Abstract

Corresponding Author: Bing Zhang. Abstract: Although it is generally agreed that rapid, effective cooling treatment increases survival in Exertional Heat Stroke(EHS), the protective mechanism of Arginine Vasopressin(AVP) and Vasopressin 2 Receptor(V2R) modulating water metabolism under cooling condition are unclear. PURPOSE: To determine the regulatory mechanism of AVP and V2R in water metabolism during EHS rats were treated with cooling. METHODS: We arranged 4 groups of male SD rats for this study,namely Normal Control group(NC, n = 8), EHS Onset group(EHSO, n = 9), EHS Rest group(EHSR, n = 9) and EHS Cooling group(EHSC, n = 8). In 36 °C high temperature and 75% high humidity environment, the rat model of EHS was established by exercising to exhaustion and raising rectal temperature to about 42 °C. Cold water immersion for 5 min at 19 °C was employed as the cooling treatment for EHS rats. Blood and kidney were harvested. AVP in serum was measured by ELISA. PCR and WB were respectively used to detect V2R mRNA expression and V2R protein expression in kidney. Mann-Whitney U of nonparametric test was used to analyze the data. RESULTS: When EHS symptoms occured in rats, AVP, V2R mRNA expression and V2R protein expression which modulate water metabolism were significantly up-regulated(EHSO vs. NC) (AVP: 66.02 ± 24.55 vs. 33.52 ± 11.13 pg/ml, p < 0.01; mRNA: 3.46 ± 1.46 vs. 1.15 ± 0.34, p < 0.01; Protein: 2.96 ± 1.96 vs. 1.00 ± 0.00, p < 0.01). After cold water immersion, AVP level in serum showed little change, V2R mRNA expression and V2R protein expression were apparently down-regulated(EHSC vs. EHSO)(AVP: 58.14 ± 21.79 vs. 66.02 ± 24.55 pg/ml, p > 0.05; mRNA: 1.70 ± 0.49 vs. 3.46 ± 1.46, p < 0.01; Protein: 1.42 ± 0.72 vs. 2.96 ± 1.96, p < 0.05). CONCLUSION: AVP, V2R mRNA expression and V2R protein expression can be used as pathophysiological markers in the pathogenesis of EHS. Cooling treatment for exertional heat stroke improves water metabolism through V2R rather than AVP.

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