Modulation of myocardial function and [Ca2+] sensitivity by moderate hypothermia in guinea pig isolated hearts.
Modulation of myocardial function and [Ca2+] sensitivity by moderate hypothermia in guinea pig isolated hearts.
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DOI：
10.1152/ajpheart.1999.277.6.h2321
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发表时间：
1999-12
期刊：
影响因子：
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通讯作者：
D. Stowe;S. Fujita;J. An;R. A. Paulsen;S. G. Varadarajan;S. Smart
中科院分区：
文献类型：
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作者：
D. Stowe;S. Fujita;J. An;R. A. Paulsen;S. G. Varadarajan;S. Smart
心脏低温改变收缩力和细胞内Ca2+浓度（[Ca2+]i）稳态。我们研究了在37°C、27°C和17°C条件下，分离的豚鼠心脏灌注期间，左心室压（LVP）是如何随着细胞质[Ca2+]离子在细胞外CaCl2浓度（[CaCl2]e）范围内的变化而改变的。使用Ca2+指示剂indo 1测量跨壁LV相[Ca2+]，并在校正自身荧光，温度和非胞质Ca2+后校准（以nM为单位）。非胞质[Ca2+]i，胞质舒张期和收缩期[Ca2+]i，期相[Ca2+]i和收缩期每拍释放的Ca2+（面积Ca2+）绘制为0.3-4.5 mM [CaCl2]e的函数，收缩性指标[LVP，最大LVP发育率（+dLVP/d t）和弛缓（-dLVP/d t），以及每拍LVP曲线积分（LVParea）]绘制为[Ca2+]i的函数。低温升高收缩期[Ca2+]，略微改变收缩期LVP，但升高舒张期LVP和[Ca2+]i。舒张和非胞质[Ca2+]与[CaCl2]的关系在17°C和27°C时向上移动，而相态[Ca2+]与[CaCl2]的关系在17°C时向上移动，而在27°C时没有。随着体温的降低，相[Ca2+]与LVP、+ LVP/d和LVP面积的关系逐渐降低，从而使最大的Ca2+激活LVP降低，心脏对Ca2+脱敏。因此，轻度低温适度增加舒张期和非胞质Ca2+，对收缩期Ca2+或释放（面积）Ca2+影响不大，而中度低温显著增加舒张期、非胞质期、峰值收缩期和释放Ca2+，并导致最大Ca2+激活的LVP和心肌对收缩期Ca2+的敏感性降低。
Cardiac hypothermia alters contractility and intracellular Ca2+ concentration ([Ca2+]i) homeostasis. We examined how left ventricular pressure (LVP) is altered as a function of cytosolic [Ca2+]iover a range of extracellular CaCl2 concentration ([CaCl2]e) during perfusion of isolated, paced guinea pig hearts at 37°C, 27°C, and 17°C. Transmural LV phasic [Ca2+] was measured using the Ca2+ indicator indo 1 and calibrated (in nM) after correction was made for autofluorescence, temperature, and noncytosolic Ca2+. Noncytosolic [Ca2+]i, cytosolic diastolic and systolic [Ca2+]i, phasic [Ca2+]i, and systolic Ca2+ released per beat (area Ca2+) were plotted as a function of 0.3-4.5 mM [CaCl2]e, and indexes of contractility [LVP, maximal rates of LVP development (+dLVP/d t) and relaxation (-dLVP/d t), and the integral of the LVP curve per beat (LVParea)] were plotted as a function of [Ca2+]i. Hypothermia increased systolic [Ca2+]iand slightly changed systolic LVP but increased diastolic LVP and [Ca2+]i. The relationship of diastolic and noncytosolic [Ca2+] to [CaCl2]ewas shifted upward at 17°C and 27°C, whereas that of phasic [Ca2+]ito [CaCl2]ewas shifted upward at 17°C but not at 27°C. The relationships of phasic [Ca2+]ito developed LVP, +dLVP/d t, and LVParea were progressively reduced by hypothermia so that maximal Ca2+-activated LVP decreased and hearts were desensitized to Ca2+. Thus mild hypothermia modestly increases diastolic and noncytosolic Ca2+ with little effect on systolic Ca2+ or released (area) Ca2+, whereas moderate hypothermia markedly increases diastolic, noncytosolic, peak systolic, and released Ca2+ and results in reduced maximal Ca2+-activated LVP and myocardial sensitivity to systolic Ca2+.