Int J Med Sci 2020; 17(4):525-535. doi:10.7150/ijms.39745

Research Paper

Therapeutic Hypothermia Protects Against Heat Stroke-Induced Arterial Hypotension via Promoting Left Ventricular Performance in Rats

Wen-Ching Ko1,2, Cheng-Hsien Lin2, Jie-Jen Lee2, Ching-Ping Chang3✉, Chien-Ming Chao4,5✉

1. Department of Surgery, Mackay Memorial Hospital, Taipei, Taiwan
2. Department of Medicine, Mackay Medical College, New Taipei, Taiwan
3. Department of Medical Research, Chi Mei Medical Center, Tainan, Taiwan
4. Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan 73657, Taiwan
5. Department of Nursing, Min-Hwei College of Health Care Management, Tainan, Taiwan

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Citation:
Ko WC, Lin CH, Lee JJ, Chang CP, Chao CM. Therapeutic Hypothermia Protects Against Heat Stroke-Induced Arterial Hypotension via Promoting Left Ventricular Performance in Rats. Int J Med Sci 2020; 17(4):525-535. doi:10.7150/ijms.39745. Available from http://www.medsci.org/v17p0525.htm

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Abstract

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.

Keywords: myocardial injury, therapeutic hypothermia, heatstroke, cardiac mechanical efficiency, arterial elastance