A hospital/school science fair mentoring program for middle school students.

The Massachusetts General Hospital (MGH) and the James P. Timilty Middle School established a partnership to enhance science education, promote faculty development, and improve the health status and academic performance of all Timilty students. This article describes one of the Partnership's Science Connection programs, the Science Fair Mentoring Program, designed to enhance middle school science education, inform urban early adolescents about professions in the health field, inspire them to pursue postsecondary study in the health sciences, and prepare them for rigorous academic work in high school. In this program, hospital-based clinical and research staff mentor young adolescent students. The authors describe the planning, implementation, and evaluation of the Science Fair Mentoring Program as an innovative learning experience.

Exercise during pregnancy and maternal and fetal plasma corticosterone and androstenedione in rats.

Adrenocortical glucocorticoid and androgen secretion is stimulated by exercise. Excesses of these hormones in fetuses can cause abnormalities in development. We measured maternal and fetal plasma corticosterone and androstenedione concentrations in Sprague-Dawley rats immediately after maternal exercise in exercise-trained mothers and at rest in sedentary mothers. To do this, we developed a technique for fetal blood sampling and assessed its effect on maternal and fetal plasma corticosterone concentrations. Under halothane anesthesia, maternal blood was collected by cardiac puncture and fetal blood was collected from carotid and jugular vessels. Corticosterone was not affected by the blood collection procedure. Corticosterone was significantly higher in exercised mothers and their fetuses after 30 min of running than in sedentary mothers and their fetuses at rest. Androstenedione was significantly higher in exercised mothers after 30 min of running than in sedentary mothers at rest, but fetal androstenedione was not different between groups. We conclude that this maternal exercise protocol elevates plasma corticosterone but not androstenedione concentrations in fetal rats.

Effect of low and high doses of nitrous oxide on preproenkephalin mRNA and its peptide methionine enkephalin levels in the hypothalamus.

The effect of exposure to nitrous oxide (N2O) on the levels of preproenkephalin mRNA in the hypothalamus of rats was examined. In the first experiment, rats were exposed to 1000 ppm N2O for 8 h a day over 4 days. Compared with controls (which were exposed to air over the same duration), the N2O exposed animals exhibited significant elevations in preproenkephalin mRNA levels in the hypothalamus. In a second experiment, rats were exposed to 60% N2O or air for 12, 24 and 48 h duration, and hypothalamic levels of preproenkephalin mRNA as well as methionine enkephalin were analyzed. Compared with controls, N2O exposed rats exhibited significant elevations in preproenkephalin mRNA levels. The levels on preproenkephalin mRNA were significantly higher after 48 h of N2O exposure than after 12 h of N2O exposure. Similarly, the concentration of methionine enkephalin was significantly higher after 24 and 48 h of exposure of N2O than after exposure to 12 h of N2O or air. These results indicate that (a) exposure to N2O results in significant elevations in preproenkephalin mRNA levels, (b) the increased preproenkephalin mRNA levels appear to be proportional to the concentration of N2O exposure as well as the duration of N2O exposure, and (c) N2O-induced elevation in preproenkephalin mRNA levels is associated with corresponding increase in tissue concentrations of methionine enkephalin. In total, these results suggest that N2O selectively stimulates synthesis of methionine enkephalin in the diencephalic region of the brain.

Interleukin-1 alpha stimulates dopamine release by activating type II protein kinase A in PC-12 cells.

