Acclimation to heat of the beagle dog

Four beagle dogs showed evidence of heat acclimation (reduced post-exercise heart rate and body temperature) within 10 days of first exposure of one hour a day in a hot environment (38 ± 2°C). One hour of daily exercise (110 m/min, 0% grade) in the heat (as with human subjects) was adequate to produce the effects of heat acclimation. The physiological changes observed were due to heat exposure alone since the work which was done for training (110 m/min, 4% grade) at the control temperature (20 ± 2°C), was reduced in the heat (0% grade).     

Early chick neuroretinal responses following direct exposure to methotrexate

Explants of 4.5-day-old chick embryonic neuroretinas with mesenchyme were exposed to Methotrexate (MTX) in medium 199 with embryo extract. Proliferative responses of the cultured neuroretinas were followed radioautographically by administration of ³H-thymidine to the cultures. The DNA synthetic, mitotic and pyknotic responses of the ventricular cells of the neuroretina were followed over a 16-hour period. The responses observed suggested that MTX caused a synchronization of the ventricular cells in the pre-mitotic phases with no direct inhibition of mitosis. Furthermore, prolonged exposure to MTX resulted in the accumulation of labeled pyknotic cells, indicating a decline in the regenerative capacity of the proliferative ventricular cells.     

Testicular function of rats following exposure to microwave radiation

Male Sprague-Dawley rats were exposed for 6 h per day for nine days to pulse-modulated microwave radiation (1.3 GHz, at 1-microseconds pulse width, 600 pulses per second). Exposures were carried out in cylindrical waveguide sections at a mean dose rate of 6.3 mW/g; sham controls were treated similarly and received no irradiation. At time periods corresponding to 0.5, 1.0, 2.0, and 4.0 cycles of the seminiferous epithelium, groups of four sham-irradiated and four irradiated rats were killed and the testes removed for analysis. Net mass of the testes, epididymides, and seminal vesicles; daily sperm production (DSP) per testis and per gram of testis; sperm morphology; and the number of epididymal sperm were determined. There were no statistically significant differences between the sham-irradiated and irradiated groups with respect to any measured variable. In a group of seven surrogate animals of similar body mass, the dose rate of 6.3 mW/g caused a net change in body temperature (via rectal probe) of 1.5 degrees C.     

Testosterone modifies response to chronic heat exposure in rats

Eight weeks of heat exposure (34±0.5°C) in sham-orchiectomized rats leads to an increase of body temperature, slowing of body growth rate, and decrease of serum corticosterone level, as compared with animals maintained at 21±2°C. Orchiectomy decreases body temperature, slows growth rate, and increases plasma corticosterone concentration both in control and heat exposed animals. Testosterone administration reverts these parameters to initial values. We conclude that testosterone plays a role in the regulation of heat balance in male rats.     

Causes of cell death following exposure to different fungicides and heat

The lethal effects of several agricultural fungicides, the mutagen ICR-170, and heat have been studied in multinucleated spores from heterokaryotic mycelia ofPhycomyces blakesleeanus. The fungicides captafol, captan, Manzate (maneb), Benlate (benomyl), and ZZ-melprex (dodine) induce exclusively cytoplasmic lethality. The mutagen ICR-170 causes three different kinds of lethal events: mitotic, recessive, and cytoplasmic. Heat exposure of dormant spores results in only cytoplasmic lethal damage. Germination increases heat sensitivity, particularly that of nuclei; while most of the lethality in germinating spores is still cytoplasmic, there is a definite contribution of mitotic lethality, i.e., events blocking the division of the affected nuclei.     

