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Three weeks of sodium cyanate (NaCNO) intraperitoneal treatment in rats (n = 15) induced high hemoglobin O2 affinity, i.e., low PO2 at 50% hemoglobin saturation (P50), 20.5 +/- 1.4 Torr, in comparison with the mean control values, 34.5 +/- 1.6 Torr (n = 15). NaCNO rats showed a reduction in mean body weight, 376 +/- 27 g, in comparison with controls, 423 +/- 23 g (P less than 0.001). Despite arterial O2 partial pressure (PaO2) within normal limits NaCNO-treated rats had a higher systolic right ventricular pressure (SRVP), 33.7 +/- 3.1 Torr, in comparison with control value, 29.0 +/- 2.5 Torr (P less than 0.001). Right ventricle weights were significantly increased (P less than 0.001). After 60 min of an hypoxic challenge (fractional concentration of inspired O2 = 0.10) NaCNO-treated rats increased SRVP of only 7 +/- 4% compared with 46 +/- 9% in the control animals. Inducing high hemoglobin affinity in rats (n = 10; 6 wk NaCNO treatment) resulted in increases in hematocrit ratio and hemoglobin concentration (P less than 0.001). The characteristics of the red blood cell (RBC) itself changed; values of mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration being significantly increased (P less than 0.001) when compared with mean control values. The count of nucleated RBC's appeared to be significantly higher from the 2nd wk of NaCNO treatment. Chronic NaCNO treatment was demonstrated to exert "hypoxia-like" effects since it induced prevention of normal growth, polycythemia, pulmonary hypertension, right ventricular hypertrophy, and blunted pulmonary pressor response to acute hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

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In anesthetized, normoxic or hypoxic rats the hemodynamic, metabolic and O2 transport characteristics following exchange transfusion with human erythrocytes containing a high O2 affinity hemoglobin (Hemoglobin Creteil, beta 89 Ser----Asp) have been studied. The in vivo oxygen partial pressure at 50% oxygen hemoglobin saturation (P50) decreased from 37.4 +/- 2.1 to 12.7 +/- 0.7 mm Hg; the arterial oxygen tension was reduced significantly from 109.9 +/- 7.7 to 87.3 +/- 12.0 mm Hg. There was a decrease in right ventricular partial pressure of oxygen (PvO2), (P less than 0.001), oxygen consumption (VO2), (P less than 0.001), arterio-venous difference, (P less than 0.001), and peripheral vascular resistance index, (P less than 0.01). Exchange transfusion with normal rat blood (P50 = 37.2 +/- 2.4 mm Hg) or with 2,3-diphosphoglycerate-enriched human red blood cells (P50 = 34.7 +/- 2.2 mm Hg), did not modify these variables in normoxic rats. In hypoxia, the reduction in P50 was associated with a further decrease in PvO2 an increase in serum lactate concentration and a VO2 decrease.

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PO2 temperature formulae supplied by manufacturers on automatic blood gas apparatus, PO2 corr. = PO2 37 degrees C X 10F X delta T were studied and compared to the experimental determination of the delta log PO2/delta T ratio (Hérigault et al. [10]). Acid-base status at 37 degrees C appeared to have a measurable influence on the PO2 temperature factor; alkalosis increased the delta log PO2/delta T ratio, and the contrary was found for acidosis in comparison with normal acid-base status at 37 degrees C. For the same PO2, measured at 37 degrees C, all the proposed formulae of commercial blood gas automatic apparatus did not give the same temperature corrected PO2. The observed difference between the corrected PO2 may be important and greater than the precision of the initial measurement. To correct the measured PO2 for temperature, a relationship between delta log PO2/delta T and PO2 is proposed, between PO2 zero and PO2 180 mmHg, which takes into account measured pH and PO2 values at 37 degrees C:delta log PO2/delta T = [(-0.35 pH + 0.658) X 10(-4) X PO2] + 0.035.

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The variation with saturation of the temperature coefficient of PO2 in human blood (delta log PO2/delta T) was determined by continuous recording of the oxygen dissociation curve (ODC), at 37 degrees C and 25 degrees C, on the same blood samples. PCO2 and pH were held constant through an ODC run, and PCO2 was reduced at 25 degrees C to the value measured by anaerobic cooling of the same sample. delta log PO2/delta T was calculated from isosaturation points on the 37 and 25 degrees C curves. The temperature coefficient was also computed as an independent check on this method by determination of the effects of temperature (25, 30, 37 and 40 degrees C) on hemoglobin ligand interaction: fixed acid Bohr effect (delta log PO2/delta pH), carbamino-formation (delta log PO2/delta log PCO2) and hemoglobin oxygen affinity. The values of delta log PO2/delta T ratio obtained from the two different approaches were found to be in good agreement. The coefficient decreased when [H+] concentration was increased. A linear relationship between the Bohr factor and the temperature was found: delta log PO2/delta pH = 0.00267 T-0.520 (r = 0.85; n = 40) At 25 degrees C, the carbamino-formation was one order of magnitude lower than at 37 degrees C. Acid-base state and saturation value appeared to be major determinant factors for the temperature correction coefficient to be applied to blood PO2 values measured at standard (37 degrees C) temperature.

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