Saliva Spreading Research Articles

Elastocapillary effect in self-repair of proboscises of butterflies and moths

HypothesisSelf-repair in living organisms, without tissue regeneration or regrowth, is rare. Recent discovery that butterflies can self-repair the proboscis after the two halves (galeae) have been separated raised a question about the physical mechanism allowing them to reunite the parts. We discovered that butterflies pump saliva during repair of their proboscises. We then hypothesized that saliva spreading along the food canal of the proboscis would create capillary forces capable of bringing the galeae together. ExperimentTo test the hypothesis, we distinguished capillary forces from muscular action of the galeae by sedating butterflies and video tracking retraction of the saliva menisci during galeal separation. To theoretically show capillary adhesion, the elastic moduli of the galeae were measured, and the galeal profiles were extracted from videos as a function of time. The values were then fitted with a mathematical model based on an augmented Euler-Bernoulli beam theory whereby each galea was treated as a beam bent by capillary forces due to saliva. We also evaluated friction forces that prevented disjoining of the galea at the tip of their separation. FindingsThe results showed that butterflies use saliva to repair their proboscises via capillary adhesion, and theoretically supported the role of saliva in providing the necessary capillary forces to bring the galeae together. Tangential shear forces acting parallel to the galea at the tip of their separation are caused primarily by friction between the cuticular linking structures.

Aquaporins, evaporative water loss and thermoregulation in heat-acclimated Mongolian gerbils (Meriones unguiculatus).

Evaporative water loss is an essential strategy to maintain stable body temperature in heat-exposed rodents. However, the thermoregulatory role and adjustment of evaporative heat loss capacity is unclear during prolonged heat exposure. Here, we studied the role of evaporative water loss in thermoregulation in Mongolian gerbils during heat acclimation. After 3 weeks of heat acclimation, gerbils exhibited a lower body temperature than the controls, and no difference in evaporative losses of water from the lung or saliva spreading compared with the controls. Heat acclimation did not alter the expression of aquaporin-1 and aquaporin-5 in the lungs and the expression of aquaporin-5 in the salivary glands. The expression of aquaporin-2 in the kidneys was kept stable, while the expression of aquaporin-1 in the kidneys was down-regulated. In addition, resting metabolic rate and non-shivering thermogenesis of heat-acclimated gerbils were reduced to 51% and 55% of the control group, respectively. Taken together, heat-acclimated Mongolian gerbils can reduce the metabolic thermogenesis without enhancing the evaporative water loss capacity for thermoregulation.

Parotid and mandibular gland secretion by red kangaroos, Macropus rufus, in response to heat stress

Salivary flow rates from ipsilateral parotid and mandibular glands were measured in conscious red kangaroos over a 70–90-min period during episodes of saliva spreading induced by heat stress. At the onset of saliva spreading, mandibular flow rose rapidly to plateau at 1.12 ± 0.10 mL min–1 for the collection intervals after the first 10 min of licking. Parotid flow increased more slowly and progressively, reaching secretion rates similar to those of the mandibular gland after 40 min of saliva spreading, exceeding mandibular flow after 70 min and showing no indication that it had reached maximum secretion at 90 min of saliva spreading. The ion concentrations of both parotid and mandibular salivas during saliva spreading were similar to those previously reported for parasympathomimetic stimulation. The low osmotic concentration of mandibular saliva relative to plasma (40%) makes it a functionally better evaporative coolant than parotid saliva, which was nearly isosmotic with plasma. The increased production of hydrogen ions associated with the increased secretion of bicarbonate by the parotid gland would tend to offset the respiratory alkalosis due to panting thereby helping to maintain acid/base balance during periods of prolonged heat stress.

