Glucose metabolism during liver transplantation in dogs

Arterial and hepatic venous blood levels of glucose were studied in 12 dogs during orthotopic liver transplantation performed under ketamine anesthesia without exogenous glucose administration. During the early part of surgery, arterial blood glucose levels were stable: 161 +/- 12 mg/dl (mean +/- SEM) after laparotomy and 183 +/- 16 mg/dl 5 min before the anhepatic stage. During the anhepatic stage, arterial blood glucose levels decreased progressively to 135 +/- 9 and 88 +/- 8 mg/dl, 5 min in the anhepatic stage and 5 min before reperfusion of the graft liver, respectively (P less than 0.05). Reperfusion of the graft liver resulted in an increase in arterial glucose levels to 206 +/- 17 and 240 +/- 24 mg/dl, 5 and 30 min after reperfusion, respectively (P less than 0.05). Hepatic venous blood glucose levels increased after reperfusion (405 +/- 37 and 346 +/- 41 mg/dl, 5 and 30 min after reperfusion, respectively) and were significantly higher than in arterial blood (P less than 0.05). Arterial plasma insulin, measured in five animals, did not change significantly during the procedure, whereas plasma glucagon levels, stable during the preanhepatic and anhepatic stages, increased steadily after reperfusion of the graft liver, from 66.1 +/- 14.2 to 108.4 +/- 38.1 pg/ml (P less than 0.05). This study shows that in dogs with ketamine anesthesia mild hypoglycemia occurs during the anhepatic stage of liver transplantation without exogenous glucose administration followed by hyperglycemia on reperfusion of the graft liver, possibly secondary to the release of glucose from the donor liver.     

肝硬化病人肝移植术中脑氧代谢的变化

目的观察肝硬化病人原位肝移植术中脑氧代谢的变化。方法16例拟行原位肝移植术的终末期肝硬化病人，年龄25～67岁，体重45—80kg，Child分级B级3例、C级13例，心功能I或Ⅱ级，ASAⅢ或Ⅳ级。持续监测心输出量（CO）、平均动脉血压和体温；分别在术前（基础值）、切肝前10min、无肝期20min、新肝期30min和术毕采集桡动脉、肺动脉（混合静脉血）和左颈内静脉血，进行血气分析，记录血红蛋白、动脉、颈静脉的血氧饱和度（SaO2、SivO2）、血氧分压（PaO2、PjvO2），计算脑氧代谢和机体氧供指标：动脉血氧含量（CaO2）、颈静脉血氧含量（CjvO2）、动．颈静脉血氧含量差（Ca-jvO2）、氧供（DO2）、氧耗（VO2）、脑氧摄取率（CERO2）、脑血流／脑氧代谢率比值（CBF／CMRO2）。结果与基础值比较，切肝前、新肝期及术毕CO升高，无肝期CO降低；术中Hb、CaO2、Ca-jvO2、CERO2均降低，Sjv02、CBF／CMR02升高；无肝期DO2、VO2、CjvO2降低，其余时期DO2升高，术毕VO2升高；新肝期PaCO：升高，pHa降低；无肝期和新肝期pHv和pHjv均降低，术中及术毕BEa、B瞄和BEjv降低（P＜0．05）。结论肝硬化病人在肝移植围术期不存脑缺氧，脑氧摄取率降低。     

Effect of liver transplantation on hepatic glucose metabolism in a patient with type I glycogen storage disease

BACKGROUND: In type I glycogenosis, mutation of the glucose-6-phosphatase gene results in absent glucose-6-phosphatase activity in liver cells leading to fasting hypoglycemia. Liver transplantation is expected to normalize glucose homeostasis. METHODS: Endogenous glucose production (6,6 2H2 glucose) was measured after an overnight fast and during exogenous 13C-labeled glycerol infusion in a patient with glycogenosis type I 24 months after liver transplantation and in a group of healthy subjects. RESULTS: Compared with healthy subjects, the glycogenosis patient had normal fasting glucose production and glucose and insulin concentrations after liver transplantation, but mildly elevated plasma glucagon concentrations. Gluconeogenesis from exogenous glycerol (13C glucose synthesis) was similar and did not lead to enhancement of glucose production in both healthy controls and the patient. CONCLUSIONS: Liver glucoregulatory function is restored by orthotopic liver transplantation in type I glycogenosis.     

