Journal of applied physiology
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Respiratory properties of whole blood during development were studied in embryos of the bar-headed and Canada geese. In both species, affinity of the blood for O2 [expressed as O2 half-saturation pressure (P50)] increased with development, to a low and stable value. The low and stable P50 at pH 7.4 for the bar-headed goose, 20.1 +/- 0.3 Torr, is significantly lower than that for the Canada goose, 26.9 +/- 0.8 Torr. ⋯ Hill's coefficients, buffering capacity, red cell 2,3-diphosphoglycerate, and blood hemoglobin concentrations are similar in both species. We suggest that the affinity of the whole blood for O2 is an important genetically based adaptation to ensure a high O2 content in the blood in the face of reductions in ambient PO2 associated with nesting at high altitudes. The higher Bohr effect may ensure high tissue PO2 in the presence of the high-affinity hemoglobin.
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Continuous recordings have been made of pH, PO2, and PCO2 of arterial blood (pHa, PaO2, PaCO2) in an extracorporeal circulation during periods of hypoxia (inspired PO2 45-10 Torr) in sea bass, Morone labrax. During moderate hypoxia hyperventilation was accompanied by an increase in pHa. ⋯ Recovery from hypoxia is associated with an increase in lactate concentration reaching values of more than 6 meq X l-1 following deep hypoxia, and pHa falls to 7.73. PaO2 recovers rapidly, but recovery of PaCO2 is not so rapid and together with the residual hyperventilation indicates that the fish is paying off an O2 debt.
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The adequacy of constant airway gas flow sustenance of arterial blood gas tensions was investigated in anesthetized-paralyzed mongrel dogs. Gas delivery was achieved via a main-stem bronchi cannulation system constructed of two polyethylene tubes bifurcating at the carina, which rested on the posterior surface of the trachea outside of an endotracheal tube positioned in the upper third of the trachea. Equal flows (total flow = Vin) of humidified air were delivered through each limb of the cannulation system at constant flow rates with Vin ranging from 8 to 28 l/min. ⋯ Arterial O2 tension varied directly (PaO2 = 0.72 Vin + 74.6), and arterial CO2 tension varied inversely (PaCO2 = -0.73 Vin + 51.2) with Vin during ambient gas, constant-flow ventilation (CFV). During prolonged CFV (greater than 2 h), no evidence of CO2 accumulation or deterioration of PaO2, was observed. This study demonstrates that in apneic dogs normal blood gases can be achieved and maintained over prolonged periods with constant airway flow at low intratracheal pressures.
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Assessment of ventricular performance during positive end-expiratory pressure (PEEP) requires accurate measurement of transmural cardiac pressures. We investigated the influence of PEEP on the atrial and juxtacardiac pressures estimated by different methods in eight dogs. Left atrial pressure was measured by hydraulic and transducer-tipped catheter systems. ⋯ Similar phenomena were also observed in three human subjects. We conclude that lung distension lifts and tilts the heart in a supine preparation causing a hydrostatic increase of intracavitary pressure and attenuation of the esophageal pressure increment. These effects help to account for the apparent alterations of ventricular compliance and performance previously attributed to PEEP.
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We sought to determine why large lung compartment hypoxic pulmonary vasoconstriction fails to redistribute blood flow at a low fraction of inspired oxygen (FIO2) level (0.06) when the remaining small lung compartment is ventilated with room air. In 10 pentobarbital-anesthetized dogs, we decreased large compartment FIO2 from 1.0 to 0.06 while the small compartment FIO2 was constant at 0.21, 0.3, 0.5, or 1.0. When small compartment FIO2 was 0.21 and 0.3, large compartment FIO2 decreases from 1.0 to 0.15-0.10 caused a disproportionate increase in large compartment pulmonary vascular resistance (PVR) and further large compartment FIO2 decreases from 0.15-0.10 to 0.06 caused a decrease in large compartment PVR while small compartment PVR continued to increase. ⋯ When small compartment FIO2 was 0.21 and 0.3, small compartment alveolar oxygen tension (PAO2) and PVR were always inversely related. When small compartment FIO2 was 0.21, 0.3, and 0.5, large compartment PVR either decreased or remained constant whenever mixed venous oxygen tension (PVO2) was less than 30-32 Torr and large compartment PAO2 was less than 50-60 Torr. We conclude that both small compartment hypoxic pulmonary vasoconstriction and primarily failure of large compartment hypoxic pulmonary vasoconstriction occurred when large compartment FIO2 was low (0.06) and small compartment FIO2 was 0.21 or 0.3.