丁二醇诱导的酮症可提高小鼠对缺氧的耐受性。

Butanediol induced ketosis increases tolerance to hypoxia in the mouse.

作者信息

Kirsch J R, D'Alecy L G, Mongroo P B

出版信息

Stroke. 1980 Sep-Oct;11(5):506-13. doi: 10.1161/01.str.11.5.506.

DOI:10.1161/01.str.11.5.506

Abstract

In previous studies from our laboratory a positive correlation between elevated blood ketone levels and the survival time (ST) during hypoxia (4-5% oxygen) was observed in fasted and alloxan diabetic mice. To test the hypothesis that ketosis was somehow increasing the tolerance of mice to hypoxia, we induced ketosis by either oral (PO), intraperitoneal (IP), or intravenous (IV) 1,3-butanediol (BD). Blood beta-hydroxbutyrate increased from 0.33 +/- 0.06 mM to 3.32 +/- 0.08 mM for PO, 1.2 +/- 0.2 mM for IV and 0.83 +/- 0.15 mM for IP. BD was associated with an increase in ST to 458% (n = 19) when given PO, 217% (n = 12) by IP route, and 560% (n = 13) by the IV route. The effect of ambient temperature (Ta) on this phenomenon was evaluated at 12, 22, 32, and 34 degrees C. At each Ta, IV BD at 1.4 mmole/mouse was associated with an increase in ST to 525, 559, 151, and 145% of control, respectively. The absolute ST of both control and treated mice was greater at Ta of 12 and 22 degrees C. Hypoxia, however, was associated with a decrease in body temperature in each group. It is concluded that the artificial induction of ketosis by BD is associated with an increase in ST of mice exposed to hypoxia.

摘要

在我们实验室之前的研究中，在禁食和四氧嘧啶糖尿病小鼠中观察到血液酮水平升高与缺氧（4-5%氧气）期间的存活时间（ST）之间存在正相关。为了检验酮症以某种方式增加小鼠对缺氧耐受性的假设，我们通过口服（PO）、腹腔注射（IP）或静脉注射（IV）1,3-丁二醇（BD）诱导酮症。口服时血液β-羟基丁酸从0.33±0.06 mM增加到3.32±0.08 mM，静脉注射时为1.2±0.2 mM，腹腔注射时为0.83±0.15 mM。口服BD时ST增加到458%（n = 19），腹腔注射途径时为217%（n = 12），静脉注射途径时为560%（n = 13）。在12、22、32和34摄氏度下评估环境温度（Ta）对该现象的影响。在每个Ta下，每只小鼠静脉注射1.4毫摩尔BD时，ST分别增加到对照的525%、559%、151%和145%。对照小鼠和处理小鼠的绝对ST在12和22摄氏度的Ta下更大。然而，缺氧与每组体温下降有关。结论是，BD人工诱导酮症与暴露于缺氧的小鼠的ST增加有关。