Metabolic and ventilatory responses to anemic hypoxia in conscious rats.

Abstract

We investigated the metabolic and ventilatory effects of anemia, which is characterized by a decrease in blood O2 content with no changes in arterial PO2 (PaO2). Anemia was obtained in conscious chronically instrumented adult male rats by substituting blood with equal volumes of Ringer lactate solution via the tail artery. Three hours later, we measured resting O2 consumption (VO2) by an open flow method and ventilation (VE) by the barometric method. Hemodilution to 80-90, 70-80, or 60-70% of the starting hematocrit and hemoglobin values had no major effects on VO2, VE, or mean arterial blood pressure (MAP). A 50-60% hemodilution reduced VO2 and MAP, with a modest increase in VE; the rats were hypocapnic, with normal PaO2. Infusion of vasopressin in a dosage sufficient to increase MAP to the basal value resulted in a reduction in VE, a further drop in VO2, and a return to normocapnia. Three days after hemodilution, hematocrit and hemoglobin were still low but ventilatory and metabolic parameters were normal. In conclusion, in this rat model of anemic hypoxia, 1) hypometabolism occurred without a drop in PaO2, implying that its manifestation does not require activation of the carotid body, and 2) the transient hypocapnia resulted from the VE stimulating effects of the hypotension.