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1. A-V differences and milk concentrations of respiratory gases, pH, HCO3 and H2CO3 have been measured in lactating goats and cows. 2. The pH and [HCO3 minus] of milk were significantly lower than those of plasma while milk PCO2 was virtually identical to that of mammary venous blood. [H2CO3+ dissolved CO2] was similar in milk and blood. 3. 14-C (from injected [14-C]HCO3 minus was found to cross the mammary epithelium in both directions. 14-C also passed across the duct epithelium and since this epithelium has previously been shown to be impermeable to ions it is argued that 14-C crossed in an unionized form, i.e. as CO2 and/or H2CO3. 4. Hourly milking with the aid of oxytocin raised milk pH, [HCO3 minus], [H2CO3], [Na] and E1Cl], and lowered [K], [lactose] and [phosphate]. These effects are discussed in relation to the hypothesis proposed previously for the action of oxytocin on milk composition. 5. A scheme for the distribution and movements of CO2, H2CO3 and HCO3 minus between extracellular fluid and milk is suggested, and discussed in relation to Cl minus transport.
In 4 spontaneously breathing, barbiturate-anesthetized dogs, hyperthermia was induced with 2,4-dinitrophenol while rectal temperature, heart rate, mean blood pressure, end-tidal carbon dioxide, and carbon dioxide production (milliliters per minute) were measured continuously. The latter was determined with a pneumotachygraph (to obtain respired volume) and an infrared carbon dioxide analyzer that measured inspired and expired carbon dioxide concentration. Of the five physiologic measurements, the increase in carbon dioxide production preceded the increase in rectal temperature by more than 120 seconds. End-tidal carbon dioxide was an unreliable indicator in the spontaneously breathing animal of approaching hyperthermia during spontaneous breathing due to a transient tachypnea, which decreased end-tidal carbon dioxide. The carbon dioxide production (milliliters per minute) increased immediately and reached three to five times the control value. Blood pressure and heart rate were insensitive indicators of approaching hyperthermia.
In 18 healthy children three to 13 years of age, the transcutaneous partial pressure of carbon dioxide (PtcCO2) (Radiometer electrode) and the alveolar partial pressure of carbon dioxide (PACO2) (Beckman analyzer) were measured simultaneously during the breathing of room air and 5 percent carbon dioxide. The PtcCO2 electrode was placed on the anterior thorax and heated to 42 degrees C. The PACO2 was calculated on the 4/5 part of the carbon dioxide expired trace. Minute ventilation (VE) was measured in 11 cases. There was a significant correlation between PtcCO2 (in millimeters of mercury) and PACO2 (in millimeters of mercury) while breathing room air (PtcCO2 = 0.82 PACO2 + 19.7; r = 0.55; p less than 0.02) and while breathing 5 percent carbon dioxide (PtcCO2 = 0.77 PACO2 + 22.5; r = 0.61; p less than 0.01); however, the ratio of PtcCO2 over PACO2 was significantly lower while breathing 5 percent carbon dioxide (p less than 0.01) than while breathing room air. When considering the relationship between the increase in VE (delta VE while breathing 5 percent carbon dioxide and the changes in PACO2 (delta PACO2) or in PtcCO2 (delta PtcCO2), a significant correlation was found only between delta VE and delta PACO2, ie, delta VE = 0.41 delta PACO2 + 0.44 (r = 0.63; p less than 0.01). These results suggest that breathing carbon dioxide modified the factors acting on PtcCO2, possibly by changes in the vasomotor tone of cutaneous blood vessels. These modifications appeared to be variable from subject to subject. Therefore, we conclude that PtcCO2 does not appear to be an accurate quantitative index to assess ventilatory response to carbon dioxide.
There has been a recent renewal of interest in the antioxidant properties of pyruvate which are usually attributed to its capacity to undergo oxidative decarboxylation in the presence of hydrogen peroxide. The interaction of pyruvate with other oxidizing biological intermediates, however, has been scarcely considered in the literature. Here we report that peroxynitrite, the oxidant produced by the reaction between superoxide anion and nitric oxide, reacts with pyruvate with an apparent second-order rate constant of 88 +/- 7 M-1 s-1 at pH 7.4 and 37 degrees C. Kinetic studies indicated that pyruvate reacts with peroxynitrite anion (k = 100 +/- 7 M-1 s-1, peroxynitrous acid (k = 49 +/- 7 M-1 s-1, and a highly oxidizing species derived from peroxynitrous acid. Pyruvate decarboxylation was proved by anion exchange chromatography detection of acetate in incubations of peroxynitrite and pyruvate at pH 7.4 and 5.5. Formation of carbon dioxide radical anion was ascertained by EPR spin-trapping studies in the presence of GSH and the spin-trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO). The use of pyruvate labeled with 13C at the 1-position led to the detection of the labeled DMPO carbon dioxide radical anion adduct. In the absence of GSH, oxygen consumption studies confirmed that peroxynitrite mediates the decarboxylation of pyruvate to free radical intermediates. Comparing the yields of acetate and free radicals estimated from the oxygen uptake studies, it is concluded that pyruvate is oxidized by both one- and two-electron oxidation pathways, the latter being preponderant. Hydrogen peroxide-mediated pyruvate oxidation does not produce detectable levels of carbon dioxide radical anion except in the presence of iron(II)-ethylenediamine-N,N,N',N'-tetraacetate (EDTA). The apparent second-order rate constant of the reaction between pyruvate and hydrogen peroxide was determined to be 1 order of magnitude lower than that of the reaction between pyruvate and peroxynitrite. The latter process may contribute to the antioxidant properties of pyruvate.
