INTERACTIONS BETWEEN THE CIRCULATORY EFFECTS OF CENTRAL HYPOVOLEMIA AND ARTERIAL HYPOXIA IN CONSCIOUS RABBITS

1. Eight conscious rabbits were repeatedly subjected to progressive re duction in central blood volume by gradually inflating a thoracic infe rior vena caval-cuff so cardiac index (CI) fell at a constant 8.5% of baseline/min. 2. Caval-cuff inflations were performed after 10 min exp osure to 100, 21, 12-14 and 8-10% O-2, with and without the addition o f 3-4% CO2, in randomized order. 3. The haemodynamic response to progr essive reduction in central blood volume was biphasic. In Phase I, sys temic vascular conductance index (SVCI) fel linearly, supporting mean arterial pressure (MAP). When CI had fallen to a critical level, Phase II occurred in which SVCI rose abruptly, MAP plummeted and respirator y drive progressively increased. 4. During Phase I, there were indepen dent linear relationships between Pa-CO2 (but not Pa-O2) and the rates at which SVCI and MAP changed during the progressive fall of CI. The higher the level of Pa-CO2, the greater was the rate of fall of SVCI a nd the less the rate of fall of MAP. 5. There was an inverted U-shaped effect of Pa-O2 on the level of CI at which Phase II occurred: (a) du ring hyperoxia (100% O-2), Phase II occurred later than during normoxi a (21% O-2); and (b) across the normoxic and hypoxic gas mixtures (21- 8% O-2, with and without added CO2), there was an independent linear r elationship between Pa-O2 (but not Pa-CO2 or Pa-O2 X Pa-CO2) and the l evel of CI at which Phase II occurred. That is, the lower the level of Pa-O2, the later was the onset of Phase II. This interaction is best explained by an increased level of central sympathetic vasoconstrictor drive during hypoxia.