A recent study from this laboratory [A. R. Gwosdow, N. A. O'Connell, and A. B. Abou-Samra. Am. J. Physiol. 263 (Endocrinol. Metab. 26): E461-E466, 1992] showed that the inflammatory mediator interleukin-1 alpha (IL-1 alpha) stimulates catecholamine release from primary cultures of rat adrenal cells. The present studies were conducted to determine whether 1) IL-1 alpha stimulates catecholamine/dopamine release from the adrenal medullary cell line PC-12 and 2) the adenosine 3',5'-cyclic monophosphate (cAMP)-protein kinase A (PKA) pathway is involved in IL-1 alpha-induced dopamine release from PC-12 cells. The results indicate that IL-1 alpha significantly (P < 0.05) elevated dopamine release after a 24-h incubation period. IL-1 alpha did not stimulate cAMP accumulation at any time period between 5 min and 2 h. In contrast, forskolin-treated cells elevated (P < 0.05) intracellular cAMP levels and increased dopamine release. Because IL-1 alpha did not affect cAMP accumulation, the effect of IL-1 alpha on PKA activity was investigated. IL-1 alpha increased (P < 0.05) PKA activity at 15 and 30 min and returned to control levels by 1 h. Forskolin also increased (P < 0.05) PKA activity. The type of PKA activated (P < 0.05) by IL-1 alpha was type II PKA. In contrast, forskolin activated (P < 0.05) type I and type II PKA. Inhibition of PKA with the PKA inhibitor H-8 blocked PKA activity and dopamine secretion by both IL-1 alpha and forskolin in PC-12 cells. These observations demonstrate that 1) IL-1 alpha stimulated dopamine release from PC-12 cells by activating PKA, 2) the mechanism of IL-1 alpha activation of PKA does not involve detectable increases in intracellular cAMP accumulation, and 3) IL-1 alpha activates type II PKA, which is used by IL-1 alpha to stimulate dopamine secretion from PC-12 cells.

Effects of anesthesia with halothane and methoxyflurane on plasma corticosterone concentration in rats at rest and after exercise.

To determine whether halothane and methoxyflurane are suitable anesthetics for cardiac puncture in studies of plasma corticosterone concentration in rats, four experiments were done. Blood samples were taken immediately after rats became anesthetized with halothane or methoxyflurane. Decapitation without anesthesia was used to determine baseline corticosterone concentration. Another group of rats was anesthetized with ether as a positive control (known to stimulate corticosterone secretion). Corticosterone values in halothane- and methoxyflurane-treated rats were not significantly different from those measured after decapitation. Corticosterone concentration in halothane-treated rats was significantly lower than that in either methoxyflurane- or ether-treated rats. Cardiac puncture was done after 3 min of exposure to each of the three anesthetics. The results indicated that there were no differences in corticosterone values among the three anesthetics, suggesting that corticosterone concentration was lower immediately after halothane was used as the anesthetic, because halothane induced anesthesia in less time than that required for activation of adrenocortical secretion. To determine whether there was a difference among anesthetics in stimulating corticosterone secretion when anesthesia was maintained for a period before blood sample collection, cardiac puncture was done after 15 min of exposure to each of the three anesthetics. Corticosterone values were similar, suggesting that any of the three anesthetics was acceptable in this situation. To determine whether halothane or methoxyflurane affected exercise-induced increases in corticosterone values, exercise-trained rats were run for 30 min; then blood samples were collected by cardiac puncture immediately after induction of anesthesia with halothane, methoxyflurane, or ether, or after decapitation without anesthesia. Corticosterone values were not different among the three anesthetics or decapitation.

Mechanisms of interleukin-1-induced hormone secretion from the rat adrenal gland.

The aim of these studies was to determine the intraadrenal mechanism of interleukin-1 (IL-1)-induced corticosterone release from the rat adrenal gland. To accomplish this, the role of catecholamines and eicosanoids on IL-1-induced corticosterone release was determined. Experiments were conducted on primary cultures of dispersed rat adrenal cells. Dose-dependent increases (P < 0.05) in corticosterone concentration were observed when primary adrenal cells were incubated with different doses (10(-10) to 10(-8) M) of IL-1 alpha. IL-1 alpha and IL-1 beta elevated corticosterone release after a 24 hr incubation period. ACTH elevated corticosterone levels at 4 and 24 hr. The stimulatory effect of IL-1 on corticosterone release was mimicked by epinephrine (1 microM), and was selectively blocked by the alpha-adrenergic antagonist, phentolamine (10 microM). The beta-adrenergic antagonist, propranolol (10 microM), did not change IL-1 induced corticosterone release. Neither phentolamine nor propranolol had an effect on ACTH stimulated corticosterone release. Both IL-1 alpha and IL-1 beta significantly elevated (P < 0.05) epinephrine levels after a 24 hr incubation period compared to media-treated controls. Untreated adrenal cells fixed for immunohistochemical staining with a specific anti-rat tyrosine hydroxylase antibody indicate that the primary adrenal cell preparation contained 3.1 +/- 0.45% tyrosine hydroxylase positive cells. On the ultrastructural level, the chromaffin cells were found to be in direct cellular contact with cortical cells. Although IL-1 alpha significantly increased (P < 0.05) prostaglandin E2 (PGE2) levels from primary adrenal cells, the presence of the cyclooxygenase inhibitor, indomethacin (10 microM) significantly inhibited IL-1 alpha-induced PGE2 secretion without altering the effect of IL-1 alpha on corticosterone release. Inhibitors of the lipoxygenase system (5-lipoxygenase, 10 microM) and the lipoxygenase and cytochrome P450 monooxygenase systems (nordihydroguaiaretic acid, 10 microM) did not effect IL-1 alpha-induced corticosterone or PGE2 release. These observations indicate that IL-1 stimulates the local release of catecholamines, which, in turn, stimulates corticosterone release through an alpha-adrenergic receptor; this mechanism is independent of PGE2.

