The role of arginine vasopressin in thermoregulation during fever.
Fever is the most common symptom of disease and, unlike hyperthermia, is a regulated elevation of body temperature that appears to have an upper limit. During fever, there is an upward displacement of the hypothalamic set point mediated by pyrogenic cytokines (Kluger, 1991; Saper & Breder, 1994). Hyperthermia, on the other hand, is an increase in body temperature without a change in the hypothalamic set point (Dinarello, Cannon, & Wolf, 1988).
More than 50 years ago, DuBois (1949) reported that fever rarely exceeds 41.1[degrees]C. However, his observations were made prior to the wide use of antibiotics and modem-day medical technology. Practitioners know today that thermoregulatory neurons in the preoptic region and anterior hypothalamus (POAH) and in adjacent septal areas are influenced by endogenous pyrogens to produce fever and secrete antipyretic factors to attenuate fever (Boulant, 1997; Mackowiak & Boulant, 1996). Therefore, body temperature in fever appears to have an upper limit due to influences of endogenous antipyretic substances such as the following:
* arginine vasopressin (AVP)
* alpha-melanocyte-stimulating hormone (([alpha]-MSH)
* corticotropin-releasing factor (CRF)
* adrenocorticotropic hormone (ACTH)
* thyrotropin-releasing hormone (TRH)
* gastric inhibitory peptide
* neuropeptide [gamma]
* tumor necrosis factor (TNF)
* uromodulin (Kluger, 1991).
At least three pituitary hormones appear to function as endogenous antipyretics: AVP, ([alpha]-MSH, and ACTH. Among the endogenous antipyretic factors, AVP, which modulates fever by lowering the hypothalamic core temperature set point (Pittman, Malkinson, Kasting, & Veale, 1988), has been studied most extensively.
AVP has long been known for its participation in control of arterial blood pressure (Oliver & Shafer, 1895) and water excretion by the kidneys (Farini, 1913; Von den Velden, 1913). Even though there is early evidence of AVP's antipyretic activity (Cushing, 1932), most research on this topic has occurred within the last 20 years. This article reviews the pharmacodynamics of AVP and addresses the role of AVP during fever, including its role during dehydration and fever, its interaction with antipyretic drugs, and its neuromodulator role during febrile convulsions.
Vasopressin, also known as antidiuretic hormone, is produced in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus and stored in the posterior pituitary, ha the rat, vasopressinergic cells also have been identified in the lateral ventricle, stria terminalis, stria medullaris, septum, hippocampus, amygdala, medulla oblongata, and spinal cord (Buijs, 1978; Buijs, Swaab, Dogterom, & Van Leeuwen, 1978). AVP is a nonapeptide with a 6-amino acid ring and a 3-amino acid side chain. In humans and most other mammals, arginine is found in position 8; in pigs and related species, lysine is found in position 8 (Klonoff & Karam, 1995).
Two types of AVP receptors have been identified. Vasoconstriction is mediated by V1 receptors on smooth muscle cells (Holmquist, Ludin, Larsson, Hedlund, & Andersson, 1991). In addition, V1 receptors also have been localized on principal cells of the cortical collecting duct (Ando & Asano, 1993) but are absent from cells of papillary collecting ducts of the kidney (Portilla, Shyman, & Morrison, 1987). V1-like receptors have been reported in brain regions such as the ventral septal area (VSA), lateral septum, bed nucleus of the stria terminalis, hippocampus in a number of animal species (Poulin, Lederis, & Pittman, 1988; Szot, Ferris, & Dorsa, 1990), rostral end of third ventricle, chorus, and area postrema (Gerstberger & Fahrenholz, 1989).
Antidiuresis is mediated by V2 receptors detectable on the basolateral membrane of principal cells in the collecting ducts (Kirk, 1988; Leite & Suki, 1990), luminal membrane cells of terminal inner medullary collecting ducts (Nonguchi et al., 1995), and smooth muscle cells in the renal pelvis (Kimoto & Constantinou, 1990). It has been suggested that V2 receptors, not V1 receptors, are localized near the anterio-ventral third ventricle and the paraventriculal, supraoptic, suprachiasmatic nuclei, and neurohypophysis of the hypothalamus (Cheng & North, 1989; Gerstberger & Fahrenholz, 1989). However, the antipyretic effect of AVP is mediated by the V1 receptors in the fibers and terminals of the VSA (Kasting, 1989).