The effects of intermittent heat acclimation on water balance in rats

Heat exposure can lead to thermal dehydration in rats, as they use saliva spreading for evaporative cooling. The effects of heat acclimation in rats on thermal dehydration and subsequent water intake are not well understood. In this study, male Sprague‐Dawley rats were exposed to 37.5°C (Intermittent Heat Acclimation ‐ IHA) with or without water or to 25°C with water for 4 hours/day for 7 consecutive days. Water losses and intakes were determined during the exposure period and a 3 hour drink period on days 1 and 7. On day 8, rats from each experimental group were exposed to either 25°C with water or 37.5°C without water for 4 hours and then blood samples were taken for estimation of cellular and extracellular dehydration. Heat exposure increased water intake both during and after the exposure and having access to water during heat exposure increased evaporative water loss but did not alter urine output. IHA decreased evaporative water loss during heat exposure, while not altering urine output during or after heat exposure. IHA also increased water intake in the heat and decreased drink period water intake and total water intake without changing blood indicators of cellular or extracellular dehydration. IHA reduces evaporative water loss during heat exposure leading to a subsequent reduction in total water intake without altering physiological thirst drives. Supported by a NSF REU Site Award (DBI‐0754293)°

Arginine vasopressin does not mediate heat loss in the tail of the rat

It has been reported that hypothermia induced by arginine vasopressin (AVP) is brought about by a coordinated response of reduced thermogenesis in brown adipose tissue (BAT) and increased heat loss through the tail of rats. However, it is well known that AVP is one of the strongest peripheral vasoconstrictors. Whether the AVP-induced hypothermia is associated with an increase in heat loss through the tail is questionable. Therefore, the present study assessed the relationship between the effects of AVP on tail skin temperature and the induced hypothermic response, and to determine if peripheral AVP administration increases heat loss from the tail. Core, BAT and tail skin temperature were monitored by telemetry in male Sprague–Dawley rats before and after intraperitoneal administration of AVP or vasopressin receptor antagonist. We also analyzed simultaneously of the time-course of AVP-induced hypothermic response and its relationship with changes in BAT temperature, and effect of AVP on grooming behavior. The key observations in this study were: (1) rats dosed with AVP induced a decrease in heat production (i.e., a reduction of BAT thermogenesis) and an increase of saliva spreading for evaporative heat loss (i.e., grooming behavior); (2) AVP caused a marked decrease in tail skin temperature and this effect was prevented by the peripheral administration of the vasopressin V1a receptor antagonist, suggesting that exogenous AVP does not increase heat loss in the tail of rats; (3) the vasopressin V1a receptor antagonist could elevate core temperature without affecting tail skin temperature, suggesting that endogenous AVP is involved in suppression of thermogenesis, but not mediates heat loss in the tail of rats. Overall, the present study does not support the conclusion of previous reports that AVP increased tail heat loss in rats, because AVP-induced hypothermia in the rat is accompanied by a decrease in tail skin temperature. The data indicate that exogenous AVP-induced hypothermia attributed to the suppression of thermoregulatory heat production and the increase of saliva spreading for evaporative heat loss.

Central neural pathways for thermoregulation

Central neural circuits orchestrate a homeostatic repertoire to maintain body temperature during environmental temperature challenges and to alter body temperature during the inflammatory response. This review summarizes the functional organization of the neural pathways through which cutaneous thermal receptors alter thermoregulatory effectors: the cutaneous circulation for heat loss, the brown adipose tissue, skeletal muscle and heart for thermogenesis and species-dependent mechanisms (sweating, panting and saliva spreading) for evaporative heat loss. These effectors are regulated by parallel but distinct, effector-specific neural pathways that share a common peripheral thermal sensory input. The thermal afferent circuits include cutaneous thermal receptors, spinal dorsal horn neurons and lateral parabrachial nucleus neurons projecting to the preoptic area to influence warm-sensitive, inhibitory output neurons which control thermogenesis-promoting neurons in the dorsomedial hypothalamus that project to premotor neurons in the rostral ventromedial medulla, including the raphe pallidus, that descend to provide the excitation necessary to drive thermogenic thermal effectors. A distinct population of warm-sensitive preoptic neurons controls heat loss through an inhibitory input to raphe pallidus neurons controlling cutaneous vasoconstriction.