IL-1 is expressed in human adrenal gland in vivo. Possible role in a local immune-adrenal axis.

IL-1 is an important mediator in the dialogue between the immune system and the hypothalamo-pituitary-adrenal axis. A direct influence of IL-1 upon adrenal steroidogenesis has been demonstrated in experimental animals. We therefore designed a study to see if IL-1 is expressed within the normal human adrenal gland. The combination of in situ hybridization and specific immunostaining to IL-1 beta was eminently suited to demonstrate both mRNA and protein production. The specific immunostaining of the different cells combined with in situ hybridization (IL-1) allowed us to identify the exact cellular source of IL-1. IL-1 mRNA occurred in the zona reticularis in 17 alpha-hydroxylase positive steroid cells surrounding the adrenomedullary cells. Some CD68+ macrophages in this zona showed a positive signal. A weak signal was seen to IL-1 mRNA in few chromaffin cells, while IL-1-like immunoreactivity was more frequent. We conclude that in the normal situation in man IL-1 is mainly expressed in specialized cortical cells. The occurrence of the major glucocorticoid inducing factor in the normal human adrenal gland itself provides evidence for an autocrine or paracrine reaction under physiological conditions.

Interleukin-1 regulates corticosterone secretion from the rat adrenal gland through a catecholamine-dependent and prostaglandin E2-independent mechanism.

Studies from this and other laboratories have shown that interleukin-1 alpha (IL-1 alpha) stimulates corticosterone and prostaglandin (PG) release from primary cultures of rat adrenal cells. A previous report from our laboratory (1) indicated involvement of the alpha-adrenergic system in IL-1 alpha-stimulated corticosterone secretion from primary cultures of rat adrenal cells. The present experiments were conducted to determine the role of catecholamines and eicosanoids in IL-1-stimulated corticosterone release from primary rat adrenal cells. Primary adrenal cells were incubated for 24 h at 37 C with IL-1 alpha (10 nM), medium, or the appropriate agonist. After incubation, the supernatant was removed and assayed for epinephrine, prostaglandin E2 (PGE2), and corticosterone concentrations. At this time, untreated adrenal cells were fixed for immunohistochemical staining with a specific antirat tyrosine hydroxylase antibody. The results indicate that the primary adrenal cells contained 3.1 +/- 0.45% tyrosine hydroxylase-positive cells. On the ultrastructural level, the chromaffin cells were found to be in direct cellular contact with cortical cells. IL-1 alpha significantly increased (P < 0.05) epinephrine, PGE2, and corticosterone levels above those in medium-treated controls from primary adrenal cells. In the presence of the alpha-adrenergic antagonist phentolamine (10 microM), IL-1 alpha-stimulated (P < 0.05) corticosterone release was inhibited, whereas IL-1 alpha-induced PGE2 release was not affected. Conversely, the presence of the cyclooxygenase inhibitor indomethacin (10 microM) significantly inhibited IL-1 alpha-induced PGE2 secretion without altering the effect of IL-1 alpha on corticosterone release. Inhibitors of the 5-lipoxygenase system (10 microM CGS 8518) and the lipoxygenase and cytochrome P450 monooxygenase systems (10 microM nordihydroguaiaretic acid) did not effect IL-1 alpha-induced corticosterone or PGE2 release. These observations indicate that IL-1 alpha stimulates corticosterone release through an alpha-adrenergic mechanism that is independent of PGE2 release from primary rat adrenal cells.

Interleukin-1 increases protein kinase A activity by a cAMP-independent mechanism in AtT-20 cells.

