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

General pharmacological properties of cefepime (CFPM), a new injectable semisynthetic cephalosporin and its metabolite N-methylpyrrolidine-N-oxide (NMP-N-oxide) were studied in laboratory animals. The results obtained are summarized as follows: 1. CFPM reduced spontaneous locomotor activity but potentiate the anesthesia at the highest dose in mice. Furthermore, significant hypothermia and analgesia were observed at the same dose in mice. No effects were found on the other CNS function in mice and rats or on EEG activities in rabbits. 2. Muscle relaxant activity was not observed in mice treated with CFPM even at the highest dose. 3. CFPM had no effect on the intestinal smooth muscle and did not show any antagonism against some smooth muscle contracting drugs. 4. The respiration, blood pressure, heart rate and ECG were affected by CFPM. Those changes, however, might have been principally caused by L-arginine blended with CFPM product. 5. No effect of CFPM on the intestinal movement or gastric secretion was found even at the highest dose of CFPM. 6. The pH neutralizer L-arginine caused alterations in the renal function and electrolyte metabolism but CFPM did not. 7. Whole blood clotting time tended to be lengthened by CFPM at the highest concentration but this effect seemed to have been caused by L-arginine. Other parameters of the coagulation system or red blood cell resistance were not affected by CFPM. 8. NMP-N-oxide, a metabolite of CFPM, had almost no effect on any of the tested parameters except for its slight effect on the circulatory system. These findings indicate that CFPM has scarcely any pharmacological properties which might be leading to severe adverse reactions in clinical use.
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PMID:[General pharmacology of cefepime]. 150 98

The measurement of the plasma amino acid was made in 15 patients with chronic respiratory failure and 15 persons of control. The results showed: (1) The plasma acid model changed. Lysine increases and arginine decreases, due to hypothermia. Hypercapnia imbalance of acid and alkali and changes of hepatic dysfunction etc. (2) The prognosis of respiratory failure as well as its severity was judged according to the decreasing extent of arginine and BCAA. The more worse the condition of the disease, the more lowering of the level of arginine and BCAA. (3) The changes of blood gas analysis and hepatic dysfunction may effect on the metabolism of plasma amino acid in some degree. (4) Hypoxemia in infected patients with respiratory failure may cause peripheral deficit of energy. We suggested that patients should be given BCAA and arginine for more energy as anti-infection and oxygen therapy were used.
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PMID:[The determination and evaluation of the plasma amino acid in respiratory failure]. 191 67

The effect of hypoxia, cold and hypoxic-cold stress was studied on plasma and brain amino acid levels of rats. Hypoxia caused a considerable increase in plasma taurine and phosphoserine levels, while the remaining amino acids (except valine, cystine, iso-leucine, leucine and anserine) decreased significantly. On the other hand cold stress significantly increased the plasma taurine, asparagine and decreased glutamine, glycine, alanine, methionine and histidine levels. The hypoxic-cold stress combination produced marked decrease in most of the plasma levels of amino acids (except phosphoserine, taurine and anserine). During brain amino acid studies, hypoxia significantly elevated taurine, aspartic acid, valine and leucine levels while the concentrations of other amino acids were not significantly altered. Cold stress was found to elevate taurine and valine levels, while leucine and phenyl-alanine levels were significantly decreased. Exposure of animals to hypoxic-hypothermia affected significantly the brain levels of valine, methionine, leucine and arginine. Since, the change in amino acid levels in brain is less prominent, as compared with plasma, in response to stress, it appeared that brain possesses higher adaptive mechanisms to counteract the stress induced amino acid level imbalance.
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PMID:Effect of hypoxia and/or cold stress on plasma and brain amino acids in rat. 274 Jun 20

Intracerebroventricular (ICV) administration of kyotorphin (L-Tyr-L-Arg) and cyclo (N-methyl-L-Tyr-L-Arg), its analog, produced significant dose-dependent hypothermic responses in mice at an ambient temperature of 24 degrees C. The hypothermic action of kyotorphin was much greater than that of Met-enkephalin (Met-ENK) but less than that of cyclo NMTA. This action was slightly but not significantly reversed by intraperitoneally administered naloxone (8 mg/kg), an opioid receptor antagonist. Met-ENK utilized as a control peptide in this study also produced a dose-dependent hypothermia which was slightly antagonized by naloxone (8 mg/kg, IP). Thyrotropin releasing hormone (TRH) injected ICV produced hyperthermia dose-dependently. The hypothermia induced by kyotorphin, its cyclic analog and Met-ENK was prevented by a small dose of TRH (0.18 microgram = 0.5 nmol/animal) which by itself had little effect on body temperature. A TRH neuronal system in the brain may explain the mechanism of kyotorphin-induced hypothermia. However, there was little evidence of involvement of opioid receptors. The present study demonstrates a potent action of kyotorphin and its analog on thermoregulation.
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PMID:Actions of intracerebroventricular administration of kyotorphin and an analog on thermoregulation in the mouse. 642 2

