After that read the text aloud, trying to imitate the intonation. The mechanism of febrile increasing temperature in adults is characterized by the limitation of heat emission with the simultaneous intensification of heat

The mechanism of febrile increasing temperature in adults is characterized by the limitation of heat emission with the simultaneous intensification of heat production. Limitation of heat loss is realized by means of sympathetic vasoconstriction of skin blood vessels. The decrease in skin temperature is responsible for the afferent signalization of cold thermo receptors and shivering. The spinal oscillator is responsible for the shivering reflex (simultaneous contraction of flexors and extensors). Contractile and non-contractile thermogeneses are increased by 20 to 60%, first, on account of sympathetic reflexes and stimulation of the adrenal medulla and, further, on account of the activation of the hypothalamus – hypophisis–thyroid axis. These changes are the first stage of the fever – stadium incrementi – (the stage of increasing temperature lasting 3 to 4 hours). Domination of carbohydrates oxidation causes the increase of the respiratory coefficient up to 1.0.

Stadium fastigii, or acme (the stage of constant temperature) is the evidence of a new set-point of temperature homeostasis having been reached. From this point thermoregulation is accomplished through the normal mechanisms. Heat production and heat emission are balanced. Skin vessels are widened. Breathing is frequent. Heart beats are frequent. Skin temperature is increased. Chill and shivering are gone. Diuresis is limited. Activation of the hypothalamus– hypophysis–adrenal cortex axis and hypothalamus–hypophysis–thyroid axis causes changes in the hormonal status (increased cortisol, aldosterone and thyroid hormone levels) and, as a consequence, there are changes in metabolism. The dominance of contrainsulin hormones results in gluconeogenesis activation, decrease in protein synthesis and intensification in aminoacid and fat disintegration. The resulting aminoacids and fatty acid metabolites, like the metabolites of Krebs[8]’ cycle, serve as gluconeogenesis substrates. The dominance of fat oxidation causes a decrease of the respiratory coefficient down to 0.7. Rubner[9]’s urinary coefficient (total carbon (C) / total nitrogen (N) in urine) increases as a result of urinary excretion of a considerable amount of underoxidized carbon as part of ketones (“Disoxidative carbonuria”).

Stadium decrementi (the stage of temperature decrease) occurs as a result of recourse of the set-point of temperature homeostasis down to the normal level after the exogenous pyrogens have been exhausted, while the endogenous ones are no longer formed.

The levels of natural antipyretics, sometimes called “anti-pyrogenes”: arginine-vasopressin, ACTH_{1 - 39}, MSH, endorphins, somatostatin and others) are increased. The previously increased levels of some hormones (aldosterone, cortisol, thyroid hormones) return down to normal. Metabolism is normalized. The respiratory coefficient rises up to 0.8, the Rubner’s urinary coefficient decreases. Heat loss is considerably intensified. Skin vessels are enlarged. Diuresis and sweating are increased. Heat emission exceeds heat production.

Temperature fall may be gradual (lytic) or rapid (critical). In the latter case abrupt dilatation of blood vessels (“vagal enlargement”) may cause sharp decrease of peripheral resistance and arterial blood pressure. This may be complicated by vaso-vagal collapse.