Secretion and Control of Vasopressin
Two afferent pathways, one from baroreceptors and one from osmoreceptors, control the secretion of AVP in the presence of hypovolemia or hyperosmolality. Decreased extracellular volume causes the baroreceptors to decrease their firing rate, signaling the hypothalamus to increase secretion of AVP. When body water is lost, osmoreceptors in the hypothalamus sense an increased body fluid osmolarity and stimulate the secretion of AVP. During fever, AVP reduces fever through a receptor-mediated action (Pittman, Naylor, et al., 1988). Evidence now exists that AVP acts as a neurotransmitter in the brain to exert antipyretic action during fever (Cooper, Kasting, Lederis & Veale, 1979; Kasting, Veale, Cooper, & Lederis, 1981; Naylor, Ruwe, Kohut, & Veale, 1985; Wilkinson & Kasting, 1987).
Thermoregulation During Fever
Fever is a complex adaptive host response initiated by autonomic, neuroendocrine, and behavioral mechanisms as part of the acute phase response to infection (Cooper, 1995). Fever occurs in response to a challenge with endotoxins via the release of endogenous pyrogens by systemic mononuclear phagocytes (Blatteis & Sehic, 2000). Endogenous pyrogens (cytokines such as interleukin [IL]-1, tumor necrosis factor, and IL-6) stimulate an upward resetting of the hypothalamic set point (Cooper; Saper; 1998). Body temperature is sensed below the set point, triggering heat-producing and heat-conserving mechanisms. When heal production is greater than heat loss, heat is retained mad the core temperature is raised (Kluger, 1991). The body responds to the higher core temperature by initiating sweating and vasodilation during the defervescent phase of fever (Cooper). Increased sweating decreases plasma volume, which attenuates skin blood flow and sweating, causing a further increase in core temperature (Doris & Baker, 1981).
A new hypothesis has been espoused about the initial rapid febrile response to an endotoxin involving the vagus nerve. Before the peripheral cytokines reach the POAH, a febrile response is elicited. There is evidence to suggest that activation of subdiaphragmatic vagal afferent nerves may be an alternative neuronal communicator between peripheral cytokines and the hypothalamus (Blatteis & Sehic, 1997). In support, subdiaphragmatic vagotomy blocks the induction of IL-1-beta gene expression in the brain (Hansen, O'Connor, Goehler, Watkins, & Maier, 2001; Laye et al., 1995). in other words, the initial onset of the febrile response may be due to a neuronal rather than humoral pathway. During this acute phase, whether activated by neuronal or humoral activity, body temperature is rising to approximate the new set point, and a hypothermic state is present. As a result, heat-generating and heat-conserving mechanisms are initiated.
Antipyretic Properties of AVP
Experimental evidence indicates the antipyretic action of AVP exists in specific central sites. For example, AVP perfused into the VSA of the sheep, rat, and rabbit suppresses endotoxin fever (Cooper et al., 1979; Kasting et al., 1981; Naylor et al., 1985; Wilkinson & Kasting, 1987), whereas AVP injected into the third cerebral ventricle and the lateral septum in rabbits (Bernardini, Lipton, & Clark, 1983), the lateral cerebral ventricle in macaque monkeys (Lee, Mora, & Myers, 1985), and the fundus striati in rats (Kremarik, Freund-Mercier & Pittman, 1995) increases or has negligible effects on core temperature response to lipopolysaccharide (LPS) injection. Therefore, the VSA of the limbic system is believed to be the site where the antipyretic effects of AVP are mediated. These findings reinforce the differences in actions of AVP with different methods of application. Because of species-specific anatomical and physiological differences in thermoregulation, attention also needs to be paid to the animal model used if inference to other species, especially humans, is to be made.
Support for the antipyretic properties of AVP has been documented by an enhanced febrile response following AVP blockade. V1 antagonists injected into the VSA of febrile rats enhanced file febrile response; however, V2 antagonists had no effect (Cooper, Naylor, & Veale, 1987). When live bacteria were injected into rats, fever was enhanced following administration of V1 antagonists (Cridland & Kasting, 1992). These results suggest that endogenous AVP functions as a neuromodulator in natural fever as well as in endotoxin-induced fever.
In rats infused with IL-1 into the lateral cerebral ventricle to induce fever, pretreatment with an AVP V1 antagonist into the VSA enhanced the magnitude and duration of the febrile response (Cooper et al., 1987). Similar results were reported when rats received chronic infusion of V1 antagonist prior to injection of live bacteria (Cridland & Kasting, 1992). Back, Roth, Kluger, and Zeisberger (1994) investigated the effects of V1 receptor antagonist on the febrile response to intramuscular injection of LPS 20 [micro]g/kg and reported that electrical stimulation of the PVN of guinea pigs attenuated the febrile response. However, this response was partly reversed by a simultaneous intraseptal microinfusion of a V1 receptor antagonist. Taken together, these results support a role for AVP in antipyresis with natural and induced fevers.
