SEARCH · PubMed Health

Results for “CARBON DIOXIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed1995

[Evaluation of anastomosis between intrahepatic or extrahepatic vessels by intra-arterial digital subtraction angiography using carbon dioxide].

Carbon dioxide (CO2) intraarterial subtraction angiography (IADSA) was performed in 31 patients with various hepatobiliary diseases. The injection sites of CO2 were proper hepatic artery (10/31; group A), segmental hepatic artery (18/31; group B), and peripheral inferior phrenic artery (3/31; group C), respectively. In group A, only the third order branches of the portal venous system were visualized anterogradely in 8 of 10 patients. In group B, the microcatheter was placed coaxially through a 5 French guiding catheter at the main arterial supply of the tumor in 7 patients and at the peripheral segmental branch of the hepatic artery in 11 patients. The portal venous system was visualized retrogradely in all of the patients regardless of the injection site. The injected CO2 may flow back into the portal vein through the anastomosis known as the peribiliary or periportal plexus. In group C, not only the portal vein but also the pulmonary artery or pericardial vein were visualized by this method. CO2-IADSA was useful to image the minute communications between the various vessels, which have been not hitherto visualized by iodinated contrast medium.

Adult↗

PubMed1986

Gas exchange during controlled ventilation in children with normal and abnormal pulmonary circulation: a study using the single breath test for carbon dioxide.

Carbon dioxide single breath tests (SBT-CO2) were obtained during anesthesia and controlled ventilation in 42 children about to undergo thoracic surgery. The tests were obtained with a computerized system based on the Servo ventilator. The system made on-line corrections for compressed volume, apparatus deadspace, and rebreathing. Children with normal pulmonary circulation had excellent gas exchange with high PaO2 values, a mean alveolar deadspace fraction (VDalv/VTalv) of 0.10, and a gently sloping phase III of SBT-CO2. Children with pulmonary hyperperfusion (left to right shunting) due to an atrial septal defect or a ventrical septal defect had significantly lower PaO2 values, steeper phase III slopes, and a greater spread of values for VDalv/VTalv. Children with pulmonary hypoperfusion due to pulmonary stenosis in combination with intracardiac right to left shunting had extremely low PaO2 values, and "adult" values for VDalv/VTalv. They required increased ventilation to maintain CO2 homeostasis. In the pooled material, the airway deadspace was strongly correlated to height, weight, and age. The airway deadspace was unaffected when tidal volume was increased by 37%, and ventilatory frequency simultaneously reduced by 30%, a maneuver that left alveolar ventilation unchanged. This is probably because an end-inspiratory pause was used; when frequency is reduced the length of the end-inspiratory pause increases, allowing proximal diffusion of the alveolar/fresh gas interface.

Anesthesia↗

PubMed1981

Transpleural diffusion of carbon dioxide.

Carbonic anhydrase in lung tissue might play a role in speeding the movement of CO2 between blood and alveolus. To test this hypothesis, we measured the transpleural diffusion rate of CO2 and compared it to that of oxygen, argon, and nitrogen, before and after inhibition of carbonic anhydrase activity with acetazolamide. Experiments were performed in exsanguinated dog lungs, which allowed study of CO2 dynamics in the absence of carbonic anhydrase activity from erythrocytes. The relative rate of movement of CO2 and the other gases into and out of the lung, agreed with that predicted solely on the basis of molecular weight and solubility. We conclude that there is no evidence for facilitated diffusion of CO2 across the pleural tissue.

Animals↗

PubMed2004

Amidations using N,N '-carbonyldiimidazole: remarkable rate enhancement by carbon dioxide.

Carbon dioxide catalyzes the reaction of imidazolides with amines to form amides. A substantial rate enhancement is observed in the presence of CO(2) compared to the CO(2)-free case. The scope and limitations of this reaction are discussed.

Journal Article↗

PubMedDate not supplied

Euthanasia of mink (Mustela vison) by means of carbon dioxide (CO2), carbon monoxide (CO) and nitrogen (N2).

