[Airway Management Using McGrath MAC in a Pediatric Patient with a Laryngeal Saccular Cyst].

An 18-month-old female infant was scheduled for resection of a laryngeal saccular cyst inducing narrow airway. Since the cyst protruded from the left side of the epiglottis and the vocal cord was compressed to the right side, a difficult airway was anticipated. In addition, there was a risk of tracheal occlusion by rupture of the cyst Awake intubation was considered to be dangerous. Slow induction with sevoflurane and neuromusclar blockade was attempted, preparing reversal of the neuromusclar blockade. Fortunately, mask ventilation was achieved without difficulty. It was necessary to insert a tracheal tube avoiding the cyst We used McGrath MAC (Aircraft Medical Co., UK), which enabled us to manipulate the tracheal tube. A tracheal tube was successfully inserted under McGrath monitor guidance.

[Case of anesthesia for thoracoscopic thymectomy in a pediatric patient with myasthenia gravis: reversal of rocuronium-induced neuromuscular blockade with sugammadex].

Neuromuscular blocking drugs (NMBDs) can predispose patients with myasthenia gravis to postoperative paralysis and respiratory complications. We had a 12-year-old female patient undergoing thoracoscopic thymectomy. She had suffered from MGFA class IIa (mild systemic) myasthenia gravis for 4 months. Anesthesia was induced with 3 mg x kg(-1) of thiopental and 0.2 mg x kg(-1) of rocuronium, which was given incrementally to achieve 100% blockade. Anesthesia was maintained with oxygen, air, 2% sevoflurane and 0.2 microg x kg(-1) x min(-1) of remifentanil. 0.05 mg x kg(-1) of rocuronium was added when the TOF ratio recovered to 20%. Towards the end of the surgery, remifentanil was withdrawn and 4 microg x kg(-1) of fentanyl was given. Intercostal nerve block with 0.2% ropivacaine was performed to relieve postoperative pain. TOF ratio was 32% at the end, when we gave 2 mg x kg(-1) of sugammadex to get 100% reversal of neuromuscular blockade in 120 seconds. There was no residual paralysis and respiratory complications postoperatively.

Impact of protein and carbohydrate supplementation on plasma volume expansion and thermoregulatory adaptation by aerobic training in older men.

We examined whether protein-carbohydrate (CHO) supplementation immediately after exercise each day during aerobic training facilitated plasma volume (PV) expansion and thermoregulatory and cardiovascular adaptations in older men. Fourteen moderately active older men [68 +/- 5 (SD) yr] were divided into two groups so as to have no significant differences in anthropometric measures, PV, and peak oxygen consumption rate (Vo(2peak)). Each group was provided with a mixture of protein and CHO (3.2 kcal, 0.18 g protein/kg body wt, Pro-CHO, n = 7) or a non-protein and low-calorie placebo (0.5 kcal, 0 g protein/kg body wt, CNT, n = 7) immediately after cycling exercise (60-75% Vo(2peak), 60 min/day, 3 days/wk) each day for 8 wk at approximately 19 degrees C ambient temperature (T(a)) and approximately 43% relative humidity (RH). Before and after training, we measured PV, cardiac stroke volume (SV), and esophageal temperature (T(es)) during 20-min exercise at 60% of pretraining Vo(2peak) at 30 degrees C T(a) and 50% RH. Moreover, we determined the sensitivity of the chest sweat rate (DeltaSR/DeltaT(es)) and forearm vascular conductance (DeltaFVC/DeltaT(es)) in response to increased T(es) during exercise. After training, PV increased by approximately 6% in Pro-CHO (P < 0.001), with an approximately 10% increase in SV during exercise (P < 0.001), but not in CNT (P > 0.07). DeltaFVC/DeltaT(es) increased by 80% and DeltaSR/DeltaT(es) by 18% in Pro-CHO (both P < 0.01) but not in CNT (P > 0.07). Moreover, we found a significant interactive effect of group x training on PV, SV, and DeltaFVC/DeltaT(es) (all P < 0.02) but with no significant effect of group (P > 0.4), suggesting that the supplement enhanced these responses to aerobic training. Thus postexercise protein-CHO supplementation during training caused PV expansion and facilitated thermoregulatory and cardiovascular adaptations, possibly providing a new training regimen for older men.

Protein and carbohydrate supplementation after exercise increases plasma volume and albumin content in older and young men.