Disparate results concerning the antipyretic abilities of AVP have been reported in Brattleboro rats that are deficient in AVP. Following administration of endotoxin, endogenous pyrogens, or prostaglandin, the febrile response in Brattleboro rats was not enhanced (Eagan, Kasting, Veale, & Cooper, 1982; Ruwe, Veale, & Cooper, 1988). In contrast, male rats with reduced secretion of AVP produced by long-term castration had enhanced febrile responses (Pittman, Malkinson, et al., 1988). These results do not rule out the role of AVP during antipyresis but rather suggest that several endogenous antipyretics may be involved in the febrile response (Moltz, 1993).
AVP concentration in the plasma and limbic septum increased during osmotic stimulation in rats (Demotes-Mainard, Chaveau, Rodriguez, Vincent, & Poulain, 1986; Landgraf, Neuman, & Schwarzberg, 1988). There is evidence that hypovolemia and hyperosmolality, both strong stimuli of AVP, are antipyretic (Kasting, 1986; Kasting et al., 1981). In ewes injected intravenously with S. abortus LPS, Kasting et al. showed that loss of blood volume through hemorrhage (i.e., 20% of estimated blood volume) attenuates fever in sheep. In a similar study (Kasting, 1986), hemorrhage of 20% blood volume in rats also reduced the febrile response to E. call LPS. In addition, infusion of hypertonic saline, another potent stimulus of AVP, also attenuated LPS-induced fever. These findings suggest that AVP is centrally released during osmotic stimuli and hypovolemia and that 24-hour water deprivation, resulting in a combination of hypovolemia and hyperosmolality, would also be expected to release central AVP and, therefore, induce antipyresis.
In support, water deprivation exerted an antipyretic effect in guinea pigs (Roth, Schulze, Simon, & Zeisberger, 1992). However, contrasting results are reported in dehydrated rats (Morimoto, Murakami, Ono, & Watanabe, 1986) and rabbits (Richmond, 2001). There is insufficient research to determine the influence of water deprivation on fever. Because both dehydration (Epstein, Castel, Glick, Sivan, & Ravid, 1983) and fever (Kasting, Carr, Martin, Blttme, & Bergland, 1983; Sharpies, Seckl, Human, Lightman, & Dunger, 1992) elicit central release of AVP, the dehydrated, febrile animal would be expected to have levels of AVP significant enough to exert antipyretic activity.
Vasopressin Interaction with Antipyretic Drugs
Acetaminophen has replaced aspirin as the most commonly used antipyretic (Maison et al., 1998; Prescott, 2000). However, recent evidence supports the antipyretic efficacy of nonsteroidal antiinflammatory drugs (NSAIDs). There is evidence that the NSAID indomethacin reduces fever more quickly and that its effects last longer than those of acetaminophen and ibuprofen, another NSAID (Autret et al., 1994; Purssell, 2002). Indomethacin, as an antipyretic, is 35 times more potent than aspirin (Van Arman, Armstrong, & Kim, 1991). Nonsteroidal antipyretic drugs inhibit prostaglandin synthesis by decreasing cyclo-oxygenase (Dascombe, 1985). However, it has been hypothesized that other antipyretic mechanisms exist, such as an interaction with AVP (Wilkinson & Kasting, 1990, 1993).
During endotoxin fever, AVP-V1 antagonists infused within the ventral septum block salicylate antipyresis but had no effect on the antipyretic action of acetaminophen (Wilkinson & Kasting, 1990). AVP levels in the VSA of conscious rats increased following antipyresis of endotoxin-induced fever with indomethacin but not with acetaminophen (Wilkinson & Kasting, 1993). This information would suggest that salicylate and indomethacin-induced antipyresis are mediated by the neuromodulatory function of endogenous AVP from within the VSA.
Febrile Seizures and Vasopressin
Little is known about the mechanism responsible for chidhood febrile seizures. However, support for AVP as a neuromodulator in febrile seizures is present in animal studies. Motor disturbances and seizures were observed following intracerebroventricular (ICV) administration of AVP in rats (Kasting, Veale, & Cooper, 1980). The mean AVP level for rats after hyperthermia-induced seizures was significantly higher than control levels (Burnard Pittman, Veale, & Lederis, 1982). Rats with IL-1 alpha induced fever elicited a heightened motor response following ICV injection of AVP (Poulin & Pittman, 1993 AVP infused in the VSA, the site of antipyretic action of AVP, also initiates seizure activity in rats, which was enhanced with each exposure (Pittman, Naylor, et al., 1988).
Similar findings in sheep were reported. AVP per fused into the brain of sheep caused antipyresis, and following subsequent perfusions, AVP levels wet increased and seizure activity was observed (Veal, Cooper, & Ruwe, 1984). However, when AVP was diffused in the VSA of Brattleboro rats, seizure activity was attenuated (Pittman, Naylor, et al., 1988). Although antipyretic properties of AVP are mediated by V1 receptors, there is evidence that the effects of AVP on febrile seizure activity are medicated by V2 receptors (Gulec & Novan, 2002). Collectively, these results suggest that AVP released during fever causes antipyresis; however, when disproportionately high, AVP may promote seizure activity. To clarify the mechanism, further research on fever-induced seizures is needed.
