Steigen T K, Tveita T, Hevrøy O, Andreasen T V, Larsen T S
Department of Medical Physiology, University of Tromsø, Norway.
Ann Thorac Surg. 1998 May;65(5):1235-40. doi: 10.1016/s0003-4975(98)00137-4.
Reduced myocardial function after hypothermia may be metabolic in origin, but the relationship between myocardial metabolism and the various components of hypothermia-mediated dysfunction has not been thoroughly investigated.
In the present study we measured myocardial uptake and oxidation of glucose and oleate in mongrel dogs undergoing cooling to 25 degrees C followed by rewarming to 37 degrees C, using radiolabeled substrates.
Segment work index declined from 39.3 +/- 5.1 to 15.1 +/- 2.4 mm Hg in response to cooling from 37 degrees to 25 degrees C and did not recover completely on rewarming (27.2 +/- 4.2 mm Hg, p < 0.05). Oleate uptake declined from 3,251 +/- 619 to 1,043 +/- 356 nmol.min-1.100 g-1 (p < 0.05) when the dogs were cooled from 37 degrees to 25 degrees C. Simultaneously, oxidation rate fell from 1,089 +/- 158 to 354 +/- 83 nmol.min-1.100 g-1 (p < 0.05). On rewarming, oleate uptake was restored to prehypothermic values, whereas its rate of oxidation remained depressed (480 +/- 129 nmol.min-1.100 g-1; p < 0.05). Uptake and oxidation of glucose also declined significantly during cooling. However, both uptake and oxidation of glucose recovered fully on rewarming.
The results of the present study demonstrate a reduced capacity to oxidize fatty acids by the myocardium during rewarming after hypothermia.
低温后心肌功能降低可能源于代谢，但心肌代谢与低温介导的功能障碍的各个组成部分之间的关系尚未得到充分研究。
在本研究中，我们使用放射性标记底物，测量了杂种犬冷却至25℃然后复温至37℃过程中心肌对葡萄糖和油酸的摄取及氧化情况。
随着温度从37℃降至25℃，节段作功指数从39.3±5.1降至15.1±2.4 mmHg，复温时未完全恢复（27.2±4.2 mmHg，p<0.05）。当犬从37℃冷却至25℃时，油酸摄取量从3251±619降至1043±356 nmol·min⁻¹·100 g⁻¹（p<0.05）。同时，氧化率从1089±158降至354±83 nmol·min⁻¹·100 g⁻¹（p<0.05）。复温时，油酸摄取恢复至低温前值，但其氧化率仍降低（480±129 nmol·min⁻¹·100 g⁻¹；p<0.05）。冷却期间葡萄糖的摄取和氧化也显著下降。然而，复温时葡萄糖的摄取和氧化均完全恢复。
本研究结果表明，低温后复温期间心肌氧化脂肪酸的能力降低。
