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

Figures

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  Figure 1. Kaplan-Meier analysis followed by log-rank tests were performed to determine the percent survival in NC rats (⚪), in heated rats without TH following HS (HS+non-TH) (◼) and in heated rats with TH (HS+TH) (▲). Data are expressed as the means±SD of 10 rats per group. *P<0.001, HS+non-TH vs. NC; +P<0.001, HS+TH vs HS+non-TH.

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  Figure 2. Time course of the change in ambient temperature (A, Ta), colonic temperature (B, Tco) and mean arterial blood pressure (C, MABP) in NC rats (⚪), in rats without TH following HS (HS+non-TH) (◼), and in rats receiving TH following HS (HS+TH) (▲). The Tco (D) and MABP (E) were obtained 0, 70, and 90 min after the initiation of heat exposure (ambient temperature in non-heated controls ) in heat stroke rats. All heated groups were exposed to heat (43 oC) for exactly 70 min and were then allowed to recover at room temperature (26 oC). Data are expressed as the means±SD of 10 rats per group. *P<0.01, HS+non-TH vs. NC; +P<0.05, HS+TH vs. HS+non-TH.

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  Figure 3. Representative LV pressure-volume loops obtained from the steady-state of (A) an NC rat, (B) an HS+non-TH rat, and (C) an HS+TH rat at time “0 min” (―), time “70 min” (…), and time “90 min” (-·-·) after onset of heat stress. As depicted in (B), the HS+non-TH rat displayed a characteristic right shift and declined in the amplitude of the pressure-volume signal in the pressure-volume loops at the time “90 min”. The abnormal amplitude of the pressure-volume signal in the pressure-volume loop at the time “90 min” (or the time point for the onset of HS) was significantly reversed by the TH, as demonstrated in HS+TH rats. The definitions of the group abbreviations are provided in the legend of Figure 1.

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  Figure 4. Histological analysis of myocardial tissues. Representative hematoxylin and eosin (H&E) staining results for myocardial sections in rats of the (A) NC, (B) HS+non-TH and (C) HS+TH groups. (D) Semiquantitative analysis of H&E staining in the rats (n=6 per group). *P<0.05, compared with NC, +P<0.05, compared with HS+non-TH. At twenty min after HS onset, gross observation, and 400x magnification with H&E staining revealed apparent differences in the degree of injury between the different experimental groups. Scale bars: 50 µm.

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  Figure 5. Temporal associations are driving the HS reactions, including hyperthermia, hypotension, splanchnic vasoconstriction, cardiac oxidative stress, cardiac inflammation, and lethality following heat stress, which can be affected by therapeutic hypothermia (TH) treatment. (+), aggravation, and (-), mitigation. Environmental heat stress increases cutaneous blood flow and metabolism and progressively decreases splanchnic blood flow (including heart, intestine, brain, and others). Decreasing mean arterial pressure by heat stress causes myocardial ischemia. Myocardial ischemia causes myocardial oxidative stress and inflammation and results in a reduction in both cardiac mechanical efficiency and arterial elastance, causing further hypotension. SOD, superoxide dismutase; MDA, malondialdehyde; TBARS, thiobarbituric acid reactive substances; TNF-α, tumor necrosis factor-alpha; IL-6, interleukin-6; IL-10, interleukin-10.