Role of Respiratory Failure in Heatstroke Syndrome in Rats

• Main Authors: Chun-Mei Wang, 王春美
• Other Authors: Yu Ru Kou, Ph.D.
• Format: Others
• Language: zh-TW
• Published: 2001
• Online Access: http://ndltd.ncl.edu.tw/handle/93059053981791521764

碩士 === 國立陽明大學 === 生理學研究所 === 89 === 英文摘要 Heatstroke, characterized by hyperthermia, disturbance of central nervous system, and hot/dry skin is especially prevalent in hot climates. When occurs, it usually results in many serious systemic complications with a high mortality rate. To improve the clinical outcomes, much interest has been paid to investigate the mechanisms underlying the heatstroke-induced death. Previous studies suggest that central disorders leading to cardiovascular failure is the major cause of death following onset of heatstroke. However, other studies also show that hyperthermia has a great impact on the respiratory system and may induce respiratory failure. Thus, the contribution of respiratory failure to the heatstroke-induced death remains to be investigated. Accordingly, the present study was conducted to investigate 1) whether ventilatory supports may prolong the survival time in heatstroke rats, 2) whether afferent nervous system that controls breathing, respiratory muscle fatigue, and hydroxyl radicals may play a role in the heatstroke-induced death. Fifty-six male Sprague-Dawley rats were anesthetized and several cardiopulmonary parameters were monitored. The heatstroke was induced by exposing the rats to an ambient temperature of 42.5 ℃. Following the induction of heatstroke, rectal temperature, arterial blood pressure, heart rates, minute ventilation, and pH all increased, while arterial PO2 and PCO2 decreased. After the onset of heatstroke, these cardiopulmonary parameters abruptly deteriorated resulting in death. The time to reach respiratory failure was similar to that to reach cardiovascular failure. The survival time measured between the onset of heatstroke and death in control animals was 9.6 ±0.82 min. This survival time was significantly prolonged by a combination of ventilating animals with 100% O2 and correcting arterial pH, or by pretreatment with metaproterenol (an adrenergic β2 agonist that may enhance the respiratory muscle contractility). This survival time was not significantly altered by bilateral denervation of cervical vagi (the major sensory system for detecting changes in pulmonary conditions), by bilateral denervation of peripheral arterial chemoreceptors (the major sensory system for detecting changes in arterial blood gases and pH), by pretreatment with dimethylthiourea (a hydroxyl radical scavenger), or by pretreatment with milrinone (a phosphodiesterase Ⅲ inhibitor that may avoid respiratory muscle fatigue). In spite of the prolongation of the survival time by these experimental interventions, animals in all groups virtually die. These results suggest that respiratory failure resulting from alternations of arterial blood gases and pH and insufficient of respiratory muscle function may play a role in the heatstroke-induced death. Hence, similar to the cardiovascular failure, this respiratory failure apparently is due to dysfunction of the central nervous system following the onset of heatstroke.