Total and hindlimb oxygen deficit and "repayment" in hypoxic anesthetized dogs

Abstract

Whole-body (WB) and hindlimb [(HL), paw excluded] O2 uptake (VO2) were measured in 26 anesthetized paralyzed dogs while they were ventilated with 9% O2-91% N2 for 15- and 30-min periods and with room air during recovery periods. Ten of the dogs were pretreated with 1 mg/kg propranolol (beta-Blockade). O2 deficit during hypoxia and the excess O2 used during recovery were obtained by assuming that VO2 would have followed the time course described by a line connecting prehypoxic and postrecovery VO2. Amounts of O2 deficit and excess were corrected for changes in O2 stores. O2 excess was seldom as great as O2 deficit in either WB or HL and the two quantities were not obviously related. The rate of HL O2 deficit accumulation decreased with time in hypoxia, whereas WB O2 deficit remained constant. All of HL VO2 was attributed to skeletal muscle so that WB O2 deficit and excess could be partitioned into muscle and nonmuscle portions. The rate of nonmuscle O2 deficit accumulation increased with time, but the nonmuscle portion of O2 excess decreased after the longer hypoxic period. beta-Blockade accentuated but did not change these qualitative relationships. We concluded that neither WB nor HL O2 deficits were fully matched by O2 excess and that regional patterns of O2 deficit accumulation and “repayment” did not necessarily parallel those for WB.