A recent study from this laboratory has shown that the inflammatory mediator, interleukin-1 alpha (IL-1 alpha), stimulates protein kinase A (PKA) activity and adrenocorticotropic hormone (ACTH) secretion from AtT-20 cells without any detectable increase in intracellular cAMP accumulation. The present studies were conducted to determine if cAMP is involved in IL-1 alpha activation of PKA and if PKA is responsible for IL-1 alpha-induced ACTH release from AtT-20 cells. The data are consistent with a novel mechanism of PKA activation that does not involve cAMP. Inhibition of adenylate cyclase with 2'5'-dideoxyadenosine (2'5'-DDA) did not affect IL-1 alpha-induced increases in PKA activity and ACTH secretion. In contrast, CRF-stimulated PKA activity and ACTH secretion were inhibited by 2'5'-DDA. Additional evidence was obtained using the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX). IBMX did not alter IL-1 alpha-induced PKA activity or ACTH secretion, yet IBMX potentiated CRF-induced cAMP accumulation. Inhibition of PKA with the PKA inhibitor, H-8, blocked activation of PKA and ACTH secretion by both IL-1 alpha and CRF in AtT-20 cells. These observations demonstrate that 1) the mechanism of IL-1 alpha activation of PKA is independent of adenylate cyclase or cAMP and 2) PKA is used by IL-1 alpha to induce ACTH secretion from AtT-20 cells.

Evaporative water losses through a temporary wound dressing under simulated wound conditions.

Patients with burns lose large amounts of water through evaporation from open wounds. Because the wound covering is the first line of defense for maintenance of body fluid balance in these patients, quantification of the evaporative water loss through wound coverings at the bedside would improve the accuracy of estimations of body water loss. The present experiment evaluates the use of a small ventilated capsule system automated with miniature resistance-type dew-point sensors for measurement of evaporative water loss through biologic dressings under simulated wound conditions. Evaporative water loss from wounds was simulated by pilocarpine-induced profuse sweating on the forearm. Evaporative water loss through uncovered skin was compared with that of skin covered with commercially available temporary wound dressings. Compared with an adjacent unstimulated area, forearm dew-point temperature in the capsule (Tcdp) and sweat rate increased immediately after pilocarpine exposure and remained significantly elevated and relatively constant for an additional 60 minutes. Evaporative water loss of the forearm was 29 +/- 4.8 gm/m2/hr (mean +/- SE) at baseline and rose significantly to 275 +/- 18.2 gm/m2/hr after pilocarpine exposure. The pilocarpine-stimulated sweat rate and Tcdp at neutral conditions were similar to those obtained from walking on a treadmill for 60 minutes in a 30 degrees C room. Compared with pilocarpine-induced evaporative water loss of the uncovered skin, temporary wound dressings significantly reduced evaporative water loss by 40% to 60%. No significant differences were observed between varieties of temporary wound dressings differing in thickness and/or porosity.(ABSTRACT TRUNCATED AT 250 WORDS)

Interleukin-1 activates protein kinase A and stimulates adrenocorticotropic hormone release from AtT-20 cells.

Studies from this and other laboratories have shown that interleukin-1 (IL-1) stimulates ACTH secretion directly from AtT-20 cells. The present studies were conducted to determine the signal transduction mechanisms activated by IL-1 to stimulate ACTH release. IL-1 significantly (P < 0.05) elevated ACTH release after incubation periods of 4, 8, and 24 h. IL-1-induced ACTH release was not additive to that of CRF, cholera toxin, 8-bromo-cAMP, or forskolin. In contrast, IL-1 and the phorbol ester phorbol 12-myristate 13-acetate together produced a greater increase (P < 0.05) in ACTH release than either agent alone. IL-1 did not stimulate cAMP accumulation at any time period between 5 min and 24 h and did not affect cAMP accumulation induced by CRF, cholera toxin, or forskolin. The lack of additivity between IL-1 and CRF, cholera toxin, 8-bromo-cAMP, and forskolin suggests that IL-1 stimulates ACTH release by a pathway that shares some common step(s) with CRF. Because IL-1 did not affect cAMP accumulation, the effect of IL-1 on protein kinase A (PKA) was investigated. IL-1 began to increase (P < 0.05) PKA activity at 15 min and remained elevated for 2 h before returning to control levels. IL-1 stimulation of PKA and the lack of additivity between IL-1 and CRF, forskolin, and cholera toxin indicate that PKA is the intracellular mediator used by IL-1 to stimulate ACTH release in AtT-20 cells.