Nutrition and metabolism in kidney disease

Nutritional and metabolic derangements are highly prevalent in patients with chronic kidney disease (CKD) and patients on renal replacement therapy. These derangements, which can be termed uremic malnutrition, significantly affect the high morbidity and mortality rates observed in this patient population. Uremic malnutrition clearly is related to multiple factors encountered during the predialysis stage and during chronic dialysis therapy. Several preliminary studies suggested that interventions to improve the nutritional status and metabolic status of uremic patients actually may improve the expected outcome in these patients, although their long-term efficacy is not well established. It therefore is important to emphasize that uremic malnutrition is a major comorbid condition in CKD and renal replacement therapy patients, and that all efforts should be made to try to understand better and treat these conditions effectively to improve not only mortality but also the quality of life of chronically uremic patients. In this article we review the current state of knowledge in the field of nutrition and metabolism in all stages of CKD and renal replacement therapy, including kidney transplant. We also address questions that face investigators in this field and suggest where future research might be headed.     

Magnesium metabolism in health and disease

Magnesium (Mg) is the main intracellular divalent cation, and under basal conditions the small intestine absorbs 30–50% of its intake. Normal serum Mg ranges between 1.7–2.3 mg/dl (0.75–0.95 mmol/l), at any age. Even though eighty percent of serum Mg is filtered at the glomerulus, only 3% of it is finally excreted in the urine. Altered magnesium balance can be found in diabetes mellitus, chronic renal failure, nephrolithiasis, osteoporosis, aplastic osteopathy, and heart and vascular disease. Three physiopathologic mechanisms can induce Mg deficiency: reduced intestinal absorption, increased urinary losses, or intracellular shift of this cation. Intravenous or oral Mg repletion is the main treatment, and potassium-sparing diuretics may also induce renal Mg saving. Because the kidney has a very large capacity for Mg excretion, hypermagnesemia usually occurs in the setting of renal insufficiency and excessive Mg intake. Body excretion of Mg can be enhanced by use of saline diuresis, furosemide, or dialysis depending on the clinical situation.     

Albumin metabolism in health and disease

Studies performed at the University of Cape Town on the metabolism of albumin have been reviewed. The control of albumin metabolism in protein energy malnutrition, in acute exposure to alcohol and after partial hepatectomy in the rat is discussed.     

Amino acid metabolism in isolated perfused rat liver

Conflicting evidence concerning hepatic amino acid (AA) metabolism in the isolated perfused rat liver (IPRL) led us to investigate the response of IPRL using perfusates with various AA contents. Perfusion (n = 4) with whole rat blood diluted in Krebs buffer (1:3, v/v) led to acute proteolysis on account of AA deprivation, as shown by the large release of AA (approximately 1400 mumoles in 120 min), especially branched-chain AA (BCAA) (e.g., Leu, 35.4 +/- 10.4 nmole.min-1.g-1 the first hour, 34.3 +/- 5.5 nmole.min-1.g-1 the second hour). In a first attempt to prevent proteolysis, livers (n = 4) were perfused with the previous medium supplemented with AA known for their antiproteolytic activity, at twice their physiological concentrations. Results during the first hour showed uptake of several AA (mainly alanine, glutamine, and proline), reduced release of BCAA (leucine, 12.5 +/- 6.3 nmole.min-1.g-1), and an increase in glucose and urea production. However, during the second hour, because of the use of a recirculating system, progressive AA depletion induced a reappearance of proteolysis. A two-step AA loading technique, i.e., the addition of antiproteolytic AA at the beginning of the perfusion and the addition of a balanced AA mixture at 60 min caused a further decrease in proteolysis during the 2 hr of perfusion (n = 6). Under these conditions, most AA were taken up by the liver with uptake values comparable to those observed in vivo.     

Gallstones in chronic liver disease

Gallstones occur more commonly in patients with cirrhosis. The incidence increases with severity of liver disease, and the majority remain asymptomatic. When symptoms do occur, morbidity and mortality are much higher than in noncirrhotic patients. Asymptomatic gallstones in cirrhotic patients are best managed conservatively with close follow-up and surgery if symptoms occur. The management of asymptomatic gallstones found incidentally at abdominal surgery for another indication is controversial. Laparoscopic cholecystectomy is the treatment of choice for symptomatic cholelithiasis in patients with well-compensated liver disease, whereas patients with choledocholithiasis are best managed endoscopically. Symptomatic cholelithiasis in the decompensated patient remains a challenge, and these patients are best managed in specialized hepatobiliary centers. This review examines the evidence currently available on gallstones in chronic liver disease and the factors that infiuence its management.