Translation of muscle mRNA in rats following acute exposure to Pb2+ or Cd2+

The hindleg muscle of rats was studied 2 days following the i.p. administration of 0.5 mg Pb2+ /100 g body wt or 0.12 mg Cd2+ /100 g body wt or both Pb2+ and Cd2+. The incorporation of [14C]leucine into proteins was measured using mRNA obtained from the muscle polysomes. The translatability of this poly(A)+ RNA in a mRNA-dependent reticulocyte lysate was elevated similarly in each of the preparations from heavy metal treated rats compared to control rats. Evidence for increased mRNA activity for glyceraldehyde-3-phosphate dehydrogenase and actin was obtained.     

Neonatal behavioral toxicity in rats following prenatal exposure to methanol

Although methanol (MEOH) may assume a significant role as a fuel, which implies wide availability, little is known of its toxicity apart from acute poisoning episodes in human adults. Even less is known about its toxicity in developing organisms. This experiment studied the early behavioral development of rats whose mothers had consumed MEOH during gestation by measuring the responses of suckling (postnatal day 1) and nest-seeking (postnatal day 10). Primigravida Long-Evans rats were divided into three groups (N = 10). Two of the groups consumed drinking solutions of 2% MEOH instead of distilled water either on gestational days 15-17 (MEOH 1) or 17-19 (MEOH 2). No maternal toxicity was apparent as measured by weight gain, gestational duration, and daily fluid intake. Daily MEOH consumption averaged 2.5 gm/kg over the 3-day period in both MEOH groups. Litter size, birth weight, and infant mortality did not differ among the three groups. Postnatal growth and date of eye opening were unaffected. MEOH pups required longer than controls to begin suckling on postnatal day 1. On postnatal day 10, they required more time to locate nesting material from their home cages. These data suggest that prenatal MEOH exposure induces behavioral abnormalities early in life that are unaccompanied by overt toxicity.     

Chronic low-sodium diet in rats: responses to severe heat exposure

To determine the effects of sodium (Na+) deficiency on the responses to severe heat stress (35.5 degrees C), immature (mean wt 150.4 g) male rats (n = 21) were fed a low-Na+ diet for 71 days. Rates of weight gain and food consumption were significantly (P less than 0.001) reduced in the low-Na+ group, whereas water consumption was unaffected. Prior to heat exposure circulating Na+ levels were unaffected by dietary Na+ restriction, but both circulating potassium (K+) and hematocrit levels were significantly (P less than 0.001) increased. After 24-h exposure to severe heat stress, circulating Na+ levels did manifest a significant (P less than 0.001) decrement in the low-Na+ group. K+ levels increased significantly (P less than 0.01) in the control group after 6 h of heat exposure but remained depressed in comparison with the low-Na+ group after 48 and 72 h. Although plasma renin activity (PRA) was not increased by chronic consumption of the low-Na+ diet or by severe heat exposure in the control group, severe heat stress in the low-Na+ group did elicit significant (P less than 0.005) increments in PRA after 24 h of exposure. Alternatively, plasma aldosterone levels were significantly (P less than 0.001) elevated by both the low-Na+ diet and heat stress. We concluded from these studies that chronic consumption of the low-Na+ diet had severe effects on hematologic, endocrinological, and thermoregulatory variables as well as thermal sensitivity to prolonged and sedentary exposure to severe heat stress.     

Thermoregulatory responses to acute body heating in rats acclimated to continuous heat exposure

Thermoregulatory responses to an acute heat load with intraperitoneal heating (IH) or indirect external warming (EW) by increasing ambient temperature (Ta) were investigated with direct and indirect calorimetry in rats acclimated to environments of 24.0 degrees C (Cn), 29.4 degrees C (H1), and 32.8 degrees C (H2) for greater than 15 days. The rats were placed in a direct calorimeter where the air temperature was maintained at 24 degrees C for the initial 3 h. IH was then made for 30 min through an electric heater implanted chronically (6.5 W.kg-1) in the peritoneal cavity, and EW was performed by raising the jacket water temperature surrounding the calorimeter from 24 to 39 degrees C (0.19 degrees C.min-1). Hypothalamic (Thy) and colonic temperature immediately before the start of the heat load tended to be higher as the acclimation temperature increased. During IH, the threshold Thy for the tail skin vasodilation (Tth) was significantly higher in H2 than in Cn rats. During EW, however, there was no difference in Tth between the groups. Metabolic heat production (M) was slightly suppressed during IH and significantly depressed only in H2 rats. During EW, M was suppressed in all the groups. The magnitude and duration of suppression were greater in H2 rats than in the other two groups. The responses in nonevaporative heat loss and thermal conductance (C) to the rise in Thy did not differ among the three groups during IH. According to the rise in Thy, however, there was a greater C increase in H2 than in Cn and H1 rats during EW.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cyanobacterial Acclimation to Photosystem I or Photosystem II Light