Gaps and Unexplored Areas in the Literature
Evidence supports a role for endogenous AVP in thermoregulation during fever. Changes in the concentration of AVP have been demonstrated during fever, dehydration, febrile convulsions, and administration of antipyretic drugs. However, gaps in the literature related to AVP and fever still exist. Research clarifying the antipyretic mechanisms of vasopressin during dehydration is need ed. Dehydration is a frequent cause of morbidity in vulnerable populations such as children, the elderly, and immunocompromised persons. An understanding of the mechanism of body temperature regulation during dehydration and fever is needed to reduce morbidity, and even mortally, in high-risk populations. Also, further research is needed to determine whether an increase in AVP during dehydration affects the production of endogenous pyrogens.
During fever, vasopressin enhances the efficacy of the antipyretic properties of indomethacin and salicylate. Although indomethacin is not routinely prescribed for fever reduction in the clinical setting, ibuprofen is often prescribed. The safety and efficacy of NSAIDs in dehydrated patients, especially children and the elderly, need to be explored. Whether NSAIDs are safe and effective antipyretics, especially during dehydration, is crucial information for the healthcare practitioner. Finally, the role of AVP as a neurotransmitter in febrile seizures needs to be explored further. Based on the evidence that NSAIDs may increase the level of AVP and that enhanced levels of AVP may contribute to febrile seizures, the safety and efficacy of NSAIDs in the presence of febrile seizures need to be investigated.
Implications for Practice
Patients who have undergone neurosurgical procedures are at risk for developing a fever. It is important to evaluate each neurosurgical patient's temperature elevation postoperatively because an elevated temperature does not necessarily mean the presence of fever or an infection. Cytokines that are released during surgery-induced inflammation (Lin, Calvano, & Lowry, 2000) at, the same cytokines released after a febrile stimulus. In addition, the same causes of postoperative fever in general surgery patients (i.e., hypoventilation, dehydration infection, stress, pulmonary congestion, atelectasis) are present in the neurosurgical patient (Barker, 2002). Because of the nature of neurosurgery, additional stressors are present (e.g., invasive lines, catheters) that may contribute to the induction of postoperative fever or infection (Barker).
Research results suggest that dehydration enhance the febrile response. The daily fluid requirement during fever increases by 15% for each 1[degrees]C elevation in body. temperature (Brensilver & Goldberger, 1996). During defervescence, thermoregulatory responses to elevated body temperature such as cutaneous vasodilation to transfer heat from the core to the periphery and evaporative heat loss via sweating or panting (Boulant, 1997) induce body water losses, inducing dehydration (Morimoto & Itoh, 1998). Therefore, in the immediate post-operative period, temperature monitoring, along with the detection and prevention of dehydration, is crucial to the recovery of the neurosurgical patient.
Neurosurgical nurses frequently encounter patient with fever as a result of the sequelae of surgery. Fever unlike hyperthermia, is a regulated elevation of body temperature and is a part of the acute phase response to infection. Endogenous antipyretics, such as AVP, modulate the thermoregulatory response during fever. AVP, which is produced in the SON and PVN and stored in the posterior pituitary, reduces fever through a receptor-medicated action. Results of animal research studies suggest the the antipyretic action of AVP exists within the VSA of the limbic system. Although osmotic stimuli such as hypovolemia and hyperosmolality stimulate the release of AVP, the effects of dehydration on fever are unclear.
Evidence suggests that there may be a synergistic relationship between AVP receptors and cyclo-oxygenase enzyme during antipyresis, and the presence of AVP may enhance the efficacy of nonsteroidal antipyretic drugs. Although the antipyretic effect of AVP release is beneficial, excessively high levels of AVP may enhance seizure activity during fever. In view of the discovery that AVP levels are increased during antipyresis with indomethacin and not acetaminophen, it is possible that the use of acetaminophen may be more beneficial in febrile seizures than NSAIDs.
I would like to acknowledge Vernon Bishop, PhD, Barbara J. Holtzclaw, PhD RN FAAN, and Duane Proppe, PhD, of the University of Texas Health Science Center at San Antonio for their early editorial comments.
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Questions or comments about this article may be directed to: Charlotte A. Richmond, PhD RN, Mount Sinai Medical Center, 4300 Alton Road, #205A, Miami Beach, FL 33140. She is the scientific director of anesthesia research in Department of Anesthesia at Mount Sinai Medical Center and Miami heart Institute, Miami beach, FL.
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|Author:||Richmond, Charlotte A.|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Oct 1, 2003|
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