The time periods and the behavioural pattern of mink euthanized with carbon dioxide (CO2), 100% and 70%, carbon monoxide (CO), 4%, and nitrogen (N2), 100%, are described. The time between the placement of the animal in a glass box and the first symptoms of incoordination (phase I), the period of loss of consciousness (phase II), and, finally, the coma phase until cessation of respiration (phase III) using three groups each of 10 pastel male mink each were recorded. Phase I times ranged from 14 s for CO2, 31 s for N2, and 49 s for CO. In phase II, the difference was even more pronounced, being 5 s for CO2, 15 s for CO, and 45 s for N2. In phase III, the time was 58 s for N2, 134 s and 151 s for CO2 and CO respectively. Hence, the critical period from the time when the animals were placed in the glass box till unconsciousness occurred (phase I and II) was 19 s for CO2, 64 s for CO, and 76 s for N2. The total course of euthanasia was 153 s for CO2, 215 s for CO, and 134 s for N2. The following minimum times will be required before it can be judged to be safe to remove the animals: CO2 and N2: 5 min, and for CO: 6.5 min. In a supplementary experiment, involving a mixture of 70% CO2 and 30% atmospheric air, it was not possible within the allotted time to kill adult male mink.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

[Potentiation by carbon dioxide of carbon monoxide-induced death in the hypoxic condition].

This study was aimed at clarifying the effect of carbon dioxide (CO2) on the toxicity of carbon monoxide (CO) in the hypoxic condition. In order to evaluate the coexistent toxicity of CO2 and CO under hypoxic hypoxia, we investigated the difference of CO toxicity between under the hypoxic and hypercapnic hypoxia in point of lethality in conscious male mice. Furthermore, we measured blood gases (pO2 and pCO2), pH, COHb concentration, and blood pressure (BP) and heart rate (HR) in urethane anesthetized male rabbits inhaled with 2 toxic gases: N2-toxic gas (O2 5.0%, CO 1.8%, N2 93.2%) and CO2-toxic gas (O2 5.0%, CO2 16.0%, CO 1.8%, N2 77.2%). The animals were inhaled with the 2 toxic gases until the BP reached 0 or 20 mmHg. In the latter case, when the BP reached 20 mmHg, the animals were inhaled with air and were intravenously infused with saline (20 ml/kg/30 min). Conscious mouse experiment: In the both types of hypoxia, LC50 were decreased with the decrease of O2 concentration and the LC50 of CO in hypercapnic hypoxia was significantly lower than that in nitrogen-replacement hypoxia in the range of 12% and 9% of O2 concentration in male mice. BP 0 mmHg-group experiment in rabbits: All the rabbits inhaled with N2-toxic gas or CO2-toxic gas died. The time to BP 0 mmHg in CO2-toxic gas group (7.8 +/- 0.33 min) was shorter than that in N2-toxic gas group (11.5 +/- 1.00 min). Although both toxic gases lowered pO2 level and elevated COHb% of the blood, CO2-toxic gas extremely elevated pCO2 level by 80-100 mmHg corresponding to lowering the serum pH by 0.37-0.45. BP was firstly elevated during 2-3 minutes by inhalation of these toxic gases and was finally lowered to die. HR decreased continuously after the inhalation of toxic gases until the animals died. BP 20 mmHg-group experiment in rabbits:Recoveries of COHb%, pCO2 level and pH of the blood in N2-toxic gas intoxication were significantly faster than those in CO2-toxic gas group. The times to COHb 10% were 64.2 min and 78.2 min in N2-toxic gas and CO2-toxic gas, respectively. But, there was no significant difference between N2-toxic gas and CO2-toxic gas intoxications in the recoveries of pO2 level, BP and HR. The above results suggest that CO2 potentiates the CO-intoxication under hypoxic hypoxia and our methods of coexistent gas toxicity may be useful for examining the gas toxicity in fire accident.

Animals↗

PubMed2005

Monitoring of end tidal carbon dioxide and transcutaneous carbon dioxide during neonatal transport.

OBJECTIVE: To assess the accuracy of measurements of end tidal carbon dioxide (CO2) during neonatal transport compared with arterial and transcutaneous measurements. DESIGN: Paired end tidal and transcutaneous CO2 recordings were taken frequently during road transport of 21 ventilated neonates. The first paired CO2 values were compared with an arterial blood gas. The differences between arterial CO2 (Paco2), transcutaneous CO2 (TcPco2), and end tidal CO2 (Petco2) were analysed. The Bland-Altman method was used to assess bias and repeatability. RESULTS: Petco2 correlated strongly with Paco2 and TcPco2. However, Petco2 underestimated Paco2 at a clinically unacceptable level (mean (SD) 1.1 (0.70) kPa) and did not trend reliably over time within individual subjects. The Petco2 bias was independent of Paco2 and severity of lung disease. CONCLUSIONS: Petco2 had an unacceptable under-recording bias. TcPco2 should currently be considered the preferred method of non-invasive CO2 monitoring for neonatal transport.

Blood Gas Monitoring, Transcutaneous↗

PubMed1978

Quality control of measurements of pH, carbon dioxide tension, and total carbon dioxide in plasma.

