Brozmanova Andrea, Jochem Jerzy, Javorka Kamil, Zila Ivan, Zwirska-Korczala Krystyna
Department of Physiology, Comenius University, Jessenius Faculty of Medicine, Martin, Slovakia.
Int J Hyperthermia. 2006 Mar;22(2):135-47. doi: 10.1080/02656730500531988.
Under conditions of heat stress and hyperosmotic dehydration, both animals and humans reduce thermoregulatory evaporation and regulate deep body temperature at elevated levels. Regarding the mechanisms, the main role in producing these thermoregulatory changes during dehydration is attributed to the increased osmolality of body fluids, although the role of the decreased plasma volume without changes in plasma osmolality (hypovolemia/isosmotic dehydration) has not been so far investigated. There are also controversial experimental results regarding the effects of dehydration on heat stress-induced cutaneous vasodilation. Therefore, this paper studied the effects of hypovolemia/isosmotic dehydration on cardiorespiratory responses to hyperthermia and its physical treatment in 17 anaesthetized adult rabbits. The animals were divided into two groups: normovolemic group (NV; n = 10) and hypovolemic group (HV; n = 7). In the HV group, hypovolemia/isosmotic dehydration (decrease in plasma volume by 16.1 +/- 1.2%) was induced by furosemide (5 mg kg-1 i.v.) without change in measured plasma Na+ concentration. Hyperthermia (the rise in body temperature (BT) to 42 degrees C by a gradual body surface heating) caused significant increase in minute ventilation (VE) in both groups. However, VE values were significantly higher in the HV rabbits compared to the NV animals despite the lower breathing frequency (p < 0.05). The panting was absent in the HV rabbits at the BT of 42 degrees C, unlike the NV animals. From cardiovascular variables, the vasoconstrictor response in visceral (mesenteric) region during hyperthermia in hypovolemic/isosmotic animals was attenuated (p < 0.05), whereas the heat stress-induced cutaneous vasodilation was not influenced by hypovolemia. Recovery of the BT by body surface cooling was accompanied by further increase in VE in the NV group, whereas VE decreased (p < 0.05) in the HV animals. Cooling led to recovery of the cardiovascular parameters. There were found no significant cardiorespiratory differences between the groups (NV:HV) during cooling. The lower frequency of breathing and attenuation of the mesenteric vasoconstriction during exogenous hyperthermia are present not only during hyperosmotic dehydration induced by water deprivation, but they also occur under conditions of furosemide-induced isosmotic dehydration/hypovolemia in rabbits. The heat stress-induced cutaneous vasodilation regarding its biological importance was not influenced by hypovolemia/isosmotic dehydration. Therefore, it is suggested that hypovolemia alone is sufficient to produce described respiratory, thermoregulatory and cardiovascular changes in dehydrated rabbits during exogenous hyperthermia, whereas hyperosmolality is not a requisite.
在热应激和高渗性脱水条件下，动物和人类都会减少体温调节性蒸发，并将深部体温调节至较高水平。关于其机制，脱水过程中产生这些体温调节变化的主要作用归因于体液渗透压的升高，尽管血浆渗透压不变但血浆量减少（低血容量/等渗性脱水）的作用迄今尚未得到研究。关于脱水对热应激诱导的皮肤血管舒张的影响，也存在有争议的实验结果。因此，本文研究了低血容量/等渗性脱水对17只麻醉成年兔高温心肺反应及其物理治疗的影响。动物分为两组：正常血容量组（NV；n = 10）和低血容量组（HV；n = 7）。在HV组中，通过静脉注射呋塞米（5 mg kg-1）诱导低血容量/等渗性脱水（血浆量减少16.1 +/- 1.2%），而测得的血浆Na+浓度无变化。高温（通过体表逐渐加热使体温（BT）升至42℃）导致两组的分钟通气量（VE）均显著增加。然而，尽管呼吸频率较低，但HV组兔的VE值显著高于NV组动物（p < 0.05）。与NV组动物不同，HV组兔在BT为42℃时无喘息现象。从心血管变量来看，低血容量/等渗性动物高温期间内脏（肠系膜）区域的血管收缩反应减弱（p < 0.05），而热应激诱导的皮肤血管舒张不受低血容量影响。体表降温使BT恢复时，NV组的VE进一步增加，而HV组动物的VE下降（p < 0.05）。降温导致心血管参数恢复。降温期间两组（NV:HV）之间未发现显著的心肺差异。外源性高温期间呼吸频率降低和肠系膜血管收缩减弱不仅在缺水诱导的高渗性脱水期间出现，在兔中呋塞米诱导的等渗性脱水/低血容量条件下也会发生。热应激诱导的皮肤血管舒张就其生物学重要性而言不受低血容量/等渗性脱水影响。因此，有人提出，仅低血容量就足以在脱水兔外源性高温期间产生所述的呼吸、体温调节和心血管变化，而高渗性并非必要条件。
