Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

N-Acetyl, N-propionyl, and N-pivaloyl derivatives of taurine were synthesized by applying a modified Schotten-Bauman method starting from taurine and using the corresponding acid chloride or acid anhydride for direct acylation reactions. The central nervous system actions of these lipid soluble taurine derivatives, which were presumed to pass the blood-brain barrier, were studied and compared to those of taurine in mice. A large dose (15 mmol/kg) of intraperitoneally administered taurine lengthened the pentobarbitone induced sleep by 30%. N-Pivaloyltaurine was 45 times more potent but not more effective than taurine. Neither N-acetyl- nor N-propionyltaurine lengthened the pentobarbitone induced sleep in doses up to 3 mmol/kg. Intraperitoneally administered N-pivaloyltaurine depressed the locomotor activity in a smaller dose and for a longer period than taurine. However, when administered intracerebroventricularly neither N-acetyl- nor N-pivaloyltaurine altered the locomotor activity in three times larger dose than in which taurine clearly depressed it. Intraperitoneally administered N-pivaloyltaurine decreased the rectal temperature slightly more than taurine, whereas intracerebroventricularly administered taurine was clearly more potent in inducing hypothermia than its acyl derivatives. Intraperitoneally administered N-pivaloyltaurine was about three times more potent than taurine in increasing the striatal concentration of dopamine. Intraperitoneally administered N-pivaloyltaurine only in a very large dose (3 X 15 mmol/kg) slightly and transiently increased the cerebral taurine concentration. Carboxylesterase inhibition by bis-p-nitrophenyl phosphate (BNPP) did not modify this increase. Furthermore, BNPP pretreatment modified neither the hypothermic nor the striatal dopamine concentration elevating effects of N-pivaloyltaurine. Our results suggest that N-pivaloyltaurine possesses taurine-like pharmacological actions. It is not converted to taurine to produce these actions. When administered intracerebroventricularly it is less potent than taurine. However, when administered intraperitoneally it is more potent than taurine because it seems to pass the blood-brain-barrier more easily than taurine. Thus N-pivaloyltaurine could be used to study the behavioural and other central nervous system actions of taurine.
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PMID:Comparison of central nervous system actions of taurine and N-pivaloyltaurine. 406 Oct 94

Severe electrolyte disturbances developed after the administration of hypertonic phosphate enemas in 2 chronically obstipated cats. Hyperphosphatemia, hypernatremia, and hypocalcemia were detected in both cats. Physical findings included weakness, anxiety, tachycardia, hypothermia, and dehydration. Intravenous fluid and electrolyte therapy led to prompt, dramatic improvement in both cats. Although well tolerated by most healthy animals, hypertonic phosphate enemas should be avoided in small animals, especially those that are dehydrated, severely obstipated, or suffering from renal or colonic disease.
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PMID:Electrolyte abnormalities induced by hypertonic phosphate enemas in two cats. 408 55

1. Cannabis extract prolonged sleeping time in mice in a thermally neutral environment (30-32 degrees C) in which hypothermia does not occur. The prolongation was dose related, just detectable at 50 mg/kg, and 4-fold at 500 mg/kg.2. Under these conditions, ether sleeping time was not prolonged.3. Cannabis extract inhibited the aerobic metabolism of phenazone by a microsome-rich 9,000 g supernatant of mouse liver homogenate capable of nicotinamide adenine dinucleotide phosphate (NADPH) generation.4. Delta(1)-Tetrahydrocannabinol (Delta(1)-THC) prolonged pentobarbitone sleep and inhibited phenazone metabolism, but its action was limited, and could not account for the effect of the extract. The carotenes and water-soluble fractions of the extract were inactive on pentobarbitone sleep.5. Cannabidiol was strongly active by both tests; in vivo 39.8 muM/kg (12.5 mg/kg) prolonged sleep by 190%, and in vitro 12.7 muM inhibited phenazone metabolism 20%. These actions were dose related, and could account for the effect of the extract.6. The prolongation of pentobarbitone sleep by cannabis extract in a dose of 200 mg/kg, intraperitoneally, was maximal when given 30 min before the pentobarbitone, still present at 3 h, but undetectable at 24 hours. No phase of enhanced metabolism at 24 or 48 h after single cannabis injection was detected.7. It is concluded that cannabis extract inhibits microsomal activity of mouse liver, chiefly by virtue of its cannabidiol content. It is probable that cannabis consumption by man could lead to altered disposal of many other drugs, used in medicine or otherwise.
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PMID:Effect of cannabis and certain of its constituents on pentobarbitone sleeping time and phenazone metabolism. 466 92

