Effects of hypovolemia on hypercapnic ventilatory response in experimental hyperthermia.

The present study was undertaken to evaluate the effects of hypercapnia on the cardiorespiratory control in normovolemic and hypovolemic rabbits during exogenous hyperthermia. Hypovolemia was induced by administration of furosemide, the body temperature (Tb) was gradually elevated to 42 degrees C by body surface heating. Subsequently, Tb was lowered back to the initial values by gradual cooling. Recordings were done at normothermia (TN=38 degrees C), during heating at 40 degrees C (TH1) and 42 degrees C (TH2), and in the course of Tb reverting toward the baseline values back at 40 degrees C (TC1), and finally after full return to the initial temperature value (TC2). The hypercapnic ventilatory response (HCVR) was estimated as the slope of minute volume (VE) on end-tidal CO2 (ETCO2) curves. We found that heating caused an increase in the VE slope in the normovolemic (NV), but not in hypovolemic (HV), rabbits. Between-group comparison revealed a significant increase in HCVR at TH2 and TC1 in NV vs. HV rabbits. Hypercapnia in hyperthermia (at TC2) was accompanied by a significant decrease in heart rate only in the hypovolemic group. Recovery of Tb was unaccompanied by appreciable changes in HCVR in either NV or HV groups. In the course of cooling, a decrease in heart rate during hypercapnic challenge was present in both group, in HV the drop was less prominent. We conclude that hypercapnia during heat stress in both normovolemic and hypovolemic rabbits is associated with altered cardiorespiratory responses. HCVR during exogenous hyperthermia is augmented in normovolemic, but not in hypovolemic, rabbits.

Effects of acute normovolemic haemodilution on cardiorespiratory changes in hyperthermia and its physical treatment.

As only one experimental study examining the effects of haemodilution on circulatory responses to hyperthermia has so far been published and there is no information on respiratory responses to hyperthermia during haemodilution or anaemia, this paper studied the effects of acute normovolemic haemodilution on cardiorespiratory changes during 42 degrees C hyperthermia and its recovery by body surface cooling in 16 anaesthetized adult rabbits. The animals were divided into two groups: haemodiluted group (Hct = 18.6 +/- 0.4%) and control group (Hct = 41.1 +/- 0.9%). In the haemodiluted group, acute normovolemic haemodilution was induced by 60% replacement of total blood volume with dextran. Haemodilution produced significant increases in minute volume (V(E), p < 0.02), heart rate (HR, p < 0.02) and central venous pressure (CVP, p < 0.02), but there was no significant change in mean arterial pressure (MAP). Hyperthermia caused significant increases in V(E) and HR in both the groups; however, V(E) and HR values were significantly higher in the haemodiluted group compared to the controls. CVP decreased (p < 0.05) during 42 degrees C hyperthermia only in the controls in the panting phase. MAP did not significantly change during over-heating in controls, but it significantly (p < 0.02) rose in the haemodiluted group. In the recovery phase, cooling led to significant decreases in HR and MAP in both the groups and to further increases in V(E) (p < 0.05) in controls, whereas V(E) decreased in the haemodiluted animals. There were found no significant cardiorespiratory differences between the two groups during cooling. Hyperthermia was accompanied by the higher values of minute volume and heart rate in the haemodiluted animals, indicating a greater activation of the respiratory and cardiovascular systems, which could result in diminished functional cardiorespiratory reserve and a higher risk of respiratory and circulatory failures in haemodiluted/anaemic animals during hyperthermia. In the phase of recovery of the body temperature there were no significant cardiorespiratory differences found between the two groups.

[Baroreflex regulation of the cardiovascular system during hyperthermia]. / Baroreflexná regulácia kardiovaskulárneho systému pocas hypertermie.

Baroreflex control of human skin blood flow during hyperthermia is predominantly mediated by the stimulation of cardiopulmonary low pressure baroreceptors. Under hyperthermic conditions, the active cutaneous vasodilator system represents an efferent arm of the baroreflex, when baroreceptor unloading elicits withdrawal of sympathetic active vasodilator activity. Splanchnic sympathetic nerve activity is not likely modulated by the arterial and cardiopulmonary baroreceptors during hyperthermia. Little is known regarding the effects of heat stress on baroreflex control of the heart rate and on the vascular resistance. Baroreflex control of heart rate during heat stress seems to be dependent on the species of experimental animals and on their age.

[Thermoregulation of skin blood flow]. / Termoregulacná kontrola prietoku krvi kozou.

Exposure of organism to the heat stress causes a significant increase in skin blood flow. The heat stress-induced cutaneous vasodilation initially results from the withdrawal of cutaneous sympathetic vasoconstrictor activity. In addition, there is a sympathetic active cutaneous vasodilator system which is activated during another increase of the core temperature. The mechanism for this active cutaneous vasodilation is not clear and according to several experimental studies it involves a release of a vasodilator substance bradykinin from sweat glands activated by the sudomotor nerves. According to other studies the active cutaneous vasodilation is caused by the cholinergic vasodilator nerves through release of a yet-to-be-determined neurotransmitter in the presence of the basal pool of nitric oxide. Interaction of local and reflex influences is important in the control of skin blood flow during both rest and exercise.