Cutaneous vasoconstriction

Pyrogens (e.g., bacterial matter) elevate—probably through mediation by prostaglandins (p. 196) and interleukin-1—the set point of the hypothalamic temperature controller (B2). The body responds by restricting heat loss (cutaneous vasoconstriction chills) and by elevating heat production (shivering), in order to adjust to the new set point (fever). Antipyretics such as acetaminophen and ASA (p. 198) return the set point to its normal level (B2) and thus bring about a defervescence. 

Alcohol produces dilation of the skin vessels, flushing, and a sensation of warmth. Alcohol also interferes with the normal cutaneous vasoconstriction in response to cold. The body heat is therefore lost very rapidly and the internal temperature consequently falls. At toxic alcohol levels, the hypothalamic temperature-regulating mechanism becomes depressed and the fall in body temperature becomes pronounced. For these reasons, consuming alcoholic beverages for the purpose of keeping warm in cold weather is obviously irrational. 

The rate of infection may be higher in patients treated with mild hypothermia. Cutaneous vasoconstriction, which leads to lowered tissue oxygenation subcutaneously, can reduce resistance to infection. In addition, immune function impairment, including neutrophil activity, may be the result of peripheral vasoconstriction and consequent tissue hypoxia (43,49,50). 

Most adverse effects are mediated through the Vj receptor acting on vascular and GI smooth muscle consequently, such adverse effects are much less common, and less severe, with desmopressin than with vasopressin. After the injection of large doses of vasopressin, marked facial pallor owing to cutaneous vasoconstriction is observed commonly. Increased intestinal activity is likely to cause nausea, belching, cramps, and an urge to defecate. Most serious, however, is the effect on the coronary circulation. Vasopressin should be administered only at low doses and with... 

Another factor to consider is environmental temperature. If it falls below body temperature, heat conserving mechanisms kick in (i.e. cutaneous vasoconstriction and shivering). This causes the metaboUc rate to rise. When environmental temperature increases to a point where it is high enough to raise body temperature, metabolic enzyme action accelerates. Therefore metabolic rate rises with an increase in body temperature. 

Nasal vasculature may offer some insight into this question, though research to date has been equivocal. Nasal turbinate vessels can be classified as either capacitance vessels or resistive vessels. Capacitance vessels appear to vasodilate in response to infection while resistance vessels appear to respond to cold stimuli by vasoconstriction. Buccal vascular structures also respond to thermal stimuli but appear to respond principally to cutaneous stimuli. How pharyngeal and tracheobronchial submucosal vessels react to thermal stimuli is not known, though cold-induced asthma is believed to result from broncho-spasms caused by susceptible bronchial smooth muscle responding to exposure to cold dry air.- This asthmatic response suggests an inadequate vascular response to surface cooling. 

Raynaud s phenomenon is an exaggerated vascular-response to cold temperature or emotional stress. Clinical symptoms are sharply demarcated color-changes in the skin of the digits. The underlying disorder consists of abnormal vasoconstriction of digital arteries and cutaneous arterioles due to a local defect in normal vascular responses. 

A slow intravenous injection of histamine produces marked vasodilation of the arterioles, capillaries, and venules. This causes a fall in blood pressure whose magnitude depends on the concentration of histamine injected, the degree of baroreceptor reflex compensation, and the extent of histamine-induced release of adrenal catecholamines. Vasodilation of cutaneous blood vessels reddens the skin of the face, while a throbbing headache can result from vasodilation of brain arterioles. Vasodilation is mediated through both Hj- and Hj-receptors on vascular smooth muscle. Stimulation of Hj-receptors produces a rapid and short-lived response, whereas stimulation of H2-receptors produces a more sustained response that is slower in onset. Stimulation of Hj-receptors on sympathetic nerve terminals inhibits the release of norepinephrine and its associated vasoconstriction. 

Smith KM, Macmillan JB, McGrath JC. Investigation of bl adrenergic receptor subtypes mediating vasoconstriction in rabbit cutaneous resistance arteries. Br J Pharmacol 1997 122 825-832. 

Angiotensin II (All) is one of the most potent vasoconstrictors known, and accounts for most of the endogenous activity of the angiotensin peptide family, including vasoconstriction in cutaneous, splanchnic and renal beds. It has few actions on other smooth muscle, but increases the rate and force of the heart. It has actions within the CNS that suggest a role in control of thirst and appetite for salt. 

The predominant actions of phenylephrine are on the cardiovascular system. Parenteral administration causes a rise in systolic and diastolic pressures due to peripheral vasoconstriction. Accompanying the pressor response to phenylephrine is a marked reflex bradycardia that can be blocked by atropine after atropine, large doses of the peripheral resistance is considerably increased. Circulation time is slightly prolonged, and venous pressure is slightly increased venous constriction is not marked. Most vascular beds are constricted renal, splanchnic, cutaneous, and limb blood flows are reduced, but coronary blood flow is increased. Pulmonary vessels are constricted, and pulmonary arterial pressure is raised. 

Figure 13.3 Changes in cutaneous blood flow experienced as a result of vasoconstriction to reduce heat dissipation and convective heat transfer from the skin and vasodilation with the opposite effects.

Cutaneous microdialysis has also been used to examine the role of vasoconstriction on transport of drugs through hmnan skin (Boutsiouki et al., 2001 Morgan et al., 2003). The organophosphorus insecticide malathion is observed following topical application to human volunteers in microdialysate after 30 min, with a steady state reached after 2 h (Boutsiouki et al., 2001). Adding the vasoconstrictor noradrenaline... 

A different example is the thermoneutral zone within the thermoregulatory systems of humans and other warm-blooded animals. Sweating to remove heat and thermogenesis to produce extra heat are both energy consuming. There is a temperature range where neither of these mechanisms operates, the thermoneutral zone. Temperature control within the thermoneutral zone is accomplished by vasodilation or vasoconstriction of cutaneous blood vessels. The amount of heat lost by this means is determined by controlling the skin surface temperature (see Section 2.7). 

The temperature of the skin is not constant with time and is not uniform over the entire body surface. Vasoconstriction and vasodilation influence cutaneous blood flow and skin temperature. Air temperature, too, affects the skin temperature. Equation (18-2) requires a single estimate of skin temperature. For heat stress conditions. Equation (18-2) uses a value of 35 °C. 

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