This study examined whether increased plasma volume (PV) and albumin content (Alb(cont)) in plasma for 23 h after exercise were attenuated in older subjects compared with in young adult subjects, and if this attenuation abated by supplementation with protein and carbohydrate (CHO) immediately after exercise. Eight moderately active older (approximately 68 yr) and 8 young (approximately 21 yr) men performed two trials: control (CNT) and Pro-CHO in which subjects consumed placebo (0.5 kcal, 0 g protein, 0.5 mg Na(+) in 3.2 ml total fluid volume/kg body wt) or protein and CHO mixture (3.2 kcal, 0.18 g protein, 0.5 mg Na(+) in 3.2 ml total fluid volume/kg body wt) supplementations, respectively, immediately after high-intensity interval exercise for 72 min [8 sets of 4 min at 70-80% peak oxygen consumption rate (Vo(2peak)) intermitted by 5 min at 20% Vo(2peak)]. PV, Alb(cont), and plasma globulin content (Glb(cont)) were measured before exercise, at the end of exercise, every hour from the 1st to the 5th hour after exercise, and at the 23rd hour after exercise. From 12 h before the start to the end of experiment, food intake was controlled to the age-matched recommended dietary allowances. We found that during the first 4 h after exercise in CNT, Alb(cont) recovered less in the older than the young group by approximately 0.04 g/kg (P < 0.05), while it generally recovered more with Pro-CHO than CNT by approximately 0.09 and approximately 0.04 g/kg in the young and older group, respectively, accompanied by a greater increase in PV by approximately 1 and approximately 2 ml/kg, respectively, during the 23 h after exercise (P < 0.05). Glb(cont) remained constant throughout the experiment in both trials for both age groups. Thus the attenuated responses of Alb(cont) and PV after exercise in older subjects were restored by protein and CHO supplementation immediately after exercise, similarly to young subjects.

Acute hypoosmolality attenuates the suppression of cutaneous vasodilation with increased exercise intensity.

We examined the hypothesis that elevation of the body core temperature threshold for forearm skin vasodilation (TH(FVC)) with increased exercise intensity is partially caused by concomitantly increased plasma osmolality (P(osmol)). Eight young male subjects, wearing a body suit perfused with warm water to maintain the mean skin temperature at 34 +/- 1 degree C (ranges), performed 20-min cycle-ergometer exercise at 30% peak aerobic power (VO2(peak)) under isoosmotic conditions (C), and at 65% VO2(peak) under isoosmotic (H(EX)I(OS)) and hypoosmotic (H(EX)L(OS)) conditions. In H(EX)L(OS), hypoosmolality was attained by hypotonic saline infusion with DDAVP, a V2 agonist, before exercise. P(osmol) (mosmol/kg H2O) increased after the start of exercise in both H(EX) trials (P < 0.01) but not in C. The average P(osmol) at 5 and 10 min in H(EX)I(OS) was higher than in C (P < 0.01), whereas that in H(EX)L(OS) was lower than in H(EX)I(OS) (P < 0.01). The change in TH(FVC) was proportional to that in P(osmol) in every subject for three trials. The change in TH(FVC) per unit change in P(osmol) (deltaTH(FVC)/deltaP(osmol), degrees C x mosmol(-1) x kg H2O(-1)) was 0.064 +/- 0.012 when exercise intensity increased from C to H(EX)I(OS), similar to 0.086 +/- 0.020 when P(osmol) decreased from H(EX)I(OS) to H(EX)L(OS) (P > 0.1). Moreover, there were no significant differences in plasma volume, heart rate, mean arterial pressure, and plasma lactate concentration around TH(FVC) between H(EX)I(OS) and H(EX)L(OS) (P > 0.1). Thus the increase in TH(FVC) due to increased exercise intensity was at least partially explained by the concomitantly increased P(osmol).

Ten-day endurance training attenuates the hyperosmotic suppression of cutaneous vasodilation during exercise but not sweating.

It is well known that hyperosmolality suppresses thermoregulatory responses and that plasma osmolality (P(osmol)) increases with exercise intensity. We examined whether the decreased esophageal temperature thresholds for cutaneous vasodilation (TH(FVC)) and sweating (TH(SR)) after 10-day endurance training (ET) are caused by either attenuated increase in P(osmol) at a given exercise intensity or blunted sensitivity of hyperosmotic suppression. Nine young male volunteers exercised on a cycle ergometer at 60% peak oxygen consumption rate (V(O2 peak)) for 1 h/day for 10 days at 30 degrees C. Before and after ET, thermoregulatory responses were measured during 20-min exercise at pretraining 70% V(O2 peak) in the same environment as during ET under isoosmotic or hyperosmotic conditions. Hyperosmolality by approximately 10 mosmol/kgH2O was attained by acute hypertonic saline infusion. After ET, V(O2 peak) and blood volume (BV) both increased by approximately 4% (P < 0.05), followed by a decrease in TH(FVC) (P < 0.05) but not by that in TH(SR). Although there was no significant decrease in P(osmol) at the thresholds after ET, the sensitivity of increase in TH(FVC) at a given increase in P(osmol) [deltaTH(FVC)/deltaP(osmol), degrees C x (mosmol/kgH2O)(-1)], determined by hypertonic infusion, was reduced to 0.021 +/- 0.005 from 0.039 +/- 0.004 before ET (P < 0.05). The individual reductions in deltaTH(FVC)/deltaP(osmol) after ET were highly correlated with their increases in BV around TH(FVC) (r = -0.89, P < 0.005). In contrast, there was no alteration in the sensitivity of the hyperosmotic suppression of sweating after ET. Thus the downward shift of TH(FVC) after ET was partially explained by the blunted sensitivity to hyperosmolality, which occurred in proportion to the increase in BV.