To clarify the impact of hypothermia on the hormonal control of glucose metabolism, rats were rendered hypothermic (25 C) after catheterization of the portal vein. Glucose, insulin, glucagon, and catecholamine concentrations were serially monitored, and the regional blood flows were measured, allowing the estimation of hormone outputs. Hypothermia reduced the portal blood flow by 50% without changing arterial blood pressure, blood gases, or pH. Portal plasma insulin secretion dropped (0.05 +/- 0.01 vs. 0.23 +/- 0.04 mU/min), and glucagon secretion increased (0.81 +/- 0.18 vs. 0.38 +/- 0.10 ng/min). The B cell responses to glucose, arginine, and glucagon were abolished, while the A cell response to arginine was not significantly affected. Glucose intolerance was apparent after iv glucose or arginine loads. Haloperidol and to a lesser extent phentolamine suppressed the cold-induced glucagon rise. Phentolamine and to a lesser extent haloperidol alleviated the cold-induced suppression of insulin release. Propranolol, naloxone, and atropine were relatively inactive. The cold-induced glucose intolerance was not corrected by phentolamine treatment. A marked resistance to iv insulin was apparent in these rats, which is in contrast to a normal sensitivity to iv glucagon.
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PMID:Glucagon and insulin secretion and their biological activities in hypothermic rats. 643 6

The effectiveness of cold exposure on the secretion of insulin and glucagon were examined using five adult sheep. Endocrine responses were studied in a warm environment and after cold exposure (0 C) from 4-19 days. Compared to levels at room temperature, basal plasma glucose levels were elevated during cold exposure, but basal levels of plasma insulin and glucagon were unchanged. Cold exposure significantly decreased the early insulin response to a primed iv infusion of glucose. Plasma glucose and glucagon levels during glucose infusion were unaffected by cold exposure. The decrease in plasma glucose after iv insulin injection (0.2 U/kg BW) was greater during cold exposure than at room temperature. Butyrate injection (0.625 mmol/kg, iv) resulted in a significantly lower secretion of both insulin and glucagon in the cold than in the warm environment. The glucagon response to arginine infusion (0.5 g/kg over 30 min, iv) was elevated by cold exposure, whereas the insulin response to arginine tended to be reduced. Propranolol infusion (20 micrograms/kg . min, iv) caused a slight inhibition of insulin secretion in the cold environment, but did not affect glucagon levels in either the cold or warm environment. Phentolamine infusion (20 micrograms/kg . min, iv) inhibited glucagon secretion, particularly in the cold environment, and caused a markedly greater stimulation of insulin secretion in the cold. It is concluded that cold exposure insufficient to cause hypothermia decreases insulin secretion in response to a variety of stimuli. Effects of cold on glucagon secretion depend upon the stimulating agent used.
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PMID:Effects of cold exposure on insulin and glucagon secretion in sheep. 675 53

The hypothermic effect of ethanol, tolerance to ethanol hypothermia, and the effect of desglycinamide(9)-Arginine(8)-vasopressin dicitrate (DGAVP) on ethanol hypothermic tolerance were investigated in Bailey's Recombinant Inbred strains of mice. Strains differed markedly in baseline temperatures and initial sensitivity to ethanol. There were no significant strain differences in tolerance. DGAVP attenuated the strain differences in initial sensitivity to ethanol and blocked tolerance development. These effects were accompanied by changes in the pattern of genetic control.
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PMID:Genetic analysis of tolerance to ethanol hypothermia in recombinant inbred mice: effect of desglycinamide(9)-Arginine(8)-vasopressin. 721 1

