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缺氧和氟利昂12对心脏收缩力学的影响。

Effects of hypoxia and Freon 12 on mechanics of cardiac contraction.

作者信息

Kilen S M, Harris W S

出版信息

Am J Physiol. 1976 Jun;230(6):1701-7. doi: 10.1152/ajplegacy.1976.230.6.1701.

DOI:10.1152/ajplegacy.1976.230.6.1701
PMID:7144
Abstract

Data are presented which indicate that the mechanism of tension depression and subsequent recovery from dichlorodifluoromethane (Freon 12), an aerosol gas recently described as a potent cardiac depressant agent, differs from that of hypoxia. To analyze these differences, 22 rat papillary muscles, contracting isometrically in a myograph, were studied during and subsequent to 15-min interventions of of hypoxia. Freon 12 with adequate oxygenation, or Freon 12 combined with hypoxia. During each of the three interventions the developed force (F) was markedly depressed, while peak shortening velocity (Vpm) was selectively more depressed by Freon and Freon combined with hypoxia than by hypoxia alone. While hypoxia shortened the time to peak force (TTP) and one-half relaxation time (RT1/2) markedly, Freon 12 with adequate oxygenation slightly shortened RT1/2 (P is less than 0.001) but failed to shorten TTP significantly. In contrast, Freon 12 administered during hypoxia shortened TTP and RT1/2 significantly (P is less than 0.001), more than did hypoxia or Freon 12 alone. Posthypoxic prolongation of TTP and RT1/2 was not seen during recovery from Freon 12. This prolongation was depressed during recovery from Freon 12 given either during hypoxia or during recovery from hypoxia. The results indicate that Freon 12 and hypoxia act synergically, although the mechanisms through which they mediate their actions on myocardial tissue are not identical.

摘要

所呈现的数据表明,二氯二氟甲烷(氟利昂12,一种最近被描述为强效心脏抑制剂的气雾剂)导致张力降低及随后恢复的机制与缺氧不同。为分析这些差异,对22条在肌动描记器中进行等长收缩的大鼠乳头肌在15分钟的缺氧干预期间及之后进行了研究。干预包括有充足氧合的氟利昂12、氟利昂12与缺氧联合。在这三种干预的每一种过程中,所产生的力量(F)均显著降低,而峰值缩短速度(Vpm)受氟利昂以及氟利昂与缺氧联合的影响比单独缺氧时更有选择性地降低。虽然缺氧显著缩短了达到峰值力量的时间(TTP)和半松弛时间(RT1/2),但有充足氧合的氟利昂12仅轻微缩短了RT1/2(P<0.001),但未显著缩短TTP。相反,在缺氧期间给予氟利昂12显著缩短了TTP和RT1/2(P<0.001),比单独缺氧或单独使用氟利昂12时缩短得更多。从氟利昂12恢复过程中未观察到缺氧后TTP和RT1/2的延长。在缺氧期间或从缺氧恢复期间给予氟利昂12后恢复过程中,这种延长受到抑制。结果表明,氟利昂12和缺氧协同作用,尽管它们介导对心肌组织作用的机制并不相同。

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