Thermoregulation in monotremes: riddles in a mosaic

The three extant genera of the Monotremata have evolved, probably from a pre-Cretaceous Gondwanan origin, independently of the Theria to display a variety of ancestral and derived features. A comparison of their thermoregulation reveals a diversity of physiology that might represent both plesiomorphic and apomorphic elements within this mosaic. In the tachyglossids, the echidnas Tachyglossus and Zaglossus, body temperature is often labile, rising as a result of activity and allowed to decline during inactivity. This daily heterothermy, which is not necessarily torpor, may combine with typical mammalian hibernation to provide substantial energy economy in a wide variety of often unproductive habitats. Only when incubating do free-ranging echidnas display classic mammalian thermoregulation, the facultative nature of which suggests echidna-like physiology as an example of a protoendothermic stage in the evolution of endothermy. Similarly, physiological response to heat in Tachyglossus, at least, may be plesiomorphic, relying on the cyclic loss of heat stored during activity. Tachyglossids neither exhibit a panting response nor spread saliva to facilitate evaporative cooling and Tachyglossus, though not Zaglossus, lacks functional sweat glands. By contrast, the only extant ornithorhynchid, the platypus Ornithorhynchus, does not utilise heterothermy of any kind and maintains its body temperature more tightly than several semiaquatic eutherians. Although not necessarily required, it responds to heat via sweating, but not panting or saliva spreading. The classic nature of ornithorhynchid thermoregulation stands in marked contrast to the more diverse thermoregulatory responses shown by the tachyglossids, making it difficult to determine which aspects of monotreme thermoregulation are plesiomorphic and which are apomorphic.

Regulation mode of evaporative cooling underlying a strategy of the heat-tolerant FOK rat for enduring ambient heat.

Compared with other rat strains, the inbred FOK rat is extremely heat tolerant. This increased heat tolerance is due largely to the animal's enhanced saliva spreading abilities. The aims of the present study were to 1) quantify the heat tolerance capacity of FOK rats and 2) determine the regulatory mode of the enhanced salivary cooling in these animals. Various strains of rats were acutely exposed to heat. In the heat-intolerant strains, saliva spreading was insufficient and the core temperature (Tc) rose rapidly. In contrast, FOK rats maintained an elevated Tc plateau (39.5 +/- 0.7 degrees C) for 5-6 h over a wide range of ambient temperatures (Ta) (37.5-42.5 degrees C). In hot environments the FOK rats secreted copious amounts of saliva and spread it over more than the entire ventral body surface. FOK rats had a low Tc threshold for salivation, and the salivation rate increased linearly in proportion to the Tc deviation from the threshold. No strain difference or temperature effect was observed in the saliva secretion rate from in vitro submandibular glands perfused by sufficient doses of ACh. These results suggest that 1) the ability of FOK rats to maintain a moderate steady-state hyperthermia (39.5 +/- 0.7 degrees C) over a wide Ta range is enabled by a lowered threshold Tc for salivation and functional negative-feedback control of saliva secretion and 2) strain differences in ability to endure heat stress are mainly attributable to changes in the thermoregulatory control system rather than altered secretory abilities of the salivary glands.

Differences in Thermal Salivation between the FOK Rat (a Model of Genotypic Heat Adaptation) and Three Other Rat Strains

Rats secrete saliva in response to heat. In the present study, details of thermal salivation were investigated using the FOK rat in comparison with Sprague–Dawley (SD), Donryu, and ACI rats. The FOK rat is a strain inbred for genotypic heat adaptation and endures heat for long periods. Conscious rats of all four strains were exposed to 42.5°C. The order of heat endurance times at this temperature was FOK ⪢ SD > Donryu = ACI. FOK rats spread their saliva over their entire ventral surface, their faces, and their outside legs. This saliva area was wider than those made by the other three strains. SD rats spread in an area wider than those of the Donryu and ACI rats. Saliva spreading in the FOK rats continued for 4.0–4.5 h, far longer than in the other strains. Under ketamine anesthesia and exposure to 40°C, the FOK rats secreted saliva at 1390 ± 235 μL/100 g of body weight during a 60-min observation period. This was the highest rate among the four rat strains ( p < 0.0001). The body temperature increase rate in anesthetized FOK and SD rats was lower than in the other two strains, suggesting a minor contribution of unknown factors. Ligation of the submandibular gland ducts abolished the thermal salivation of the FOK rats, whereas ligation of the parotid duct had no effect. The submandibular, sublingual, and lachrymal glands in the FOK rats were 1.3–1.5, 1.25–1.4, and 1.3–1.5 times heavier, respectively, than those in the other three strains, whereas the parotid gland of the FOK rats was not enlarged. These findings indicate that the rats’ saliva spreading and ET values are significantly correlated. A potentiated and long-lasting salivation from the submandibular gland was acquired during development of genotypic heat adaptation. This salivation is actuated in response to heat. The pronounced thermal salivation is probably attributable to adaptive changes in the superior salivatory nucleus–chorda tympani–submandibular gland pathway.

