. (1977). Thorax, 32,[317][318][319][320][321] Secondary polycythaemia in chronic respiratory insufficiency. The relationship between polycythaemia, P50 and Saco (saturation in carboxyhaemoglobin) has been studied in 50 patients who were hypoxaemic due to chronic respiratory insufficiency. These patients were divided into two groups according to their haemoglobin concentration and haematocrit: 21 polycythaemic patients with haemoglobin>16 g/dl and haematocrit>50 % aDd 29 patients without polycythaemia. PaO2, PaCO2, plasma and erythrocyte pH, haemoglobin, haematocrit, and carbon monoxide saturation and intraerythrocytic 2-3 diphosphoglycerate concentration were measured during steady-state ventilation.All polycythaemic patients were smokers and their carbon monoxide level was significantly higher than that observed in patients without polycythaemia. Additionally, their P50 and 2-3 DPG concentration were significantly lower than in patients without polycythaemia.The correlations between P5o and Hbco and between Hb and Hbco were significant (r= -0-672; r=0-552 respectively: P<0-001).Eleven non-polycythaemic patients who were smokers had a high level of Hbco but normal P50. A group of 29 normoxic subjects was also studied, 14 non-smokers and 15 smokers with a high Hbco level. The mean value of P50 was lower in smokers and their haematocrit was higher although the difference was not significant for the latter.The Hbco increase by tobacco seems to be a factor in the occurrence of polycythaemia in patients with chronic respiratory insufficiency.The level of increase of Hbco and/or its duration and perhaps other individual factors could explain why all patients with high Hbco level and hypoxaemia were not polycythaemic.
We studied the action of urea on the spin-spin relaxation rate of 2,3-diphosphoglycerate (2,3-DPG) phosphorus atoms in normal and uremic erythrocytes. At concentrations from 10 to 60 mM, urea increased the relaxation rates of 2,3-DPG P-3 phosphorus atoms. This evidenced a stronger binding of 2,3-DPG to hemoglobin (Hb), suggesting that the deoxyform of Hb was stabilized. This hypothesis was confirmed by measurements of the association constant of oxygen to hemoglobin (K) in normal erythrocytes in presence of urea concentrations in the range of those observed in uremic patients (30 mM). Indeed, the observed decrease in K suggests that the T structure of hemoglobin is stabilized. By contrast, with higher urea concentrations (120 mM), measurements of P50 showed an increase in the hemoglobin affinity for oxygen (decrease in P50). Moreover, the relaxation rates of 2,3-DPG P-3 phosphorus atoms were not modified, which is consistent with the simultaneous increase of K. This may be attributed to the formation of carbamylated hemoglobin in presence of urea. These results suggest two opposite effects of urea on Hb-O2 affinity: the first reinforces 2,3-DPG-Hb binding and leads to a decrease in O2 affinity; the second, mediated by carbamylation of Hb, hinders the binding of 2,3-DPG and increases the O2 affinity. These findings are consistent with the fact that, despite the presence of carbamylated hemoglobin, uremic patients do not present increased Hb-O2 affinity.
The authors studied the tobacco consumption of 283 blood donors and its consequences. 151 were nonsmokers and 132 were smokers (47.7% smoke more than 10 g/day). Their mean HbCO level was 4.3 ± 0.2% (highest level 15%). HbCO levels are significantly correlated with daily tobacco consumption (p < 0.001) and can be estimated with the following regression equation: HbCO% = 0.176 (tobacco in grams/day) + 1.967. For a similar consumption, inhalers exhibit significantly (p < 0.001) higher HbCO levels than noninhalers and the increase is significantly higher (p < 0.02) in inhalers who smoked 1 h or less prior to blood sampling. High HbCO levels have two consequences: in the donors they have caused a tobacco polycythemia syndrome and in the recipients they have caused acute problems in cases of massive blood transfusion and cardiovascular surgery with extracorporeal circulation
Ventilatory and bronchomotor responses to baroreceptor afferent stimulation were studied in anaesthetized rabbits breathing spontaneously. The stimuli used were either the increase in carotid sinus pressure or the electrical stimulation of the cut central end of the aortic nerve. Respiratory effects of aortic barodenervation were also studied. Normoxic, normocapnic steady state was verified by repeated measurement of PO2, PCO2 and pH in arterial blood. Stimulation of both aortic and carotid baroreceptors provoked an early decrease of tidal volume and total pulmonary resistances without change in respiratory frequency. Aortic nerve stimulation induced an important and slowly adapting ventilatory and bronchomotor effect, whereas changes in carotid sinus pressure produced slight variation in respiratory parameters. Aortic nerve section resulted in an early and prolonged increase of total pulmonary resistances. Surgical or chemical (atropine) vagotomy did not change the bronchodilation observed under stimulation of the carotid sinus; however this effect was suppressed by intravenous injection of propranolol. This observation shows the importance of the sympathetic outflow in the genesis of bronchomotor responses following baroreceptor stimulation. In conclusion the baroreceptor stimulation provokes simultaneous decrease of both ventilation and total pulmonary resistances; aortic nerves seemed to exert permanent control on bronchomotor tone.
Anemia of chronic renal failure is associated with a reduced affinity of hemoglobin for oxygen (Hb-O2 affinity). It has been reported that the correction of renal anemia by recombinant human erythropoietin (rhuEPO) treatment could be associated paradoxically with a further decrease in Hb-O2 affinity. We investigated changes in the compensatory mechanisms of chronic renal anemia during 25 weeks of rhuEPO treatment, in 19 chronic hemodialyzed (HD) patients. There was no significant variation of mean standard P50 (P50std). Average 2,3-diphos-phoglycerate (DPG) increased after 13 weeks and remained stable. The large interindividual variations prompted us to study ΔP50std and ΔHb. We demonstrated a negative correlation between ΔP50std and ΔHb. Thus, P50std increased in patients who did not immediately correct their anemia and decreased in patients whose Hb values rose. These data showed that the major factor influencing variations of Hb-O2 affinity in chronic HD patients treated by rhuEPO is the variation of Hb concentrations. In our study, it was demonstrated that the most important rise in P50std and 2,3-DPG occurred in patients who were late responders to rhuEPO.
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