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PubMed1979

[Hemoglobin oxygen combining capacity power. Reproducibility, variability; the effect of carboxyhemoglobin (author's transl)].

Hemoglobin oxygen combining power (HOCP) was measured in blood samples of 41 non smoking subjects and 36 smokers. The reproductibility and the varibility of this value were established (maximal variability was 2,5% in individual measurement). When the oxygen carrying capacity is reported to total hemoglobin (Hbt.), these two groups are not significantly different (1,344 +/- 0,004 ml O2 g-1 Hbt--n = 77-). However, when oxygen carrying capacity is reported to functional hemoglobin (Hbf = Hbt -- HbCO) there is a significative difference between smokers and non smokers (Student's t test 2 p less than 0,001) (1,404 +/- 0,005 ml O2 Hbf -- n = 77-).

Carboxyhemoglobin↗
PubMed1979

Dependence of the quantum efficiency for photolysis of carboxyhemoglobin on the degree of ligation.

A combined stopped flow-laser photolysis apparatus was used to measure the quantum efficiency for removal of carbon monoxide bound to human hemoglobin as a function of fractional CO saturation. This flow-flash technique allows the properties of partially liganded hemoglobin molecules, which are sparsely populated under equilibrium conditions, to be conveniently studied. Experiments performed at pH 7 and 20 degrees C both in the presence and absence of phosphates gave a similar dependence of quantum efficiency on fractional saturation. The observed quantum efficiency was 0.90 +/- 0.06 at 10% saturation and decreased to 0.47 +/- 0.02 as full saturation was approached. An allosteric model in which Hb(CO)1 has a quantum efficiency of 0.99 while other liganded species have quantum efficiencies of 0.47 was used to produce a good simulation of the results.

Carbon Monoxide↗
PubMed1979

First passage times as environmental safety indicators: carboxyhemoglobin from cigarette smoke.

The concentration of carbon monoxide in the blood of a cigarette smoker varies in response to the frequency and dose of CO delivered by the cigarettes he smokes and by the rate at which CO washes out of his blood. Moments of first passage times or exit times above a nominal threshold can be calculated using a stochastic differential equation that takes into account certain random variations in smoking intervals. CO doses, and washout rate. Almost any additional source of variation decreases in length of time a smoker may expect to smoke until a threshold value is exceeded. In particular the methodology proposed by Gori (1976) and Gori and Lynch (1978) for constant intervals, doses and rate may greatly overestimate the length of the "low-risk" interval for carbon monoxide concentration. One possible modification that may reduce CO hazards is to smoke less from each cigarette, even when this may be partially compensated by increased frequency of smoking.

Absorption↗
PubMed1979

[Rapid diagnosis of carbon monoxide poisoning and quantitative determination of CO-Hb in blood].

A quick diagnosis of carbon monoxide poisoning is a very difficult clinical problem. This paper describes a photometric method which permits a reliable diagnosis in a time of 7 to 10 minutes. Only 0.3 ml whole blood are necessary for the total procedure. Carboxyhemoglobin changes in absorption maximum slightly after reduction, whereas Oxyhemoglobin shows a significant change in extinction. Measurement of the hemolysate at the same wave length before and after alkaline reduction results in large differences in the extinctions (very large for Oxyhemoglobin and very small for Carboxyhemoglobin). Calibration curves are prepared by calibrating rest-extinction defined as: (formula: see text) to percent Carboxyhemoglobin. This curve can also be produced in mathematical way (as control e.g.). In practice there are the following steps: blood collecting (from fingerpad), hematolysis, first photometric measurement, reduction, second measurement, then reading the result from the calibration curve. The method can be automated (as demonstrated with the "Gilford System") providing the same results as with the manual method. All steps of quality control are given in full detail; as is the preparation of the hemolysates with various percentages of Carboxyhemoglobin.

Autoanalysis↗
PubMedDate not supplied

Augmentation of myocardial ischemia by low level carbon monoxide exposure in dogs.

This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.

Animals↗
PubMed1979

Conformation-specific antibodies to the alpha chain COOH terminus of hemoglobin A0.