Rats treated 4 hr previously with 6-aminonicotinamide showed a twenty-four fold increase of [14C]phosphogluconate in the adult brain at 30 min after injection of [U-14C]glucose indicating a blockade of the hexosemonophosphate shunt. There was a significant increase in the 14C-content of glucose and glucose-6-phosphate, and a decrease in that of amino acids. [14C]Phosphoglycerate content showed no consistent change after 6-aminonicotinamide treatment. The concentration of glucose and glucose 6-phosphate increased significantly without a significant change in the lactate pool in the brain of 6-aminonicotinamide treated rats. The rate of utilization of glucose in the brain of control rats was 0.73 mumol/min per g of brain. It decreased by 16% in rats treated with 6-aminonicotinamide; the results suggested that both glycolysis and pyruvate oxidation were affected. The amount of glucose utilized in the brain by the hexosemonophosphate shunt was approximately 0.0093 mumol/min per g of brain, i.e. 1.3% of the total rate of utilization of glucose. The observed changes were not due to hypothermia. The rate of glucose utilization was higher in animals exposed to higher ambient temperature and to stress caused by handling. The results were explained by postulating a role for the hexosemonophosphate shunt in providing neurotransmitter amino acids glutamate and gamma-aminobutyrate, and interdependence of brain function and glucose utilization.
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PMID:The effect of inhibition of hexosemonophosphate shunt on the metabolism of glucose and function in rat brain in vivo. 621 28

In order to perform intracardiac repair safely during aortic cross clamping, we designed this study to evaluate the protective effect of coenzyme Q10 (CoQ10) on hypertrophied ischemic myocardium from the aspect of energy metabolism. Six to nine months preceding the study, aortic bandings were carried out on 14 puppies to produce left ventricular hypertrophy (LVH). These dogs with LVH were then subjected to total cardiopulmonary bypass and were evenly divided into control and CoQ10-treated groups (10 mg/kg of intravenous administration plus 1 mg/kg per hr of intracoronary injection). Myocardial ischemia was induced by aortic cross clamping for 2 hr under moderate systemic hypothermia. The results indicated that the administration of CoQ10 had a protective effect on hypertrophied ischemic myocardium, since depletion of high-energy phosphate (HEP) was uniformly prevented, and accumulation of lactate was simultaneously decreased during the 2 hr of aortic cross clamping. On the other hand, there were marked exhaustion of HEP and rapid increase in lactate following the 2 hr of ischemia in the control group, these being much more predominant in the subendocardial layer.
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PMID:Effect of coenzyme Q10 on hypertrophied ischemic myocardium during aortic cross clamping for 2 hr, from the aspect of energy metabolism. 622 44

Irrespective of age or species, injured cardiac myocytes accumulate Ca2+. In this paper four different aspects of the Ca2+-overloading phenomenon are discussed. These aspects include the conditions under which it occurs, the possible routes of Ca2+ entry, the metabolic consequences of the raised tissue Ca2+ and possible protective procedures. The particular protective procedures that will be described involve the combined use of hypothermia and nifedipine (50 micrograms/l), with and without K+-induced chemical cardioplegia. Isolated, electrically paced rabbit hearts were made ischaemic for 60 to 180 min at 37, 28, 25, 15, 12 and 5 degrees C and then reperfused at 37 degrees C. In some experiments nifedipine was added to the perfusion buffer, with and without K+-induced cardioplegia. Recovery was assessed in terms of recovery of mechanical function, maintenance of the tissue stores of adenosine 5'-triphosphate (ATP) and creatine phosphate, and maintenance of the ATP-generating activity of the mitochondria. These results show that the cardioprotective effects of nifedipine and hypothermia are additive.
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PMID:Calcium and cell death. 635 69

The concentration of 6-phosphogluconate in the brain increased from 0-24 nmol/g in the controls to 1430 and 1506 nmol/g in rats treated with 50 mg of 6-aminonicotinamide/kg of body weight. A dose-dependent increase in the concentrations of glucose and glucose 6-phosphate as well as of 6-phosphogluconate was found in the brains of 6-aminonicotinamide-treated rats. The biochemical changes and symptoms of neurological disorder in 6-aminonicotinamide-treated rats were not due to hypothermia. The rate of utilization of glucose via the hexosemonophosphate shunt was determined by isolation of gluconate from 6-phosphogluconate and measurement of its [14C]content at short time intervals after injection of [U-14C]glucose into 6-aminonicotinamide-treated rats; it was 16.5 nmol of glucose utilized/min per g of brain, and represented approximately 2.3% of the overall utilization of glucose in the brain. A highly significant correlation was observed between the concentration of 6-phosphogluconate and the concentration of glucose 6-phosphate and free glucose. The validity of this correlation was supported by the results of previous investigations involving several other treatments.
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PMID:The rate of utilization of glucose via hexosemonophosphate shunt in brain. 661 64

