Desflurane consumption with the Zeus during automated closed circuit versus low flow anesthesia.

INTRODUCTION: During automated closed-circuit anesthesia (CCA), the Zeus (Dräger, Lübeck, Germany) uses a high initial fresh gas flow (FGF) to rapidly attain the desired agent and carrier gas concentrations, resulting in a desflurane consumption well above patient uptake. Because both FGF and carrier gas composition can affect consumption, we determined the Zeus' agent consumption with automated CCA and with automated low flow anesthesia (LFA) (= maintenance FGF of 0.7 L min(-1)) with 3 different carrier gases. METHODS: After IRB approval, 65 ASA PS I or II patients undergoing general surgery received desflurane in either O2, O2/air, or O2/N2O, with the Zeus to maintain the end-expired concentration (FA) at 6, 6, and 4% and the F1O2 at 1.0, 0.6, and 0.4, respectively. In addition, patients were assigned to either automated CCA (O2 n = 11; O2/air n = 11; O2/N2O n = 11) or automated LFA (selected FGF 0.7 L min(-1)) (O2 n = 12; O2/air n = 11; O2/N2O n = 9). Demographics and desflurane consumption at 2, 4, 6, 8, 10, 20, 30, 40 and 50 min were compared. RESULTS: With the same carrier gas, desflurane consumption was lower with the CCA mode than with LFA mode after 4 min in the O2 groups, 6 min in the O2/air groups, and 30 min in the O2/N2O groups. Within each mode, desflurane consumption in the O2 and O2/air groups was identical at all times. Despite the use of a lower FA in the N2O groups, initial desflurane consumption was higher than in the O2 and O2/air groups, but it was lower later (> or = 15 min) only with LFA. DISCUSSION: After 50 min, desflurane consumption with automated CCA is lower than with automated LFA. However, initial agent consumption is complex, and N2O in particular may increase initial desflurane consumption (though ultimately resulting in lower desflurane usage because of its MAC sparing effect) because initial FGF is increased to rapidly reach the target concentrations. Differences in desflurane consumption only become apparent after FGF has stabilized to the target FGF.

Inhibin B secretion in males with gonadotropin-releasing hormone (GnRH) deficiency before and during long-term GnRH replacement: relationship to spontaneous puberty, testicular volume, and prior treatment--a clinical research center study.

To evaluate the physiology of inhibin B in the human male, we measured serum concentrations in normal adult men and men with isolated GnRH deficiency before and during long-term replacement with pulsatile GnRH. At baseline, inhibin B levels in the GnRH-deficient men (n = 31) were significantly lower than normal controls (85 +/- 10 pg/mL vs. 239 +/- 14 pg/mL; P < .01) and correlated positively with pretreatment testicular volume (r = .80, P = .001) and a history of spontaneous puberty, suggesting additional maturational influences on the both testicular volume and inhibin B secretion. Pulsatile GnRH administration was associated with significant increases in inhibin B, with levels averaging 108 +/- 7 pg/mL when serum LH, FSH, and T concentrations had reached the normal adult male range (n = 22; P = .02 vs. baseline). Continued GnRH administration for at least an additional year was not associated with further increases in inhibin B concentrations. Throughout the course of long-term pulsatile GnRH replacement, serum FSH levels were negatively correlated with inhibin B concentrations (e.g. r = -.71, P < 0.01; n = 14 treated 12 months after normalization of T). Although inhibin B concentrations did not correlated with sperm density during therapy, rates of fertility were higher in patients with higher baseline levels (inhibin B > or = 60 pg/mL). Increases in serum concentrations of inhibin B occurring during GnRH replacement demonstrate the gonadotropin regulation of gonadal inhibin B secretion. However, the variation in baseline inhibin B levels before GnRH administration suggests an additional gonadotropin-independent level of modulation. The negative correlation between FSH and inhibin B secretion in GnRH-deficient men receiving long-term GnRH replacement is consistent with a putative role of inhibin B in the negative feedback regulation of FSH, although direct confirmation of this role requires further investigation.

Inhibin B in males with gonadotropin-releasing hormone (GnRH) deficiency: changes in serum concentration after shortterm physiologic GnRH replacement--a clinical research center study.

To examine the role of inhibin B in the feedback regulation of FSH secretion in the human male, we determined serial levels in 18 men with idiopathic hypogonadotropic hypogonadism (IHH) during their initial 8 weeks of GnRH replacement. Pulsatile GnRH was administered every 2 h, with the dose increased at 2-week intervals (5-50 ng/kg/bolus). Every 2 weeks, sera were assayed for inhibin B, FSH, LH, and testosterone. Serial comparisons were performed within the IHH group as well as vs. normal men (n = 20). The baseline inhibin B level in IHH patients averaged 68 +/- 11 pg/mL (mean +/- SEM), significantly less than that in normal men (239 +/- 14 pg/mL; P < 0.001). After 8 weeks of pulsatile GnRH, inhibin B levels in the IHH patients increased significantly to 118 +/- 14 pg/mL (P = 0.003). During GnRH replacement, FSH concentrations correlated negatively with inhibin B concentrations at all doses. Patients previously treated with testosterone began with somewhat lower inhibin B levels but demonstrated a significantly greater increase in serum concentrations than patients who had received prior gonadotropin or GnRH therapy. A history of cryptorchidism did not have a significant impact on inhibin B concentrations before or during GnRH replacement. The low inhibin B levels in IHH men at baseline and their prompt increase in response to pulsatile GnRH suggest acute regulation by gonadotropin stimulation of the testis. The variation in inhibin B levels at baseline and in response to GnRH suggest that prior gonadotropin exposure and seminiferous tubular development also modulate inhibin B secretion. The consistent negative correlation between FSH and inhibin B during the induction of sexual maturation with GnRH supports the role of gonadal inhibin B secretion as an important endocrine regulator of FSH in the human male.