An anti-hemoglobin antiserum obtained from a sheep immunized with human carboxyhemoglobin A0 demonstrated little difference in its reactivity with deoxy- or carboxyhemoglobin A0. However, a subpopulation of this antiserum isolated by synthetic peptide affinity chromatography clearly distinguished between these two hemoglobin species. This subpopulation, designated alpha(129-141) anti-hemoglobin antibodies, represents less than 1% of the total anti-hemoglobin antibodies. They are nonprecipitating by Ouchterlony analysis, and fluorescence-quenching studies demonstrate the interaction of a single antibody binding site per hemoglobin dimer. These antibodies bind preferentially to carboxyhemoglobin with a median affinity constant of 5 X 10(8) M-1 compared to binding to deoxyhemoglobin with a binding affinity of less than 1 X 10(8) M-1. Furthermore, the presence of these antibodies in stoichiometric amounts increases the oxygen affinity of hemoglobin, and thus antibody and oxygen binding to hemoglobin can be considered as a linked function.

Antibodies↗
PubMed1975

Determination of the pK values for the alpha-amino groups of human hemoglobin.

The rate of reaction between alpha-amino groups and cyanic acid was followed at 26 degrees and ionic strength 0.2 M as a function of pH of human hemoglobin Ao solutions to determine the pK and the pH-independent second order rate constant, kappa, for these groups in the alpha and beta chains. At a given point in time, the extent of the reaction was determined by employing the Beckmann Sequencer as a quantitative tool in which the yields of leucine and histidine in the second Edman degradation cycle were used to define the rates of reaction of the alpha and beta chains, respectively. From these results, the individual were evaluated (Garner, M.H., Garner, W.H., and Gurd, F. R.N. (1973) J. Biol. Chem. 248, 5451-5455). Values for pK for the alpha and beta chains were, respectively, 6.74 and 6.93 for cyanoferrihemoglobin, 6.95 and 7.05 for carboxyhemoglobin, and 7.79 and 6.84 for deoxyhemoglobin. Values for kappa, M- minus 1 S-minus 1, for the alpha and beta chains were, respectively, 12.5 and 17 for cyanoferrihemoglobin, 12 and 18 for carboxyhemoglobin, and 91 and 24 for deoxyhemoglobin. Limits of significance were estimated for both variables in each case. The pK results for valine 1alpha agree well with the value obtained by Hill and Davis (1967) J. Biol. Chem. 242, 2005-2012) for carboxyhemoglobin and with that of Kilmartin and Rossi-Bernardi ((1971) Biochem. J. 124, 31-45) for deoxyhemoglobin. Values obtained for sperm whale myoglobin were 7.77 for pK and 7.4 for kappa. The results are useful for the interpretation of the allosteric interactions of hemoglobin with hydrogen ions, with CO2, and with phosphate.

Amines↗
PubMed1977

Vitamin E and neonatal hemolysis.

A study was designed to determine if the presence of vitamin E deficiency during the first week of life played a contributory role in the shortened red cell life span observed in the premature infant. Carboxyhemoglobin values were used as an index of hemolysis. Ten infants received vitamin E administered intramuscularly in a total dose of 125 mg/kg during days 3 to 7 of life; ten infants served as controls. The mean percent carboxyhemoglobin level fell significantly from day 3 to day 8 in the treated group (1.08% to 0.78%) whereas the mean value remained unchanged at 0.96% in the control group. The administration of vitamin E appears to reduce but not eliminate the accelerated red cell destruction that characterizes the preterm infant. Pediatrics, 59:995-997, 1677, VITAMIN E, HEMOLYSIS, PREMATURE INFANT, CARBOXYHEMOGLOBIN.

Apgar Score↗
PubMedDate not supplied

The effect of carbon monoxide upon erythrocyte delta-aminolevulinicacid dehydratase activity.

