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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulfolane is a solvent which produces hypothermia and decreased oxygen consumption following acute exposure. In the present experiment, we investigated effects of sulfolane on a behavioral measure of toxicity at ambient temperatures which would either prevent or facilitate the development of hypothermia. Adult male Long-Evans rats (N = 10/dose) received a single i.p. injection of saline, 200, 400 or 800 mg/kg sulfolane. Motor activity in figure-of-eight mazes was assessed 1 h after dosing in testing rooms maintained at either 20.8 degrees C or at 32.3 degrees C. At the warm ambient temperature, sulfolane produced hypoactivity but not hypothermia. At the cooler temperature, sulfolane-induced hypoactivity was more pronounced, and rats were hypothermic. Therefore, a behavioral change could be detected at sublethal dosages of sulfolane in the absence of hypothermia.
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PMID:Acute behavioral toxicity of sulfolane: influence of hypothermia. 407 60

A series of pulse-doses of 7, 8, 12-trimethylbenz(a)anthracene-induced leukemia rapidly and consistently in very high yield in rats of Long-Evans (L-E) strain. The predominant type was a diffuse hepatic leukemia of erythroblastic stem cells. Progressive hypothermia and a decline in pituitary function are newly recognized signs of advanced leukemia in rat.
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PMID:Hundred day leukemia: preferential induction in rat by pulse-doses of 7,8,12-trimethylbenz(a)anthracene. 541 51

The ascending noradrenaline (NA) pathways were lesioned by injecting 6-hydroxydopamine (6-OHDA) 16 micrograms/4 microliters bilaterally into the posterior mesencephalon in male Long Evans rats. Another group of rats was pretreated with protriptyline (25 mg/kg), a NA uptake blocking agent, 15 min before they received the intracerebral injections of 6-OHDA. The controls received the vehicle only. Spectrofluorimetric determination of the catecholamine concentrations in various parts of the brain revealed a marked degeneration of the ascending NA systems in the group receiving 6-OHDA. Unexpectedly, the DA systems were also affected by the 6-OHDA treatments. Three weeks after the operation the 6-OHDA group showed a transient increase in ethanol intake. In the tilting-plane test, ethanol (2 g/kg. i.p.) impaired the performance of the 6-OHDA-treated rats significantly more than that of the controls. In contrast, the hypothermic effect of ethanol (4 g/kg, i.p.) was significantly smaller in the lesioned rats. Furthermore, the catecholamine levels in various parts of the brain could be significantly correlated with both the extent of ethanol intoxication and the hypothermia. However, the duration of ethanol-induced narcosis (4 g/kg, i.p.) was affected by the present treatments. These results give further support for the view that the central NA neurons are important in the control of ethanol intake, and that they are involved in the expression of the acute effects of ethanol administration.
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PMID:Alcohol intake and ethanol intoxication in the rate: effect of a 6-OHDA-induced lesion of the ascending noradrenaline pathways. 719 32

Trimethyltin (TMT) chloride, administered to adult male Long-Evans hooded rats, produced a unique and distinctive behavioral syndrome consisting of spontaneous seizures, tail mutilation, vocalization and hyperreactivity. The LD50 for TMT was weight dependent; in large rats (e.g., 450 g), 7 mg/kg TMT produced significant weight loss and lethality, whereas in small rats (e.g., 250 g), 7 mg/kg produced neither weight loss nor lethality. TMT produced mild hypothermia and tremors. Results are discussed in comparison with kainic acid-induced morphological alterations and septal lesion-induced behavioral alterations. Histopathological evaluations of hippocampal tissue revealed cell loss that was largely confined to regio inferior pyramidal cells. TMT offers potential as a tool for investigations of limbic system structure and function.
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PMID:The trimethyltin syndrome in rats. 720 Oct 84

