Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:003739 (CO2)
 48,959 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experiment to validate predictions concerning submersible survivability was performed in December, 1975, by members of the Canadian Forces in the CF Submersible Lockout Vehicle SDL-1 in Halifax Harbour in water of 4 degrees C temperature at a depth of 40 ft. Data was collected relevant to the life support equipment to determine if it would operate for a simulated 6-h mission followed by a 24-h immobility period, at the end of which rescue was presumed to have occurred. Physiological data was collected from the submersible occupants in order to assess the degree of thermal stress experienced in this exercise. The experiment was terminated after a duration of approximately 25 h at 1 atm internal pressure due to exhaustion of two of the three on-board power supplies, causing the CO2 scrubbers to be inoperative and the CO2 content in the breathing gas to increase to toxic levels. Only two of the three submersible occupants experienced cold stress, one in the forward sphere and one in the aft sphere. At the end of 24 h, the core temperatures of both individuals had decreased by 0.5 degrees C and, during this time, skin temperatures, particularly of the extremities, had steadily and slowly decreased. Neither individual was hypothermic, but it was considered likely that after a 3-d exposure, at least two of the crew members would have had core temperatures of 35 degrees C or lower, assuming that CO2 poisoning had not occurred earlier.
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PMID:Survival test of submersible life support systems. 1 83

Pure cultures of six pathogenic isolates of Treponema hyodysenteriae, the colonic mucosal scrapings of seven pigs with acute swine dysentery, and feces from seven unaffected pigs were diluted in phosphate-buffered saline and plated on Trypticase soy agar with 5% citrated bovine blood (TSA) and TSA with various levels of spectinomycin (TSA-S). The plates were incubated at 42 degrees C in a vented GasPak jar with a cold palladium catalyst and either 80:20 H2-CO2 by evacuation and refilling or a H2-CO2 generator envelope. Viable cell counts of the six pathogenic isolates were not altered by plating on TSA-S with 400 mug of spectinomycin per ml (TSA-S400) as compared with TSA alone. Dilutions of colonic mucosal scrapings from seven pigs with acute swine dysentery showed numbers of T. hyodysenteriae to be unchanged when plated on TSA-S400. Flora other than T. hyodysenteriae present in acute swine dysentery was inhibited, on the average, by 99.99%. Plating of dilutions of feces of unaffected pigs on TSA-S400 showed inhibition of flora that averaged more than 99.9%. Pathogenicity of T. hyodysenteriae was not altered by isolation or serial passage on TSA-S400.
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PMID:Selective medium for isolation of Treponema hyodysenteriae. 13 43

The metabolism of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide (NFTA), a carcinogen for the mouse, rat, dog, and hamster, was investigated in the rat. Radioactive NFTA administered ip to young and lactating female rats was rapidly absorbed through the peritoneum and deposited in the urine, intestinal contents, and feces. Less than 0.5% of the radioactivity was expired as CO2 during the first 24 hr. Two yellow metabolites, accounting for 5 and 27% of the radioactivity in the urine, were found by paper chromatography. One metabolite retained the 2-amino-4-(5-nitro-2-furyl)thiazole moiety. Less than 0.5% of the radioactivity in the urine was due to unchanged 14-C-NFTA. The radioactivity level in the visceral organs reached a maximum 2 hr after dosing and then gradually decreased. Liver contained considerably more radioactivity than did other visceral organs; this was mainly distributed in the cytosol and 900g pellets. Fifty per cent of the radioactivity in the liver was bound to the hot trichloroacetic acid (TCA)-insoluble fraction; that bound to the cold TCA-insoluble fraction increased gradually from 66.9% at 2 hr to 82.6% at 24 hr. The radioactivity bound to the cold and hot TCA-insoluble fractions in kidney remained at 30% and 20%, respectively. Nitroreduction of 14-C-NFTA by microsomes, as a prerequisite of the binding of metabolite to microsomal protein, was demonstrated. Addition of L-cysteine or reduced glutathione to the incubation mixture did not alter the nitroreductase activity of the microsomes; however, binding of radioactivity to protein was significantly decreased. Addition of other amino acids did not significantly decrease the nitroreductase activity or binding to protein. These results suggest that reduced NFTA binds to the protein sulfhydryl groups. Since 14-C-NFTA binds to macromolecules in vivo,nitroreductionmay be important for the metabolism of 5-nitrofurans.
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PMID:Metabolism and disposition of N-(4-(5-nitro-2-furyl)-(2-14-C)thiazolyl)acetamide in the rat. 23 64

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.
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PMID:Metabolic and respiratory responses during Helox-induced hypothermia in the white rat. 24 22

1. In vivo fatty acid synthesis by brown adipose tissue was enhanced in rats exposed to cold (5 degrees C) or altitude (4300 m) for 7 days but was unaltered in rats exposed to heat (35 degrees C) for an equivalent period. In vivo fatty acid synthesis by white adipose tissue was depressed by cold exposure while altitude and heat exposure had no effect. 2. In vitro, CO2 production and lipid synthesis were elevated in brown adipose tissue from rats fasted for 4 days. Refeeding (4 days) such rats reversed these effects, leading to depressed values relative to those of control rats. In contrast, these metabolic events in white adipose tissue were decreased by fasting and increased compared to controls during subsequent refeeding.
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PMID:Differential response of rat brown and white adipose tissue to environmental or nutritional stress. 31 66