An isolated working rat heart preparation was used to determine the effect of diltiazem, a calcium antagonist, on the myocardial metabolism and functional recovery in the ischemic and reperfused heart, under conditions of 15 degrees C of topical hypothermia. The hearts were divided into two groups according to the solution injected into aortic root at the onset of ischemia. Group I (25 hearts) were given 3 ml of cold Krebs-Henseleit bicarbonate buffer solution (KHB), and Group II (25 hearts) were given the same dose of KHB containing 300 micrograms of diltiazem. After 30 min of reperfusion following 120 min of ischemia, cardiac output (ml/min) was significantly better in Group II (24.1 +/- 3.2) than in Group I (9.5 +/- 2.5). There were no differences between the groups with regard to tissue levels of creatine phosphate, adenosine triphosphate (ATP), total adenine nucleotide (TAN), glucose-6-phosphate and lactate during the ischemia. However, ATP and TAN levels were significantly higher in Group II after 30 min of reperfusion. These data show that, although diltiazem has little effect in preventing the catabolism of high-energy phosphates during hypothermic ischemia, there was an improvement in myocardial metabolism and an enhanced functional recovery during reperfusion in the diltiazem-treated hearts.
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PMID:Effect of diltiazem on functional recovery and myocardial metabolism during hypothermic global ischemia and normothermic reperfusion. 663 97

Acidification of luminal fluid in the proximal convoluted tubule has been modeled as a pump-leak system. Using isolated perfused rabbit proximal convoluted tubules in a HCO-3/CO2-free in vitro environment, we studied "H+ leak" by imposing pH gradients across the tubule and measuring the change in pH from perfusate to collected fluid. Active acidification was inhibited by acetazolamide with and without hypothermia. At 21 degrees C a symmetrical H+ leak with an apparent permeability coefficient of approximately 0.15 cm X s-1 was found with either a lumen-to-bath or bath-to-lumen [H+] gradient. At 37 degrees C a much higher apparent permeability coefficient was found that was dependent on luminal lactate. Phosphate movement did not affect H+ fluxes significantly. Without luminal lactate, the apparent permeability coefficient was 0.31 cm X s-1. Although this permeability coefficient is larger than other ionic permeability coefficients in this segment, it is not sufficient to account for a significant H+ leak compared with rates of acidification or bicarbonate reabsorption. To investigate the role of Na+-H+ exchange in mediating the observed H+ leak, we perfused tubules with low [Na+] solutions with and without amiloride (10(-3) M). Neither the lower [Na+] nor the presence of amiloride diminished the apparent [H+] permeability coefficient. We conclude that a H+ leak pathway independent of Na+-H+ exchange is present in the proximal convoluted tubule.
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PMID:Hydrogen ion permeability of the rabbit proximal convoluted tubule. 669 75

To determine whether the calcium antagonist verapamil can produce satisfactory myocardial preservation during global ischemia, we studied three groups of eight dogs. Serial left ventricular biopsy specimens were taken for adenosine triphosphate and creatine phosphate content. Arterial and coronary sinus blood samples were obtained for lactate and oxygen content determination prior to ischemia, immediately after the ischemic interval, and after a 30 minute reperfusion period. Starling and isovolumetric ventricular function curves were determined prior to ischemic arrest and after 45 minutes of reperfusion. All animals were systemically cooled to 25 degrees C, and the aorta was clamped for 120 minutes. Group I had a potassium cardioplegic solution (30 mEq/L) chilled to 4 degrees C and injected into the aortic root. The initial dose was 200 ml and an additional 100 ml was infused at 20 minute intervals. Group II had a solution containing verapamil (0.15 mg/kg/L), diluted in Ringer's solution (4 degrees C), injected into the aortic root. The initial and subsequent doses were as in Group I. Group III received the same solution as Group II, but at room temperature. Alterations in lactate metabolism were not significantly different in any of the three treatment groups. A reduction in oxygen consumption was seen in Group III, but was not found to be statistically significant. However, the reduction in coronary flow at the end of reperfusion was statistically significant in Group III (p less than 0.05). Verapamil given at room temperature resulted in poor preservation of left ventricular function and high-energy stores. Verapamil combined with extreme hypothermia (Group II) provided excellent preservation of left ventricular compliance and contractility. Cold verapamil cardioplegia was superior to potassium cardioplegia for the preservation of adenosine triphosphate.
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PMID:Verapamil cardioplegia: improved myocardial preservation during global ischemia. 673 3


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