The activity of the delta-aminolevulinicacid dehydratase enzyme in the second reaction of the heme biosynthetic pathway has been determined in human blood in the presence of varying concentrations of carboxyhemoglobin. In vivo and in vitro carbon monoxide exposure causes a consistent, but small, significant diminution of activity. At concentrations of carboxyhemoglobin likely to be found in vivo it is unlikely to significantly influence the use of this enzyme as a measure either of lead exposure or of ethanol consumption.

Cadmium↗
PubMedDate not supplied

Carbon monoxide and ventricular fibrillation threshold in normal dogs.

In a blind, randomized study, the effect of breathing 100 ppm of carbon monoxide versus compressed, purified air for 2 hr on ventricular fibrillation threshold was investigated in twenty anesthetized normal open-chested dogs. The mean arterial carboxyhemoglobin level was 1.12% in the air control period, 0.99% after air, 1.10% in the carbon monoxide control period, and 6.48% after carbon monoxide. Carbon monoxide increased the mean arterial carboxyhemoglobin (P less than .001). Mean ventricular fibrillation thresholds were 19.9 +/- 6.5 mA in the carbon monoxide control period, 15.7 +/- 5.6 mA after carbon monoxide 20.8 +/- 6.3 mA in the air control period, and 24.5 +/- 9.5 mA after air. Carbon monoxide decreased the ventricular fibrillation threshold (P less than .005). These data show that breathing 100 ppm of carbon monoxide for 2 hr reduces the ventricular fibrillation threshold in anesthetized normal open-chested dogs.

Air↗
PubMed1975

Lactic acidosis from carboxyhemoglobinemia after smoke inhalation.

Tissue hypoxia as a result of a wide variety of clinical situations had frequently been implicated as a cause of systemic acidosis due to the accumulation of lactic acid. Four patients suffering from smoke inhalation had lactic acidosis in association with carboxyhemoglobinemia. There was no evidence of decreased tissue perfusion, hypotension, arterial hypoxemia, or anemia. The following were tested in all patients: arterial pH (7.25 to 7.40), Pco-2 (19 to 27 mm Hg), Po (63 to 116 mm Hg), HCO-2- (11 to 19 meq/litre), carboxyhemoglobin (13% to 37%), and lactic acid (5.1 to 9.3 meq/litre). After therapy with oxygen and intravenous corticosteroids, there was prompt return of lactic acid levels, carboxyhemoglobin values, and arterial pH to normal. It is concluded that the cause of lactic acidosis in the presence of carboxyhemoglobinemia during smoke inhalation is tissue hypoxia. This tissue hypoxia is due to the reduction of the oxygen-carrying capacity of the blood and the concomitant shift of the oxyhemoglobin dissociation curve to the left, both known to result from carboxyhemoglobinemia.

Acidosis↗
PubMed1975

[Risk of chronic carbon monoxide poisoning in automobile garages. Results of a study in the Lausanne region].

Clinical and physiologic data on chronic carbon monoxide poisoning are reviewed and the results of an investigation involving 7 garages in the Lausanne (Switzerland) area are reported. The aim was a practical approach to the relationships between carbon monoxide level in the air, COHb and clinical picture. The study covered working conditions (especially ventilation) but did not take into account of other factors (stresses) which may effect the parameters investigated. CO was measured by continuous recording with an MSA Carbon Monoxide Alarm and the hourly and daily averages were determined. The garage personnel replied to a questionnaire and underwent a brief clinical examination including taking of digital blood samples for measurement of hematocrit and carboxyhemoglobin level by the method of COMMINS and LAWTHER as modified by BUCHWALD. One of the garages did not meet present health requirements. Statistical analysis revealed a significant correlation between carbon monoxide and carboxyhemoglobin. The incidence of complaints was highest in poorly ventilated garages. On the basis of COHb level in the total group of employees, together with data from individual histories, it is possible to evaluate the risk of carbon monoxide poisoning in a given garage.

Air Pollution↗
PubMedDate not supplied

Interaction of carbon monoxide and cyanide on cerebral circulation and metabolism.