Effects of estrogen on thermoregulatory evaporation in rats exposed to heat

The purpose of this study was to determine the effects of estrogen (E2) replacement on thermoregulation in ovariectomized rats exposed to heat. Female Sprague-Dawley rats were ovariectomized and splenectomized and implanted with a temperature-sensitive transmitter. Each rat was studied when E2 treated (after an E2 pellet implant) and untreated. Animals were divided into two groups with opposite order of treatment and were studied over a 9-wk period. Measurements of body core temperature (Tc) and evaporative water loss (EWL) were made on unrestrained animals resting at 38 degrees C air temperature. E2-treated animals increased EWL at all levels of Tc, reduced the threshold Tc for onset of saliva spreading, and regulated Tc at a lower level during heat exposure. E2 treatment elevated plasma E2 and reduced hematocrit but did not affect plasma osmolality. These effects of E2 on evaporative cooling and Tc in heat-stressed rats are similar to those that have been reported in human females. The mechanisms of the thermoregulatory effects of E2 remain to be studied.

Thermal salivation and body water economics among Wistar rat strains.

Strain difference in thermoregulation under hot environment was studied among Wistar rat strains, especially in relation to thermal salivation and body water economics (BWE). Eight Wistar rat strains were exposed to an ambient temperature (Ta) of 42.5°C, 40%RH. Survival time (ST), saliva spreading (SS), body water loss (BWL), BWE, and wet weight of 3 salivary glands were determined. Strain difference in thermoregulatory ability was as large among Wistar rat strains as it was among non-Wistar rat strains. Crj: Wistar survived heat longer than the others. LEW/N Crj, HOS: Wistar, Wistar-Kyoto and Wistar/MS also survived heat longer than Jcl: Wistar, Wistar King A and Wistar/MK. Rats depend on extensive SS in order to survive the heat longer than 2 hr. BWE was highly efficient in strains showing more saliva spreading than others. There was no change in the wet weight of the submaxillary gland in terms of heat tolerance. These findings indicated that thermal salivation is a potential evaporative heat loss system in Ta higher than body temperature (Tb). Thermal salivation is supported by rapid body water mobilization in the early phase and by highly efficient BWE during the following long lasting hyperthermia.

Thermally induced salivary secretion in anesthetized rats.

Effect of thermal stimulation on salivary secretion was examined in urethane anesthetized (i.p., 1.0 g/kg) rats. First, rectal temperature (Tre) was maintained at various levels by warming the whole trunk with a heating blanket. Copious salivary secretion occurred when Tre reached a threshold value above 40 degrees C, which is considerably higher than the threshold for tail vasodilation. Local warming of the scrotum, face, or hypothalamus also elicited salivary secretion, but only if Tre was in a limited range just below the threshold temperature at which Tre alone would induce salivary secretion. The higher the Tre within that limited range, the lower the temperature of the site locally warmed at which salivary secretion began. Changes in temperature of the abdomen, not including the scrotum, modulated the salivary secretion elicited by scrotal warming. Hypothalamic and scrotal temperatures interacted with each other to affect salivary secretion. Temperature signals from both core and periphery thus appear to be integrated in bringing about salivary secretion. Thermally induced salivary secretion may function as a basis for saliva spreading behavior observed in rats in a hot environment.

