Vascular capacitance responses to severe systemic hypercapnia and hypoxia in dogs.
The magnitude of vascular capacitance change induced by hypercapnia, hypoxia, or hypoxic hypercapnia was estimated during the administration of experimental gas mixtures to anesthetized dogs for 25 min. Mean circulatory filling pressure (Pcf) was determined by fibrillating the heart and equilibrating arterial and venous pressures with a pump. We assumed that the total blood volume remained constant and that the magnitude of change in peripheral venous volume equaled the sum of the changes in blood volume in the cardiopulmonary and arterial beds. We further assumed that active (reflex) peripheral venoconstriction occurred if the cardiopulmonary and arterial bed blood volumes, as well as the Pcf, increased. Within 3 min, severe hypercapnia and hypoxic hypercapnia induced a 5.2 and 7.3 ml/kg reduction in systemic vascular capacity, and, by 19 min of experimental gas presentation, increased Pcf by 5.5 and 7.0 mmHg, respectively. Severe hypoxia had less effect (0.7 ml/ kg and 2.5 mmHg, respectively) at 19 min. Severe hypercapnia also increased the central venous, systemic arterial, and pulmonary arterial pressures and decreased heart rate. Hypoxic hypercapnia additionally increased cardiac output. We conclude that severe systemic hypercapnia, whether alone or in combination with hypoxia, causes a significant active reduction in vascular capacitance, but severe hypoxia is less effective.
D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D002628:Chemoreceptor Cells / Q000502:physiology*; D004285:Dogs; D006339:Heart Rate; D006400:Hematocrit; D006935:Hypercapnia / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D012119:Respiration; D013997:Time Factors; D014661:Vasoconstriction; D014664:Vasodilation