The effect of decompressive trepanation was compared to that of surgical resection of the traumatized tissue in the course of traumatic brain edema in standardized experimental brain trauma. Following a right parietal cold injury, the following parameters were monitored continuously in 12 cats: ventricular pressure, epidural pressure over both hemispheres, arterial and central venous pressure and heart rate. The EEG was evaluated continuously, using a computer (power spectra). After catheterization of the superior sagittal sinus, cerebral arteriovenous differences of glucose, lactate, O2 and CO2 were calculated. 6 animals were treated surgically when showing elevated intracranial pressure ICP and markedly altered EEG. In 3 animals, the right hemisphere was decompressed by extensive resection of bone and dura. In 3 further animals, the softened brain tissue of the cold lesion was resected and the skull defect closed. 6 untreated animals were used in controls. A decompression by skull hemiresection for ablation of the injured cortex abolished the high intracranial pressure, but only the latter method seemed to prevent further damage. This could be demonstrated by the EEG registration, and by the normalization of arteriovenous metabolite differences. Only animals treated with edema resection had a normal arousal reaction and survived the trauma. The results indicate, that only an ablation of the local injury will prevent further damage to the brain. After decompressive trepanation alone, the progression of tissue edema is not interrupted. As can be seen from the literature, the poor results obtained even from extensive decompressive operations in traumatic brain edema, indicate that the further development of edema is independent of the intracranial pressure, whereas the favorable results of resection of lobar contusions show an interruption of the spread of dysbolism.
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PMID:Comparison of the effects of surgical decompression and resection of local edema in the therapy of experimental brain trauma. Investigation of ICP, EEG and cerebral metabolism in cats. 47 64

A mixture of (1-14C)-labeled free fatty acids (FFA), complexed in bovine plasma, was infused into the abdominal aorta of conscious young steers exposed to thermoneutral or moderately cold conditions for several hours and fed 6 or 22 h before the experiment. The uptake, release, and oxidation of FFA in one hindlimb was calculated from simultaneous measurements of leg blood flow and arteriovenous difference in the specific activities of plasma 14C-FFA and blood 14CO2. Despite an invariable net release of FFA from the resting leg, uptake of 14C-FFA was considerable; of this only 14 and 3% was immediately converted to 14CO2 in fasted and fed steers, respectively. During cold exposure, increases in whole-body oxygen consumption (VO2), arterial concentration and turnover rate of plasma FFA, and a decrease in respiratory quotient were accompanied by much greater increases in VO2, uptake, and oxidation of FFA by the shivering leg. Even so, most FFA taken up were apparently not immediately oxidized to CO2, and possible alternatives for FFA metabolism in shivering muscle are discussed.
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PMID:Free fatty acid oxidation in bovine muscle in vivo: effects of cold exposure and feeding. 49 10

Breath tests that measure the oxidative utilization of 13C labeled substrates have been shown to be clinically useful, but have failed to gain wide acceptance because of the slow and costly isotopic analysis of the breath samples. Therefore we have developed a fully automated, microprocessor controlled CO2 purification and isotopic analysis system. The breath CO2 is cryogenically purified by passage through cold traps of -94 degrees C and -196 degrees to condense water and CO2, respectively. The CO2 is intorduced into a dual inlet, peak-stepping mass spectrometer and analyzed for isotopic content by comparison with a known standard. Thirty samples can be analyzed without operator intervention. Analysis time average 14 minutes per sample, and the analysis has a precision of 0.3% which corresponds to 3 parts excess 13C per 10(6) parts CO2. The speed of analysis is comparable with scintillation counting and permits next day reporting of clinical breath test results. The precision is sufficient for clinical applications as it is less than 0.7% isotopic variation in basal breath CO2.
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PMID:A microprocessor controlled mass spectrometer for the fully automated purification and isotopic analysis of breath carbon dioxide. 49 61

Twenty-four oxygen exposures lasting 80 to 271 min were performed by six immersed exercising subjects at 25 fsw (1.76 ATA) in both warm and cold water. Two types of exercise were performed, moderate work (50 watts) for long periods of time, and graded exercise (25-150 watts) lasting 85 min. In 21 degrees C water, moderate exercise lasted 228 +/- 39 min, with a mean VO2 of 1.72 +/- 0.11 liter/min. In 4 degree C water, the duration was 163 +/- 22 min, with a mean VO2 of 1.83 +/- 0.16 liter/min. The differences in duration of oxygen exposure in warm and cold water reflect termination at an inspired PCO2 of 7.6 mmHg, a level reached earlier in cold water because of CO2 absorbent exhaustion. In 21 degrees C water, the VO2 for graded exercise ranged from 1.51 to 3.00 liter/min and in 4 degrees C water, from 2.00 to 3.16 liter/min. Central nervous system oxygen toxicity was not observed during these exposures, although two divers had clinical and spirometric evidence of early pulmonary oxygen toxicity. The absence of CNS oxygen toxicity is attributed to low resistance and minimization of dead space, which caused a low inspired PCO2, although the divers' experience with oxygen diving and their excellent physical condition may have contributed as well.
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PMID:Prolonged oxygen exposures in immersed exercising divers at 25 fsw (1.76 ATA). 53 63

In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, lowered PaO2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolar PCO2 was uncontrolled or kept constant at the hyperoxic control. The V-PaO2 response was to a greater extent due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolar PCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, when PACO2 was not controlled, but a distinct decrease in ventilation, when PACO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, lowered PaO2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways--and possibly also to a lack of O2--, mainly shortening respiratory cycle duration.
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PMID:The role of the vagus nerves in the ventilatory response to lowered PaO2 with intact and eliminated carotid chemoreflexes. 57 48


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