Force and acid-base state of turtle cardiac tissue exposed to combined anoxia and acidosis.
Force and acid-base state of turtle cardiac tissue exposed to combined anoxia and acidosis.
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缺氧和酸中毒联合作用下龟心脏组织的力和酸碱状态。
DOI：
10.1152/ajpregu.1990.259.1.r15
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Jackson,DC
中科院分区：
文献类型：
--
作者：
Wasser,JS;Freund,EV;Gonzalez,LA;Jackson,DC
我们测量了在 20 摄氏度下暴露于缺氧和酸中毒 (pH 7.0) 1 小时的龟 Chrysemys picta bellii 的心室条带的收缩力。条带自发跳动（自定节奏）或响应电刺激（节奏为 12、24 或 36 次/分钟）。在对照条中和缺氧酸中毒结束时测量组织[乳酸]和细胞内pH (pHi)。在自定进度条中，在正常细胞外 Ca2+ 浓度 ([Ca2+]o) (1 mM) 下，缺氧酸中毒 1 小时后，速率和力均显着下降，分别为对照值的 54% 和 17.1%。 30 分钟时将 [Ca2+]o 增加至 10 mM，对速率和力有微小但显着的积极影响。缺氧酸中毒时起搏条的收缩力也逐渐下降，但下降幅度与起搏频率直接相关。在所有缺氧酸中毒的情况下，pHi较对照值7.53显着下降；在定速试纸中，酸中毒在 36 次/分钟 (pHi 6.75) 时最严重，而在自定速试纸中，pHi（大约 6.85）与 [Ca2+]o 无关。基于这项工作和之前的工作，我们得出结论，缺氧-酸中毒联合作用，类似于长时间缺氧淹没后在体内观察到的情况，会严重抑制心脏功能。高钙血症和心动过缓都可以改善这种极端状态下的表现，但这些影响不如单独发生缺氧和酸中毒时那么大。
We measured contractile force of ventricular strips form the turtle Chrysemys picta bellii exposed to 1 h of combined anoxia and acidosis (pH 7.0) at 20 degrees C. Strips either beat spontaneously (self-paced) or in response to electrical stimulation (paced at 12, 24, or 36 beats/min). Tissue [lactate] and intracellular pH (pHi) were measured in control strips and at the end of anoxia-acidosis. In self-paced strips, at normal extracellular Ca2+ concentration ([Ca2+]o) (1 mM), both rate and force fell significantly after 1 h of anoxia-acidosis to 54 and 17.1%, respectively, of control values. Increased [Ca2+]o to 10 mM at 30 min had a small but significant positive effect on both rate and force. Contractile force of paced strips also fell progressively during anoxia-acidosis, but the decrease varied directly with pacing frequency. Under all cases of anoxia-acidosis, pHi fell significantly from the control value of 7.53; in paced strips, acidosis was most severe at 36 beats/min (pHi 6.75), and in self-paced strips, pHi (approximately 6.85) was independent of [Ca2+]o. Based on this and previous work, we conclude that combined anoxia-acidosis, similar to that observed in vivo after prolonged anoxic submergence, profoundly depresses cardiac function. Both hypercalcemia and bradycardia improve performance in this extreme state, but these effects are not as great as when anoxia and acidosis occur alone.