Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia

To test the role of blood flow in tissue hypoxia-related increased veno-art erial Pco(2) difference (Delta Pco(2)), we decreased O-2 delivery ((D)over doto(2)) by either decreasing flow [ischemic hypoxia (IH)] or arterial Po-2 [hypoxic hypoxia (HH)] in an in situ, vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system. Twelve anesthetiz ed and ventilated dogs were studied, with systemic hemodynamics maintained within normal range. In the IH group (n = 6), hindlimb (D)over dot o(2), wa s progressively lowered every 15 min by decreasing pump-controlled flow fro m 60 to 10 ml . kg(-1)-min(-1), with arterial Po-2 constant at 100 Torr. In the HH group (n = 6), hindlimb Do, was progressively lowered every 15 min by decreasing Po, from 100 to 15 Torr, when flow was constant at 60 ml kg(- 1) min(-1). Limb (D)over dot o(2), O-2 uptake ((V)over dot o(2)), and Delta Pco(2) were obtained every 15 min. Below the critical (D)over dot o(2), (V )over dot o(2) decreased, indicating dysoxia, and O-2 extraction ratio ((V) over dot o(2) /(D)over dot o(2)) rose continuously and similarly in both gr oups, reaching a maximal value of similar to 90%. Delta Pco(2), significant ly increased in IH but never differed from baseline in HH. We conclude that absence of increased Delta Pco(2) does not preclude the presence of tissue dysoxia and that decreased flow is a major determinant in increased Delta Pco(2).