Significant elevations of carboxyhemoglobin and blood cyanide have been found in fire victims. The nature of the interaction of acute exposures to these agents is unclear. This study was undertaken to describe the of cyanide and carbon monoxide--alone and in combination--on the circulation and metabolism of the brain in anesthetized dogs. Cerebral blood flow increased to 130 and 200% of control with elevations in carboxyhemoglobin to 30 and 51% or with elevations in blood cyanide to 1.0 and 1.5 microgram/ml, respectively. Cerebral oxygen consumption remained unchanged until the higher level of carbon monoxide or cyanide was reached. When carbon monoxide and cyanide were administered simultaneously, cerebral blood flow increased in an additive manner, but significant decreases in cerebral oxygen consumption occurred at the combination of the lower concentrations. These data suggest that carbon monoxide and cyanide are physiologically additive on producing changes in cerebral blood flow, but may act synergistically on cerebral metabolism.

Animals↗
PubMed1979

Teratogenic potential of inhaled carbon monoxide in mice and rabbits.

Pregnant CF-1 mice and New Zealand rabbits were exposed to carbon monoxide at a concentration of 250 ppm for 7 or 24 hours daily during the period of major organogenesis, days 6 through 15 of gestation in mice and 6 through 18 of gestation in rabbits. Carboxyhemoglobin levels in the range of 10--15% were observed in both species (control animals had 0.7% or less). Carbon monoxide was not found to be teratogenic in either species. In mice, a significant increase in the incidence of some minor skeletal variants was observed. One litter in each of the carbon monoxide-exposed groups of mice was completely resorbed; none of the litters of control mice or of control or exposed rabbits were completely resorbed. The fetuses of mice exposed to carbon monoxide for seven hours daily were heavier than control fetuses, and those exposed for 24 hours daily were lighter than control fetuses. The reason for this result is not known.

Abnormalities, Drug-Induced↗
PubMed1979

Effects of maternal smoking on circulating catecholamine levels and fetal heart rates.

Eight pregnant chronic cigarette smokers were studied after 34 weeks of gestation to determine the effects of acute cigarette (two nonfilter cigarettes) inhalation on maternal neuroendocrine and cardiovascular changes and on the fetus. Cigarette smoking was found to induce rapid (within 2 1/2 minutes) elevations in maternal plasma norepinephrine and epinephrine levels and this was associated with a rise in maternal pulse and blood pressure. These changes are followed, with a 5 minute lag time, by a significant increase in fetal heart rate. A relatively slow but sustained increase in maternal carboxyhemoglobin (HbCO) concentration occurred. The time course of this increase in HbCO did not seem to be responsible for the acute changes in fetal heart rate. Maternal cortisol levels also showed a slow but sustained elevation. Our present findings, together with data obtained from animal models, suggest that cigarette smoking during pregnancy induces fetal hypoxia through two independent but additive pathways: (1) An acute effect is caused by nicotine activation of adrenergic discharge, resulting in vasoconstriction, a decreased uterine perfusion, and a consequent transient fetal tachycardia, and (2) a delayed but prolonged increase in HbCO may cause a sustained reduction of fetal oxygenation.

Adult↗
PubMed1979

Evaluation of smoking-induced effects on sympathetic, hemodynamic and metabolic variables with respect to plasma nicotine and COHb levels.

The effect of smoking cigarettes containing 1.5 mg and 0.08 mg nicotine per cigarette and of sham-smoking was studied in six healthy habitual smokers. Levels of carboxyhemoglobin (COHb) and plasma nicotine were measured simultaneously with hemodynamic variables, such as heart rate and blood pressure, and with the metabolic parameters, plasma DBH, cortisol, blood glucose, lactate and free fatty acids. All variables, with the exception of COHb are dose related to plasma nicotine levels. Blood pressure, heart rate and lactate show simultaneous peaks together with maximal nicotine levels, while DBH and cortisol, blood glucose and free fatty acids show a delayed reaction compared to nicotine concentrations. No effects of COHb, even with levels up to 5.6 +/- 0.5% have been observed on the variables investigated. These results demonstrate, that it is nicotine which induces considerable hemodynamic and metabolic alterations after smoking.

Adult↗