Investigation on the hemodynamic alterations and their mechanism during heat stroke under hot environment

Abstract

Heat stroke model was made under artificial hot environment in 26 mongrel dogs, and hemodynamic alterations and their mechanism were investigated. When the rectal temperature rose above 41°C the stroke volume (SV) and cardiac output (CO) significantly decreased. The central venous pressure (CVP) declined at first, but increased later and rose above the control value at 43°C. The mean arterial pressure (MAP) began to decrease at 41°C, and decreased by 25.7% (P < 0.01) at 42.5°C comparison with the control value. MAP dropped dramatically (68.4 %) at 43°C. Besides, the serum concentration of potassium increased by 6.1±1.6 mg (P < 0.01) in comparison with the control value. Naloxone (0.1–0.3 mg/kg) was injected i.v. at 40. 5°C of rectal temperature. SV and CO increased markedly at 41°C and 42 °C. CVP declined significantly, and MAP showed elevation at 41°C. These findings suggested that the circulatory failure during heat stroke might be related to the increased β-endorphin release from the anterior pituitary gland and the increase of serum potassium concentration.

Keywords

heat stroke / heat stress / hemodynamic alteration / naloxone / serum potassium concentration

References

[1] AustinMG, et al. . Observations on one hundred cases of heat stroke. JAMA, 1956, 161: 1525-9

[2] 1980;(4):4–12.

[3] GuilleminR, et al. . Beta-endorphin and adrenocorticotropin are secreted concomitantly by the pituitary gland. Science, 1977, 197: 1367-8

[4] RossierJ, et al. . Foot-shock induced stress increases beta-endorphin levels in blood but not in brain. Nature, 1977, 270: 618-20

[5] FraioliF, et al. . Physical exercise stimulates marked concomitantly release of beta-endorphin and adrenocorticotropic hormone (ACTH) in peripheral blood in man. Experientia, 1980, 36: 987-95

[6] MikiK, et al. . Circulatory failure during severe hyperthermia in dogs. Jpn J Physiol, 1983, 33: 269-78

[7] YangK, et al. . Effect of hyperthermia induced by environmental heat stress on vascular interoceptor reflexes. Acta Acad Med Wuhan, 1985, 5: 86-91

[8] HolmesRL, et al. . A heat-sensitive region in the medulla. J Physiol, 1960, 152: 93-8

[9] FadenAI, HoladayJW.. Opiate antagonists: A role in the treatment of hypovolemic shock. Science, 1979, 205: 317-8

[10] HoladayJW, et al. . Naloxone acts at central opiate receptors to reverse hypotension, hypothermia and hypoventilation in spinal shock. Brain Res, 1980, 189: 295-300

[11] 1983;18 (4):77–80.

[12] FadenAI, HoladayJW.. Naloxone treatment of endotoxin shock. J Pharmacol Exp Ther, 1980, 212: 441-7

[13] HoladayJW, FadenAI.. Naloxone reversal of endotoxin hypotension suggests role of endorphins in shock. Nature, 1978, 275: 450-1