Department of Surgery, Mackay Memorial Hospital, Taipei, Taiwan.
Department of Medicine, Mackay Medical College, New Taipei, Taiwan.
Int J Med Sci. 2020 Feb 10;17(4):525-535. doi: 10.7150/ijms.39745. eCollection 2020.
We aimed to ascertain whether therapeutic hypothermia (TH) acts as cardioprotective management for heat stroke (HS). Adult male rats under general anesthesia were exposed to whole-body heating (43°C for 70 min) to induce HS. Rats with HS displayed hyperthermia (core body temperature 42°C vs. 36°C); hypotension (30 mmHg vs. 90 mmHg mean arterial blood pressure); suppressed left ventricular (LV) performance (stroke volume 52 μl/min vs. 125 μl/min), ejection fraction (0.29% vs. 0.69%), relaxation factor (72 ms vs. 12 ms), and arterial elastance (0.31 mmHg/ μl vs. 10 mmHg/ μl); increased myocardial injury markers (e.g., creatine kinase-MB: 86 U/L vs. 24 U/L, cardiac troponin I: 3.08 ng/ml vs. 0.57 ng/ml); increased myocardial oxidative stress markers (e.g., malondialdehyde: 6.52 nmol/mg vs. 1.06 nmol/mg, thiobarbituric acid-reactive substances: 29 nmol/g vs. 2 nmol/g); decreased myocardial antioxidants (e.g., superoxide dismutase: 6 unit/mg vs. 17 unit/mg, reduced glutathione: 0.64 nmol/mg vs. 2.53 nmol/mg); increased myocardial proinflammatory cytokines (e.g., tumor necrosis factor-α 3200 pg/ml vs. 1000 pg/ml, interleukin-6: 668 pg/ml vs. 102 pg/ml); and increased cardiac damage scores (2.2 vs. 0.3). TH therapy significantly reversed the following conditions: HS-induced hyperthermia (37.5°C core body temperature), hypotension (71 mmHg), suppressed LV performance (stroke volume: 97 μl/min, ejection fraction: 0.65%, relaxation factor: 39 ms, and arterial elastance: 0.99 mmHg/μl), increased myocardial injury markers (e.g., creatine kinase-MB: 37 U/L, cardiac troponin I: 1.06 ng/ml), increased myocardial oxidative stress markers (e.g., malondialdehyde: 2.68 nmol/mg, thiobarbituric acid-reactive substances: 12.3 nmol/g), decreased myocardial antioxidants (e.g., superoxide dismutase: 13.3 unit/mg, reduced glutathione: 2.71 mmol/mg), increased myocardial proinflammatory cytokines (e.g., tumor necrosis factor-α 1500 pg/ml, interleukin-6: 108 ng/ml); and increased cardiac damage scores (0.9). We thus conclude that TH protects against HS-induced arterial hypotension by promoting LV performance in rats. These results add to the literature regarding the use of TH as cardioprotective management for HS.
我们旨在确定治疗性低温（TH）是否对热射病（HS）起到心脏保护作用。全身麻醉下的成年雄性大鼠暴露于全身加热（43°C 70 分钟）以诱导 HS。HS 大鼠表现出体温升高（核心体温 42°C 与 36°C）；低血压（30mmHg 与 90mmHg 平均动脉血压）；左心室（LV）功能抑制（每搏量 52μl/min 与 125μl/min），射血分数（0.29% 与 0.69%），弛豫因子（72ms 与 12ms），动脉弹性（0.31mmHg/μl 与 10mmHg/μl）；心肌损伤标志物增加（如肌酸激酶-MB：86U/L 与 24U/L，心肌肌钙蛋白 I：3.08ng/ml 与 0.57ng/ml）；心肌氧化应激标志物增加（如丙二醛：6.52nmol/mg 与 1.06nmol/mg，硫代巴比妥酸反应物质：29nmol/g 与 2nmol/g）；心肌抗氧化剂减少（如超氧化物歧化酶：6 单位/mg 与 17 单位/mg，还原型谷胱甘肽：0.64nmol/mg 与 2.53nmol/mg）；心肌促炎细胞因子增加（如肿瘤坏死因子-α 3200pg/ml 与 1000pg/ml，白细胞介素-6：668pg/ml 与 102pg/ml）；心脏损伤评分增加（2.2 与 0.3）。TH 治疗显著逆转了以下情况：HS 引起的体温升高（37.5°C 核心体温）、低血压（71mmHg）、LV 功能抑制（每搏量：97μl/min，射血分数：0.65%，弛豫因子：39ms，动脉弹性：0.99mmHg/μl）、心肌损伤标志物增加（如肌酸激酶-MB：37U/L，心肌肌钙蛋白 I：1.06ng/ml）、心肌氧化应激标志物增加（如丙二醛：2.68nmol/mg，硫代巴比妥酸反应物质：12.3nmol/g）、心肌抗氧化剂减少（如超氧化物歧化酶：13.3 单位/mg，还原型谷胱甘肽：2.71mmol/mg）、心肌促炎细胞因子增加（如肿瘤坏死因子-α 1500pg/ml，白细胞介素-6：108ng/ml）；以及心脏损伤评分增加（0.9）。因此，我们得出结论，TH 通过促进大鼠 LV 功能来保护 HS 引起的动脉低血压。这些结果为 TH 作为 HS 的心脏保护管理的应用提供了文献依据。