Acid-Base Balance and Body Temperature Regulation of Heat Stressed Psammomys obesus (Gerbillinae): The Effect of Bicarbonate Loss via Saliva Spreading

Psammomys obesus, a diurnal desert rodent, was exposed to air temperatures (Ta; Tb = body temperature) of 24–40 C and relative humidity (RH) > 30%. Between 24 and 38 C Ta, a positive Tb − Ta gradient for effective dry heat dissipation exists. At 40 C Ta, hyperthermia develops and is accompanied by intensive spreading of saliva essential for body cooling. The arterial blood acid-base status, determined in chronically cannulated animals, is kept normal (pH = 7.42; PCO₂ = 30.1 mm Hg) at 28-38 C Ta. During 2 h at 40 C, metabolic acidosis develops and is partially compensated for by respiratory alkalosis (PCO₂ = 21.2 mm Hg), resulting in pH 7.32. After 2 h of salivation (animals were treated with pilocarpine to increase saliva flow), the heat stressed animals' saliva remains very alkaline (standard bicarbonate [HCO₃⁻] ST = 42.1 meq/liter, pH = 8.42), but extreme [HCO₃⁻] depletion develops in the blood ([HCO₃⁻] = 10. 1 meq/liter). These data strongly suggest the existence of a mechanism having negative value for maintenance of [H +]. It enhances bicarbonate drainage from blood through long-term salivation. In gerbils exposed to extreme thermal stress, saliva spreading is an essential cooling mechanism for Tb regulation. This may result in severe acidosis, which may limit the ability to maintain normal homeostasis during exposure to heat stress.

Effect of ambient temperature on autonomic thermoregulation and activity patterns in the rufous rat-kangaroo (Aepyprymnus rufescens: Marsupialia)

1. Metabolic rate (MR), deep body temperature (Tb) and respiratory frequency (f) were measured in rufous rat-kangaroos in a controlled environment at ambient temperatures (Ta) between 5 and 37 °C. Diurnal variations inTb, total motoric activity and activity pattern were recorded in the same animals in open outdoor enclosures. 2. The lowest MR of 2.74 W kg−0.75 occurred betweenTa=25 to 35 °C. Considerable changes in thermal conductance (C) resulted in a nonlinear increase in MR below the lower critical temperature of 25 °C. Changes inC were attributed to postural changes leading to a reduction in the effective surface area. Panting and saliva spreading were the main mechanisms of heat dissipation atTa above 30 °C. 3. A. rufescens showed a reproducible motoric activity pattern during the night. Total locomotor activity and activity patterns and circadian variations inTb were not affected byTa even below 0 °C. 4. The nest had an important insulative function during the day, the resting period of the animals, but was only seldomly used at night. 5. It is concluded that the locomotor activity may contribute to the regulation ofTb mainly by minor changes in hopping speed and in the duration of resting periods, but not by changes in total activity and activity patterns.

Strain difference in thermoregulation of rats surviving extreme heat.

The survival times of unanesthetized rats in 42.5 degree C. 48% rh were studied in 12 different strains. In males, Sprague-Dawley rats (P less than 0.01) and Fisher 344/MK (P less than 0.05) showed significantly higher heat tolerance than the other 9 strains. Among Sprague-Dawley rats, females tolerated heat longer than males (P less than 0.05). There was no difference in lethal body temperature according to strains and exposure temperatures (38.5-48.5 degree C). Maximum survivable body temperature was 43.1 degree C in males and 43.3 degree C in females. The body weight loss in heat was greater in Sprague-Dawley, Fisher 344/MK, and JCL:Wistar strains. The degree of saliva spreading during the equilibrium period just below the maximum survivable body temperature correlated significantly with heat tolerance and was found to be the index of strain difference in heat tolerance. These findings demonstrated that the thermoregulatory system of rats is controlled genetically, though survival times of individuals in different strains sometimes overlap.

Body Temperature Variability in the Australian Water Rat, Hydromys chrysogaster, in Air and Water

Body and skin temperatures were recorded from water rats exposed to a range of air temperatures and also immersed in water at various temperatures. They were able to maintain stable core temperatures (mean 36.1�C, SD 0.65, n=61) at air temperatures up to 30�C. At 35�C they were unable to avoid hyperthermia despite their use of saliva spreading to enhance heat loss. Regional heterothermia was observed both in air and in water, but water rats were unable to maintain deep body temperatures at water temperatures lower than 25�C. Variations in the level of activity in cold water affected the rate of heat loss. Examination of the vascular system revealed the presence of various networks adapted for heat loss, but no major heat-conserving vascular retia. It is suggested that the poor thermoregulatory performance of water rats during aquatic excursions is largely due to the lack of heat-conserving retia, and to the poor insulative capacity of the fur when wet. The platypus, which possesses excellent fur insulation and a highly developed heat-conserving system, is a very competent homeotherm in cold water. The behavioural responses displayed by water rats which enable them to exploit the aquatic environment in south-eastern Australia are discussed.