We have measured total carbon dioxide in plasma with a new carbon dioxide analyzer, and compared the results with total carbon dioxide data derived from measurements of carbon dioxide tension and pH. The results agree sufficiently well to demonstrate that the new instrument provides a simple, efficient procedure for monitoring the precision and accuracy of pH, carbon dioxide tension, or total carbon dioxide in plasma.

Blood↗

PubMedDate not supplied

The relationship between end tidal carbon dioxide and arterial carbon dioxide during controlled hypotensive anaesthesia.

OBJECTIVES: To prospectively assess the magnitude of changes in the arterial-to-end tidal carbon dioxide gradient [P(a-ET)CO2] as well as in the ratio of physiological dead space to tidal volume (Vdphys/Vt) during controlled hypotensive anaesthesia, and to evaluate whether or not ventilatory requirements remain unaltered during this procedure. SUBJECTS AND METHODS: Twelve adult patients with American Society of Anesthesiologists' physical status I and II undergoing middle ear surgery were selected. A standard anaesthetic procedure was followed for all cases, using thiopental sodium, succinylcholine, fentanyl, atracurium and 60% N2O in 40% oxygen supplemented with isoflurane. Mean arterial blood pressure (MAP) was reduced to 60 +/- 5 mm Hg in all patients using a sodium nitroprusside infusion. The end tidal (ET) CO2, PaCO2, MAP, peak airway pressure, plateau pressure and expiratory minute volume were recorded during a period of normal arterial blood pressure (time 1) and during hypotension (time 2). RESULTS: A significant decrease in PaCO2 (7%) and ETCO2 (17%) from time 1 to time 2 (p < 0.01) was noted, as was a significant increase in P(a-ET)CO2 (48%) and in the Vdphys/Vt ratio (41.17%) (p < 0.01) during the same period. CONCLUSION: The decrease in ETCO2 does not reflect the changes in PaCO2. The larger decrease in ETCO2 is mainly due to the increase in the Vdphys/Vt ratio. During anaesthesia, once normocapnia is achieved with normal arterial blood pressure, there is hardly any need to change the ventilation after initiation of controlled hypotension.

Adult↗

PubMed2003

Simultaneous generation of methane, carbon dioxide, and carbon monoxide from choline and ascorbic acid: a defensive mechanism against reductive stress?

Indirect evidence suggests that an abnormal increase in reducing power (reductive stress) may be associated with abnormal clinical states. We have recently proposed that under such conditions biomolecules with electrophilic methyl groups (EMGs) bound to positively charged nitrogen or sulfur moieties may act as electron acceptors and that this poising mechanism may entail the generation of methane gas. Here we report for the first time the generation of methane by rat liver mitochondria. We also report the formation of methane from choline in the presence of hydrogen peroxide, catalytic iron, and ascorbic acid. In this system, carbon monoxide and carbon dioxide are formed from the ascorbate molecule in parallel with methane generation. In view of these findings, we try to explain the essential role of biomolecules with EMG moiety. We hypothesize that this concerted reaction may be a defensive response to reductive stress and may provide the protection needed against redox imbalance in living systems.

Animals↗

PubMed1988

How the rise time of carbon dioxide analysers influences the accuracy of carbon dioxide measurements.

Carbon dioxide measurements are not accurate, especially in children, if the response time of the carbon dioxide analyser is too slow and its output fails to reach the actual carbon dioxide concentration at the end of the breath. The distortion of the carbon dioxide waveform is a function of the "rise time" of the analyser. We have simulated an expired carbon dioxide curve and calculated the rise time required to measure accurately end-tidal carbon dioxide and VCO2 in adults and children. A rise time of 80 ms (10-70%) is sufficient to measure end-tidal carbon dioxide concentration with 5% accuracy in patients with rates of ventilation less than 100 b.p.m. and I:E ratios less than 2:1. We have measured the rise time of 11 commercially available carbon dioxide analysers and found that only six of the 11 responded quickly enough to be accurate for rates up to 100 b.p.m. All 11 responded rapidly enough to measure end-tidal carbon dioxide concentration with 5% accuracy when ventilatory rates were less than 30 b.p.m. To measure VCO2 with 5% accuracy, an analyser should have a rise time of 20 ms. Only one analyser met this specification. An analyser's rise time can be estimated clinically to within 10 (SD 8) ms by a simple breath hold and forced exhalation, thus providing an estimate of the accuracy of carbon dioxide measurements in adults or children.

Anesthesia, Inhalation↗

PubMed1960