  • Article Type
    REV
  • ISSN
    09106537
  • Data Source
    CJP  J-STAGE 
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