Salivary cooling, escape reaction and heat pain in capsaicin-desensitized rats.

Salivary thermolytic mechanisms (weight of salivary glands, effect of desalivation on water intake and body temperature, grooming activity) as well as escape behaviour and reaction to heat pain were studied in capsaicin-desensitized and control rats exposed to various warm ambient temperatures. Body temperature of the desensitized rats increased more than the controls' at all the ambient temperatures studied (32, 34 and 36 degrees C); however, significant differences in the mechanism of salivary cooling were obtained only at 34 and 36 degrees C. Central impairment of saliva spreading in desensitized rats seems evident. Complete surgical desalivation did not increase hyperthermia of control and desensitized animals in warm environments. Therefore other mechanisms, primarily vasodilatatory, must also be involved in the rat's thermolytic normal response. Although desensitized rats did not show a tendency to escape from the warm environment their response to heat pain was normal. In conclusion, it is suggested that heat perception in desensitized animals is impaired; however, the existence of some capsaicin-insensitive thermolytic mechanisms (prone extension of the body) cannot be excluded.

Electrical activity of the dorsal hippocampus in rats operantly trained to lever press and to lick.

One group of four rats was operantly conditioned in a Sidman avoidance procedure to lever press during one discriminative stimulus and to lick during another discriminative stimulus. Another group of four rats was conditioned in a similar manner in order to receive positive reinforcements. More dorsal hippocampal rhythmic slow activity (RSA) occurred during lever pressing than during operant licking. It was also found that dorsal hippocampal RSA accompanied walking and that dorsal hippocampal large irregular activity occurred during periods of immobility, during normal drinking and grooming and during the intense saliva spreading and grooming that were induced by exposure to a 40 degrees C environmental temperature. The data suggested that hippocampal RSA is related to type of response rather than to sensory, motivational, or learning processes. Furthermore, the data suggested that RSA is not related to the operant role of response or to relative vigor of response.

Forelimb blood flow and saliva spreading in the thermoregulation of the red kangaroo, Megaleia rufa

1. 1. Vascularity of the forelimb of the kangaroo, examined by means of latex casts, includes a profuse superficial venous network which appears highly suited to the regulation of heat exchange. 2. 2. Measurements of blood flow through the brachial artery, using electromagnetic transducers, revealed a marked increase during heat stress but no change during cold stress. 3. 3. It appears that saliva spreading over the surface of the forelimb associated with increased local blood flow could provide an important avenue of heat loss in the heat-stressed kangaroo.

Behavioral thermoregulation by the white rat at high ambient temperatures.

AbstractAt ambient temperatures greater than 40°C, rats must spread salvia on themselves to prevent lethal hyperthermia. This study examined the effect of other behavioral parameters on a rat's ability to thermoregulate. The animals were exposed to 42°C in a cylindrical wire cage; records of time spent saliva spreading and moving about the cage were made; and body temperatures were measured with thermocouples implanted in the animals' abdominal cavities. Very little time spent saliva spreading was necessary for an animal to become thoroughly wetted on its ventral surface. Once wetted, an animal's thermoregulatory ability depended on its amount of locomotion. Animals which spent a considerable amount of time climbing about the cage were unable to stabilize their body temperatures and suffered increasing hyperthermia. Those which had low levels of locomotion were able to hold a constant body temperature for an hour or more. Several of the animals were given seven successive exposures to 40°C, followed by a second exposure to 42°C. Most of these animals showed greatly improved thermoregulatory abilities in the second exposure at 42°C as compared with the first, and this improvement was associated with markedly decreased locomotion. Several animals showed increased saliva spreading, but this change was not well correlated with improved thermoregulatory ability. It was concluded that low levels of locomotion are essential for evaporative cooling by saliva spreading to be adequate, and that repeated exposures to heat can modify an animal's behavior to the type associated with prolonged thermoregulation.