Remimazolam for general anesthesia in a patient with aortic stenosis and severe obesity undergoing transcatheter aortic valve implantation.

INTRODUCTION: There is currently limited research on the clinical use of remimazolam in severely obese patients. In this report, we describe the anesthesia management of transcatheter aortic valve implantation (TAVI) in a severely obese patient using remimazolam. CASE DESCRIPTION: A 76-year-old woman (height 1.54 m; total body weight 104 kg; body mass index 43.9 kg/m2) was scheduled for TAVI via the femoral artery approach for aortic valve stenosis. Preoperative echocardiography showed an aortic valve peak flow of 4.0 m/s and an effective orifice area of 0.75 cm2. Anesthesia induction was performed with a bolus dose of 100 µg fentanyl, 15 mg remimazolam, 60 mg rocuronium, and a continuous infusion of remifentanil at 0.4 mg/h. Intraoperatively, remimazolam was administered at a rate of 35 mg/h. General anesthesia management was completed without any complications, although the patient required temporary catecholamine and inhalation anesthesia assistance due to hemodynamic changes. CONCLUSION: Owing to its pharmacological advantages, remimazolam may be an option for anesthesia induction and maintenance in severely obese patients with unstable circulation.

Low-arginine and low-protein diets induce hepatic lipid accumulation through different mechanisms in growing rats.

BACKGROUND: Dietary protein deficiency and amino acid imbalance cause hepatic fat accumulation. We previously demonstrated that only arginine deficiency or total amino acid deficiency in a diet caused significant hepatic triglyceride (TG) accumulation in young Wistar rats. In this study, we explored the mechanisms of fatty liver formation in these models. METHODS: We fed 6-week-old male Wistar rats a control diet (containing an amino acid mixture equivalent to 15% protein), a low-total-amino acid diet (equivalent to 5% protein; 5PAA), and a low-arginine diet (only the arginine content is as low as that of the 5PAA diet) for 2 weeks. RESULTS: Much greater hepatic TG accumulation was observed in the low-arginine group than in the low-total-amino acid group. The lipid consumption rate and fatty acid uptake in the liver did not significantly differ between the groups. In contrast, the low-total-amino acid diet potentiated insulin sensitivity and related signaling in the liver and enhanced de novo lipogenesis. The low-arginine diet also inhibited hepatic very-low-density lipoprotein secretion without affecting hepatic insulin signaling and lipogenesis. CONCLUSIONS: Although the arginine content of the low-arginine diet was as low as that of the low-total-amino acid diet, the two diets caused fatty liver via completely different mechanisms. Enhanced lipogenesis was the primary cause of a low-protein diet-induced fatty liver, whereas lower very-low-density lipoprotein secretion caused low-arginine diet-induced fatty liver.

Supplemental arginine above the requirement during suckling causes obesity and insulin resistance in rats.

Nutrition in early life is important in determining susceptibility to adult obesity, and arginine may promote growth acceleration in infants. We hypothesized that maternal arginine supplementation may promote growth in their pups and contribute to obesity and alteration of the metabolic system in later life. Dams and pups of Wistar rats were given a normal diet (15% protein) as a control (CN) or a normal diet with 2% arginine (ARG). Altered profiles of free amino acids in breast milk were observed in that the concentrations of threonine and glycine were lower in the ARG dams compared with the CN dams. The offspring of the CN and ARG dams were further subdivided into normal-diet (CN-CN and ARG-CN) groups and a high fat-diet groups (CN-HF and ARG-HF). In response to the high fat-diet feeding, the visceral fat deposits were significantly increased in the ARG-HF group (although not compared with the CN-HF group); no difference was observed between the CN-CN and ARG-CN groups. The blood glucose and insulin levels after glucose loading were significantly higher in the ARG-HF group compared with the CN-HF group. The results suggest that the offspring of dams supplemented with arginine during lactation acquired increased susceptibility to a high-fat diet, resulting in visceral obesity and insulin resistance. The lower supply of threonine and glycine to pups may be one of the contributing causes to the programming of lifelong obesity risk in offspring. Our findings also indicated that maternal arginine supplementation during suckling causes obesity and insulin resistance in rats.