Interleukin-1-induced corticosterone release occurs by an adrenergic mechanism from rat adrenal gland.

Interleukin-1 (IL-1) has been shown to stimulate corticosterone release from the adrenal gland directly, and indirectly through activation of the hypothalamic-pituitary-adrenal axis. The aim of this paper was to determine whether IL-1-stimulated corticosterone release occurs indirectly through the local release of catecholamines from the rat adrenal gland. To accomplish this, experiments were conducted on both quartered rat adrenal glands and primary cultures of dispersed adrenal cells. Incubation of quartered adrenals with adrenocorticotropic hormone (ACTH, 10(-12) to 10(-8) M) or IL-1 beta (10(-12) to 10(-8) M) resulted in dose-dependent increases (P less than 0.05) in corticosterone release. Corticosterone release stimulated by 10(-8) M doses of ACTH and IL-1 beta began to rise 30 min after incubation and peaked at 2 h. In primary cultures of adrenal cells, IL-1 alpha and IL-1 beta elevated corticosterone release after a 24-h incubation period. ACTH elevated corticosterone levels at 4 and 24 h. The stimulatory effect of IL-1 on corticosterone release was mimicked by epinephrine (10(-6) M), and was selectively blocked by the alpha-adrenergic antagonist phentolamine (10(-5) M). The beta-adrenergic antagonist propranolol (10(-5) M) did not change IL-1-induced corticosterone release. Neither phentolamine nor propranolol had an effect on ACTH-stimulated corticosterone release. Both IL-1 alpha and IL-1 beta significantly increased (P less than 0.05) epinephrine levels after a 24-h incubation period compared with media-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Interleukin 1 stimulation of the hypothalamic-pituitary-adrenal axis.

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

Physiological and behavioral temperature regulation of men in simulated nonuniform thermal environments between 18 and 30 degrees C.

Human thermoregulatory responses to nonuniform thermal environments was studied by simulating the situation with altered clothing distribution. Clothing was symmetrically or asymmetrically distributed over the body surface. Esophageal and local skin temperatures, metabolism, skin heat flux, evaporative heat loss and subjective responses of six sedentary men were measured at air temperatures between 18 and 30 degrees C. Clothing distribution significantly (p less than 0.05) influenced thermoregulatory responses only at 18 degrees C. At 18 degrees C, the bilaterally asymmetric clothing resulted in a higher (p less than 0.05) esophageal temperature compared to the symmetric condition. Mean skin temperatures did not differ with clothing distribution over the range of air temperatures studied, but at 18 degrees C whole body thermal sensation was warmer (p less than 0.05) for the asymmetric compared to the symmetric group. This increased perception of warm thermal sensation was significantly correlated to the difference in skin temperature across the body.

Effect of thermal conditions on the acceptability of respiratory protective devices on humans at rest.

The physiological and subjective responses of six sedentary subjects wearing half-facepiece respirators were observed over a wide range of room and respirator air conditions. Room air and dew-point (Ta:Tdp) temperatures were 25:11 degrees, 30:13 degrees, and 35:16 degrees C in still air. Respirator air temperatures were maintained independently of room conditions at 27 degrees, 30 degrees, 33 degrees, and 36 degrees C with relative humidity levels of 47% and 73%. Physiological measurements included local skin and dew-point temperatures. Subjective judgments of acceptability, thermal sensation, degree of discomfort, sense of skin moisture, and difficulty of breathing were recorded separately for the thermal environment in the room and inside the respirator. Respirator temperatures cooler than 33 degrees C were always comfortable and 100% acceptable; respirator air temperatures above 33 degrees C or higher humidity levels decreased respirator acceptability. Acceptability of the respirator environment decreased as lip temperature increased above 34.5 degrees C or when respirator dew-point temperature increased above 20 degrees C. Increased respirator air temperature and humidity often made breathing seem "slightly hard." The respirator conditions influenced the subjects' judgment of the acceptability of the surrounding thermal environment.

The effect of temperature and humidity levels in a protective mask on user acceptability during exercise.