The aqueous humors of 100 freshly enucleated rabbit eyes were assessed within 10 min postmortem by taking samples in the last stage of corneal dissection following the Dikstein-Maurice procedure. Aqueous levels of partial pressure of carbon dioxide (pCO2) averaged 58.2 +/- 8.5 mm Hg to give calculated tCO2 and bicarbonate levels of 34.9 +/- 2.2 mEq/l and 30.0 +/- 3.4 mM/l, respectively. The pH and ionized Ca2+ levels averaged 7.39 and 1.50 mM while partial pressure of oxygen (pO2) values were variable (31.5 +/- 23.6 mm Hg). The pH showed an inverse correlation to pCO2 values, and Ca2+ increased as pCO2 increased. O2 levels tended to decrease as CO2 increased. The results suggest that significant hypercapnia and hypoxia of the eye fluids can occur even within 10 min postmortem for an enucleated globe at room temperature.
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The effects of breathing 100% O2, 2% CO2, and 0.5% CO2 on the cranial blood flow of the normal human baby were investigated. A mercury in Silastic strain gauge was placed around the occipital head circumference (OFC) of a sleeping infant, and jugular flow was measured using venous occlusion plethysmography. Cranial flow was calculated using formulas derived from an electrical model. In matched sleep states cranial blood flow fell with 100% O2 (mean from eight babies = 32.8%), and rose with 2% CO2 (mean from seven babies = 40.6%). With 0.5% CO2 the flow rose in three babies and did not change in another four. These results indicate the extreme sensitivity of cerebral vasculature to the nature of the ambient gas.
Carbon dioxide was blamed for the deaths of around 1700 people in Cameroon, west Africa, in 1986 when a massive release of gas occurred from Lake Nyos, a volcanic crater lake. The clinical findings in 845 survivors seen at or admitted to hospital were compatible with exposure to an asphyxiant gas. Rescuers noted cutaneous erythema and bullae on an unknown proportion of corpses and 161 (19%) survivors treated in hospital; though these lesions were initially believed to be burns from acidic gases, further investigation suggested that they were associated with coma states caused by exposure to carbon dioxide in air. The disaster at Lake Nyos and a similar event at Lake Monoun, Cameroon, two years previously provide new information on the possible medical effects of large scale emissions of carbon dioxide, though the presence of other toxic factors in these gas releases cannot be excluded.
A system is described for measuring carbon dioxide output and alveolar carbon dioxide concentration in the neonate and for deriving the volume of alveolar ventilation. Air is drawn through a soft rubber face mask applied loosely to the face so that all expired gas is entrained. A fraction of the flow is sampled by an infra-red analyser, the signal from which is integrated to provide a measure of carbon dioxide output. Alveolar carbon dioxide concentration is measured by continuous sampling of expired gas through a nasal catheter. The response time of the catheter-analyser system is 140 ms. In 20 healthy 1-day-old neonates the mean carbon dioxide excretion was 5.86 ml/min. kg-1 (STPD) and the mean alveolar PCO2 was 4.85 kPa. From these measurements mean alveolar ventilation 147 ml/min. kg-1 (BTPS) was calculated. These results are similar to those obtained by other methods.
Carbon dioxide is a green yet feeble solvent whose full potential won't be realized until we develop a more thorough understanding of its solvent behavior at the molecular level. Fortunately, advances in molecular modeling coupled with experiments are rapidly improving our understanding of CO(2)'s behavior, permitting design of new, more sustainable "CO(2)-philes".
The reactions of propargylamine derivatives with carbon dioxide and carbon disulfide have been systematically examined in the presence of transition-metal catalysts. Pd(OAc)(2) is the best catalyst for the formation of the corresponding oxazolidinones. In addition, we found that, in the reaction of propargylamine with carbon dioxide catalyzed by palladium(0) metal catalyst in toluene, both oxazolidinone 1 and imidazolidinone 2 could be obtained under mild reaction conditions at the same time. The reaction of 1 with primary and secondary amines has been examined. A plausible reaction mechanism for the formation of 2 was proposed. In addition, in this paper, we first disclosed the ligand's effect on this reaction. Using PBu(t)(3) as a ligand with Pd(2)(dba)(3), 1 was exclusively formed in 90% yield.
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.