The organization and function of the photochemical apparatus of Synechococcus 6301 was investigated in cells grown under yellow and red light regimes. Broadband yellow illumination is absorbed preferentially by the phycobilisome (PBS) whereas red light is absorbed primarily by the chlorophyll (Chl) pigment beds. Since PBSs are associated exclusively with photosystem II (PSII) and most of the Chl with photosystem I (PSI), it follows that yellow and red light regimes will create an imbalance of light absorption by the two photosystems. The cause and effect relationship between light quality and photosystem stoichiometry in Synechococcus was investigated. Cells grown under red light compensated for the excitation imbalance by synthesis/assembly of more PBS-PSII complexes resulting in high PSII/PSI = 0.71 and high bilin/Chl = 1.30. The adjustment of the photosystem stoichiometry in red light-grown cells was necessary and sufficient to establish an overall balanced absorption of red light by PSII and PSI. Cells grown under yellow light compensated for this excitation imbalance by assembly of more PSI complexes, resulting in low PSII/PSI = 0.27 and low bilin/Chl = 0.42. This adjustment of the photosystem stoichiometry in yellow light-grown cells was necessary but not quite sufficient to balance the absorption of yellow light by the PBS and the Chl pigment beds. A novel excitation quenching process was identified in yellow light-grown cells which dissipated approximately 40% of the PBS excitation, thus preventing over-excitation of PSII under yellow light conditions. It is hypothesized that State transitions in O₂ evolving photosynthetic organisms may serve as the signal for change in the stoichiometry of photochemical complexes in response to light quality conditions.     

Apparent pA2 value of naltrexone is not changed in rats following continuous exposure to morphine or naloxone.

Chronic opioid antagonist administration increases opioid binding sites and potentiates behavioral responses to morphine. Conversely, chronic opioid agonist administration attenuates behavioral responses to morphine, though this is not necessarily accompanied by a parallel loss of binding sites. We examined the possibility that the in vivo affinity of the mu receptors might be altered as a consequence of the continuous administration of either naloxone or morphine. Rats were implanted sc with naloxone- or morphine-filled osmotic pumps; control animals were implanted with sham pumps. One week later, 24 hr after removing the osmotic pumps, cumulative dose-response curves for fentanyl analgesia were generated in the presence of 0.0, 0.03, 0.1, or 0.3 mg/kg naltrexone, using a tail-flick procedure. The analgesic ED50 (with 95% C. L.) of fentanyl in sham implanted animals, following saline pretreatment was 0.027 mg/kg (0.019, 0.039). The potency of fentanyl was decreased in rats infused with morphine, ED50 = 0.051 mg/kg (0.028, 0.093), and increased in rats that received naloxone, ED50 = 0.018 mg/kg (0.015, 0.022). The mean apparent pA2 value for naltrexone (with 95% C.L.) in the control group was 7.7 (7.5, 7.9). No differences were detected in animals that had received either naloxone or morphine for 7 days, pA2 = 7.8 (7.5, 8.1) and 7.4 (7.3, 7.6), respectively. Our results indicate that there is no change in the apparent affinity of the mu-receptor following continuous exposure to either an opioid agonist or antagonist, at a time when the analgesic potency of the agonist is decreased or increased, respectively.