The preponderance of studies of tolerance to organophosphate (OP) cholinesterase (ChE) inhibitors indicates that functional recovery accompanies neurochemical compensations for the inhibited enzyme. Contrary to prediction, rats dosed with the OP diisopropylfluorophosphate (DFP) showed progressive and persistent impairment of cognitive and motor function over a 3-week period of daily exposure, despite neurochemical and pharmacological evidence of tolerance to its inhibition of ChE. To determine whether these functional effects of DFP resulted from inhibition of ChE and downregulation of muscarinic cholinergic receptors, rats were dosed with chlorpyrifos (CPF), an OP pesticide which inhibits blood and brain ChE of rats for weeks after a single injection. Long-Evans rats were trained to perform an appetitive test of memory and motor function and were then injected s.c. with 0, 60, 125 or 250 mg/kg of CPF in peanut oil and tested 5 days/week for 7 weeks. Unconditioned behavior was also rated for signs of cholinergic toxicity. CPF inhibited ChE activity in whole blood in a dose-related manner for more than 53 days. The degree and time course of ChE inhibition in blood and brain and the downregulation of muscarinic receptors in brain after 125 mg/kg of CPF closely paralleled the previously reported effects of 25 daily injections of 0.2 mg/kg of DFP. In addition, CPF-treated rats were subsensitive to oxotremorine-induced hypothermia for at least 32 days after CPF. However, functional deficits (in working memory and motor function) appeared within 2 days after injection of CPF and recovered within 3 weeks, long before ChE activity and receptor density returned to control levels. Thus, the effects of CPF were neither progressive nor as persistent as those seen during daily DFP injections. This difference suggests that the DFP-induced behavioral changes observed previously cannot be attributed entirely to its effects on ChE activity and changes in [3H]quinuclidinyl benzilate binding.
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PMID:Behavioral and neurochemical effects of acute chlorpyrifos in rats: tolerance to prolonged inhibition of cholinesterase. 768 99

The changes in the permeability of the blood-brain barrier during pentylenetetrazol (PTZ)-induced seizures were investigated in normothermic and hypothermic rats. Six groups of rats were studied: (I) normothermic control; (II) hypothermic control; (III) normothermia plus PTZ (80 mg/kg); (IV) normothermia plus PTZ (160 mg/kg); (V) hypothermia plus PTZ (80 mg/kg); (VI) hypothermia plus PTZ (160 mg/kg). The rats were anesthetized with diethyl ether. In the hypothermic animals, colonic temperature was reduced to 20 +/- 1 degree C by submerging the animals in ice water. In normothermic animals, distinct Evans-blue leakage was observed in the occipital cortex, thalamus, hypothalamus, substantia nigra, corpus striatum, and medulla oblongata in both PTZ groups. However, hypothermic animals which received a high dose of PTZ showed the most severe blood-brain barrier breakdown. Mean levels of Evans blue in the brains of low-dose (80 mg/kg) PTZ-treated animals were 8.7 +/- 2.2 micrograms/g and 5.7 +/- 1.4 micrograms/g in the normothermic and hypothermic groups, respectively. This difference was significant (P < 0.01). The levels in the high dose (160 mg/kg) PTZ-treated animals were 10.2 +/- 3.5 micrograms/g and 15.9 +/- 3.6 micrograms/g in the normothermic and hypothermic groups, respectively (P < 0.02). In conclusion, deep hypothermia prevents the blood-brain barrier disruption induced by 80 mg/kg pentylenetetrazol and aggravates the increase in permeability after 160 mg/kg pentylenetetrazol.
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PMID:The effect of profound hypothermia on blood-brain barrier permeability during pentylenetetrazol-induced seizures. 769 98

Mild to moderate hypothermia (30-33 degrees C) reduces brain injury after brief (< 2-h) periods of focal ischemia, but its effectiveness in prolonged temporary ischemia is not fully understood. Thirty-two Sprague-Dawley rats anesthetized with 1.5% isoflurane underwent 3 h of middle cerebral artery occlusion under hypothermic (33 degrees C) or normothermic (37 degrees C) conditions followed by 3 or 21 h of reperfusion under normothermic conditions (n = 8/group). Laser-Doppler estimates of cortical blood flow showed that intraischemic hypothermia reduced both postischemic hyperperfusion (p < or = 0.01) and postischemic delayed hypoperfusion (p < or = 0.01). Hypothermia reduced the extent of blood-brain barrier (BBB) disruption as estimated from the extravasation of Evans blue dye at 6 h after the onset of ischemia (p < or = 0.01). Hypothermia also reduced the volume of both brain edema (p < or = 0.01) and neuronal damage (p < or = 0.01) as estimated from Nissl-stained slides at both 6 and 24 h after the onset of ischemia. These results demonstrate that mild intraischemic hypothermia reduces tissue injury after prolonged temporary ischemia, possibly by attenuating postischemic blood flow disturbances and by reducing vasogenic edema resulting from BBB disruption.
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PMID:Mild intraischemic hypothermia reduces postischemic hyperperfusion, delayed postischemic hypoperfusion, blood-brain barrier disruption, brain edema, and neuronal damage volume after temporary focal cerebral ischemia in rats. 801 9