Nitric oxide (NO) has been shown to be important for intracellular microbiostasis in vitro. To determine the role of NO in immune function in vivo, groups of C57BL/6 mice were given a sublethal intravenous inoculum of Listeria monocytogenes EGD, and their urine was monitored daily for nitrate, the mammalian end product of NO metabolism. Urinary nitrate levels peaked at 5 to 10 times the basal level on days 5 to 6, when spleen and liver Listeria counts declined most steeply, and decreased thereafter, when spleens and livers were nearly sterile. Peritoneal macrophages explanted from Listeria-infected mice produced nitrite spontaneously, whereas macrophages from uninfected mice did not. The inducible NO synthase mRNA was detectable in the spleens of infected mice on days 1 to 4 of infection. When Listeria-infected mice were treated orally throughout the infection with NG-monomethyl-L-arginine (NMMA), a specific NO synthase inhibitor they showed no detectable rise in urinary nitrate excretion. Mean Listeria counts in the livers and spleens NMMA-treated mice were 1 to 3 orders of magnitude greater than counts in control mice on days 4 through 8 of infection. Compared with control mice, NMMA-treated mice also showed worse clinical signs of infection, namely, weight loss, hypothermia, decreased food and water intake, and decreased urine output. Histologically NMMA-treated mice had many more inflammatory foci in their livers and spleens than control mice. The histologic observation that mononuclear cells are present at sites of infection suggests that inhibiting NO production did not block the flux of macrophages into infected viscera. As controls for possible drug toxicity, a group of uninfected mice given NMMA orally showed no detrimental effects on weight, temperature, and food and water intake. These experiments demonstrate that inhibition of NO production in Listeria-infected mice results in an exacerbated infection and thus that NO synthesis is important for immune defense against Listeria infection in mice.
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PMID:Nitric oxide produced during murine listeriosis is protective. 750 15

Since nitric oxide (NO) has been implicated in nociceptive processing, the present study examined whether NO synthase inhibition with either Nw-nitro-L-arginine (L-NA) or its methyl ester (L-NAME) would alter antinociception elicited by either continuous (CCWS) or intermittent cold-water swims (ICWS) on the tail-flick and jump tests. Whereas CCWS antinociception on both tests was significantly potentiated by a dose range of L-NA (0.1-4 mg/kg IP) and L-NAME (1 mg/kg IP), ICWS antinociception was largely unaffected by these manipulations. In contrast, administration of the less active D isomer (D-NAME) failed to alter CCWS antinociception and reduced ICWS antinociception. The ability of NO synthase inhibition to potentiate CCWS antinociception could not be explained by changes in CCWS hypothermia. Since ICWS antinociception is mediated by mu-opioid manipulations and CCWS antinociception is sensitive to delta-opioid and nonopioid manipulations, this indicates that NO synthase inhibition may be acting upon a selective form of pain inhibition.
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PMID:Nitric oxide synthase inhibition selectively potentiates swim stress antinociception in rats. 751 79

The effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthase and MK-801, an NMDA receptor antagonist on abrupt and naltrexone-precipitated abstinence symptoms were determined in male Swiss-Webster mice rendered dependent on morphine by subcutaneous implantation of a pellet containing 75 mg of morphine base for 3 days. Mice which served as controls were implanted with placebo pellets. Six hours after pellet removal, mice were injected intraperitoneally with either the vehicle or MK-801 (0.03, 0.1 and 0.3 mg/kg). Thirty minutes later the animals were injected with naltrexone subcutaneously (50 micrograms/kg) and the intensity of abstinence symptoms were determined. Of the three doses of MK-801 used, only 0.1 mg/kg dose inhibited the jumping behavior precipitated by naltrexone in morphine-dependent mice. Whereas the lower dose (0.03 mg/kg) of MK-801 increased, the higher doses of MK-801 (0.1 and 0.3 mg/kg) displayed a decrease in the formation of fecal boli. Administration of MK-801 did not affect the body weight loss observed during abrupt withdrawal (induced by removal of the pellets) in morphine-dependent mice. MK-801 at 0.1 mg/kg dose further decreased the body temperature during abrupt withdrawal in morphine-dependent mice. Other two doses of MK-801 (0.03 and 0.3 mg/kg) did not modify the hypothermia observed during abrupt morphine withdrawal. On the other hand, L-NMMA (0.02 to 4.0 mg/kg) injected intraperitoneally 15 min prior to the naltrexone administration blocked the stereotyped jumping response in a dose-dependent manner. Higher doses of L-NMMA 2.0 and 4.0 mg/kg also decreased the number of fecal boli formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of NG-monomethyl-L-arginine and MK-801 on the abstinence syndrome in morphine-dependent mice. 751 22


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