Subjective and physiological responses were obtained from six subjects wearing a ventilated face mask while exercising (3.8 met) for 15 min on a bicycle ergometer. Different combinations of ambient air temperatures (7 degrees, 16 degrees, 25 degrees C) and mask air temperatures (22 degrees, 27 degrees, 33 degrees C) were studied together with two different air humidities inside the mask (61% and 86% RH). Control experiments were performed without the mask at the same ambient temperatures. Skin temperatures, heart rates and skin wettedness were monitored during exercise. The subject's acceptance of the mask and thermal environment, thermal sensation, sensations of discomfort, sweating and skin wettedness, and their judgment of the work of breathing were assessed at the end of the 15 min exercise period. The acceptance of both the ambient thermal environment and of the thermal microclimate in the mask primarily was determined by the ambient air temperature, but it was influenced by the air temperature and humidity inside the mask. At ambient temperatures of 7 degrees C and 25 degrees C, the acceptance of the thermal work conditions decreased. In the warm environment a mask air temperature less than or equal to 27 degrees C was 100% acceptable and increased the acceptance of thermal environment. In the cool environment, a mask air temperature greater than or equal to 27 degrees C was 100% acceptable. The humidity content of the mask air was only important when the mask air was warm. Warm humid air significantly decreased acceptance of the mask conditions.

Acclimation of rats following stepwise or direct exposure to heat.

The physiological changes in male rats during acclimation were studied following direct or stepwise exposure to heat (32.5 degrees C) in a controlled-environment room. The animals were exposed to each temperature for 10 days beginning at 24.5 degrees C and returning to 24.5 degrees C in the reverse order of initial exposure. Relative humidity of 50 +/- 2% and a 12-h light-dark photoperiod (light from 0900 to 2100 h) were maintained. Physiological changes in metabolic rate (MR), evaporative water loss (EWL), plasma corticosterone, body water turnover, and food and water intake were measured. The results indicate a significantly (P less than 0.001) elevated plasma corticosterone and MR in rats exposed directly to heat from control temperature (24.5 degrees C) but not in those animals exposed stepwise via 29.0 degrees C. All kinetic parameters of water pool changed (P less than 0.01) on direct exposure to heat, whereas rats exposed in a stepwise manner increased only pool turnover. In addition, exposure to experimental temperatures resulted in reduced (P less than 0.05) relative food intake and increased (P less than 0.05) water intake. Compared with the control condition of 24.5 degrees C, EWL was significantly (P less than 0.05) elevated when the animals were exposed either directly or in a stepwise fashion to 32.5 degrees C. These data suggest that the response to elevated temperatures is influenced by the temperature to which the rat is acclimated.

Effect of thermal history on the rat's response to varying environmental temperature.

After acclimating individually housed male rats to temperatures of either 24.5 +/- 0.1 or 29.2 +/- 0.1 degrees C for 14 days, randomly paired animals from each group were acutely exposed (3 h) in series to experimental temperatures between 18.0 and 34.5 degrees C in a controlled environment room. Relative humidity of 50 +/- 0.3% and a 12-h light-dark photoperiod (light from 0900 to 2100 h) were maintained. Metabolic rate (MR) and evaporative water loss (EWL) were-measured using an open-flow system; thermistors were used to measure the rectal (Tre) and tail skin (Tts) temperatures. MR was relatively constant over a temperature range of 22.2 to 27.0 degrees C for rats acclimated to 24.5 degrees C and 20.0 to 29.2 degrees C for rats acclimated to 29.2 degrees C. Above and below these ranges, MR for both groups was significantly (P less than 0.05) elevated. At their respective acclimation temperatures, the absolute Tre and Tts of 29.2 degrees C rats were maintained at an elevated level compared with 24.5 degrees C rats. Although EWL for both groups was relatively constant between 18.0 and 27.0 degrees C, 24.5 degrees C rats displayed higher EWL changes at most environmental temperatures above 27.0 degrees C. At 34.5 degrees C, 29.2 degrees C rats dissipated 26% more metabolic heat by evaporation compared with 24.5 degrees C rats. These data suggest that acclimation temperatures of rats affected the thermoneutral zone and alter the set-point temperature around which thermal responses are regulated.

The use of cerebral ventriculography for verification of intracerebroventricular cannula placement in the live rat.

A technique using cerebral ventriculography for verification of intracerebroventricular cannula placement in the live rat is described. A radiopaque contrast medium, diatrizoate meglumine, was injected into the right lateral ventricle through a cannula stereotaxically implanted into the brain. Radiographic visualization of the radiopaque contrast material in the lateral ventricle and the subarachnoid space verified cannula placement. Transient muscular spasms were observed in about 38% of the injected rats but no lasting changes were observed in the behavior or appearance of these rats.