We investigated the effects of endotoxins on water balance, rectal temperature, and food intake in male Long-Evans rats with femoral venous catheters. Extracts of Escherichia coli or Salmonella minnesota, in doses ranging from 125 to 500 micrograms/kg IV, stimulated drinking and reduced urinary water loss for several hours. The net gain of 5 ml water 2 h after the lowest dose of E. coli endotoxin was sufficient to reduce plasma osmolality and sodium concentration 2 to 3%. Drinking occurred during the period of hypothermia that frequently precedes the onset of endotoxin-induced fever, so cannot be attributed to increased body temperature. Doses of endotoxin causing drinking inhibited both spontaneous and deprivation-induced feeding. The cause of the drinking is not known, but may involve mechanisms other than the known dehydrational signals controlling thirst.
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PMID:Stimulation of drinking by bacterial endotoxins in the rat. 824 64

Strategies for neurotoxicity testing often include initial screening tests, such as a functional observational battery (FOB) and motor activity assessment, followed by detailed characterization studies. In this study, a neurobehavioral screening battery (FOB and motor activity) was used to evaluate the effects of 3-day repeated exposure to 0, 100, 200, or 400 mg/kg/day IDPN. Adult Long-Evans rats (males and females) were tested before dosing and 1, 14, 28, 56, and 91 days after the third dose. IDPN initially produced generalized CNS depression, weakness, and hypothermia. Thereafter, marked hyperactivity, increased excitability, decreased reactivity to visual and auditory stimuli, neuromuscular weakness, equilibrium changes, and a "waltzing syndrome" (vertical and lateral head movements, circling, and retropulsion) emerged and persisted for 3 months. Males were more severely affected than females. Following neurobehavioral testing, the rats were examined for visual function using flash (three intensities) and pattern (three pattern sizes by three contrast levels)-elicited visual evoked potentials (VEPs). IDPN produced changes in pattern- and flash-elicited VEPs, thus verifying predictions made from the screening tests. However, the extent of the VEP changes produced by IDPN was insufficient to account for some of the deficits detected in the FOB, which are dependent on sensory, integrative, and motor functions. Thus, profound neurological effects of IDPN were detected using this screening battery and visual effects were confirmed using VEPs. These effects, following only three doses of IDPN, lasted for at least 3 months and thus may be permanent.
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PMID:Prolonged neurobehavioral and visual effects of short-term exposure to 3,3'-iminodipropionitrile (IDPN) in rats. 798 39

The isolated perfused liquid-filled rat lung in a "pleural bath" was the model used to study liquid exchange across the lung epithelium. Active transport and passive solute movement between the air space, the vascular perfusate, and the bath result in concentration changes of the three markers (Evans blue-tagged albumin, 22Na+, and [3H]mannitol) instilled in the air space. A mathematical model was developed to estimate the active and passive solute transports and to interpret the results. Rat lungs were perfused at left atrial and pulmonary arterial pressures of 0 and 8 mmHg, respectively. Six rat lung experiments were conducted at 37 degrees C and six at 4 degrees C. The normothermic experiments demonstrate that active transport accounts for 26% of the Na+ movement out of the air space (17.3 +/- 0.7 nm/s) and that passive mechanisms account for the remaining 74% (48.0 +/- 5.7 nm/s). Hypothermia inhibits lung liquid clearance but does not affect passive solute movement, suggesting that lung liquid clearance is effected by active Na+ transport mechanisms.
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PMID:Active transport and passive liquid movement in isolated perfused rat lungs. 828 6


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