We have studied plasma protein binding of alfentanil in 10 patients given a mean total dose of 949 micrograms kg-1 as the principal anaesthetic agent for coronary artery bypass grafting. The mean unbound fraction of plasma alfentanil increased from 0.09 to 0.16 after administration of heparin and to 0.26 after beginning cardiopulmonary bypass (CPB). After CPB until the end of surgery, the unbound fraction decreased to 0.12. These changes in the unbound fraction were associated with significant changes in plasma total and unbound concentrations of alfentanil also. Within the first 1 min of CPB, total alfentanil concentration had decreased by more than the unbound concentration and the decrease observed in the latter disappeared rapidly. From induction of anaesthesia until awakening of the patient, plasma protein binding of alfentanil was related significantly (P = 0.0166) to the serum concentration of orosomucoid (alpha 1-acid glyco-protein).

Liver oxygenation was studied with hemorrhagic hypotension and corrected using whole blood, a synthetic colloid (hydroxyethyl starch or hetastarch, HES; mol. wt. 120,000), or a crystalloid solution. Measurements were performed directly by recording pig liver tissue oxygen tension with an implanted silicone elastomer (Silastic) tube, and indirectly by calculating blood oxygen contributions. The direct method seems fairly reliable and accurately reflects different levels of bleeding and shock and their correction. Liver tissue oxygen tension (PlO2) may thus be used as an indicator of central organ response to shock management. PlO2 decreased during bleeding from 33.5 +/- 0.5 to 16.0 +/- 0.5 torr, and normalized rapidly after retransfusion. The baseline values were significantly exceeded after hetastarch infusion but were never reached with Ringer's solution. The correction of liver oxygen consumption was less complete after crystalloid infusion as well. On the other hand, the difference in liver oxygenation was less marked after crystalloid infusion and retransfusion, which restored perfusion to the baseline. The total amount of Ringer's solution needed to keep the animals hemodynamically stable during the 2-h follow-up period was four times higher than with hetastarch and some five times the blood volume shed. The cause of defective correction of liver oxygenation seems to be the poor response of liver blood flow to refilling in the Ringer group, in addition to apparent tissue edema after crystalloid infusion. According to our study, hemorrhagic hypotension related to liver oxygenation is more promptly and completely corrected with the colloid hydroxyethyl starch than with a crystalloid solution in the early phase of treatment.

No abstract

We compared the 95% response time (95% RT) of two tissue oxygen tonometers under two sets of circumstances. We first evaluated the devices during normoxia, hyperoxia, and anoxia in vitro, using a transcutaneous PO2 electrode (PtcO2) as the reference. The responses to normoxia and to different grades of hyperoxia were examined in vivo in 8 healthy volunteers to assess the relationship between changes in subcutaneous PO2 and PtcO2, an estimate of arterial PO2 (PaO2). One subcutaneous method (ScA) used a technique based on a polarographic needle electrode in situ connected to an ammeter; the second method (ScB) was based on a blood gas analyzer system first described by Hunt (Lancet 164;2:1370). ScA and PtcO2 both responded to stepwise changes in ambient oxygen concentration (21-100%) in vitro within 10 seconds; the 95% RT of ScA was 1.39 +/- 0.5 to 2.39 +/- 0.8 minutes and that of PtcO2 was 0.32 +/- 0.1 to 0.49 +/- 0.1 minutes. ScB had a lag of 3 minutes, and the 95% RT was 6.75 +/- 0.5 to 8.2 +/- 0.8 minutes. In contrast to the results in vitro, the response of ScA to changes in FiO2 in vivo was delayed compared with the rapid response of PtcO2, reflecting the physiologic delay of tissue PO2 in response to increased PaO2. The time lag and the long 95% RT of ScB were even more evident in vivo. ScA reacted three to four times faster than ScB, both in vitro and in vivo, to changes in the oxygen environment. The in vitro 95% RT of ScA to changes in ambient oxygen varied from 2 to 3.5 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract