Background Hydroxyethyl starch (HES), a commonly used resuscitation fluid, has the property to induce hyperglycemia as it contains large ethyl starch, which can be metabolized to produce glucose. group and T4, T5 in the HES group, increased significantly compared to baseline. There were no significant changes in the serial differences of mean blood glucose levels from baseline between the two groups. Conclusions Administration of 6% HES-130 increased blood glucose levels within the physiologic limits, but the degree of glucose increase was not greater than Mouse monoclonal to IL-2 that caused by administration of lactated Ringer’s solution. In conclusion, we did not find evidence that 6% HES-130 induces hyperglycemia in non-diabetic patients. Keywords: Blood glucose, Colloids, Hydroxyethyl starch derivatives, Ringer Introduction Despite serious side effects such as acute kidney injury in sepsis , hydroxyethyl starch (HES) has been widely used for intravascular volume resuscitation in various clinical settings [2,3,4,5,6]. Although recent studies have suggested careful consideration when choosing between a colloid and a crystalloid solution, colloids are still one of BI6727 the most widely used and recommended treatment options in the case of hypovolemia, according to the resuscitation guidelines and intensive care management algorithms [2,3,4,5]. Moreover, colloids can also be administered as preanesthetic brokers for the prevention of spinal anesthesia-induced hypotension . HES is usually a synthetic carbohydrate polymer and it is commonly used for fluid resuscitation . HES has been used in various clinical situations to treat hypovolemia in patients with trauma, burns, sepsis, and surgery . However, there are still concerns about serious side effects derived from using HES in patients with sepsis or who are critically ill because of its association with the risk of kidney injury and bleeding . Furthermore, HES contains large ethylated starch or glucose polymers, which can be metabolized by serum amylases to produce smaller starch polymers and free glucose . Thus, it is possible that HES could induce hyperglycemia in patients undergoing surgery, hence more susceptible to stress responses . Hyperglycemia in surgical patients is associated with numerous adverse effects and serious adverse clinical outcomes . There are few publications describing the possible effects of HES on blood glucose level and these include studies suggesting that 6% HES-450 was able to trigger changes in glycemia [8,11]. We hypothesized that this administration of 6% HES-130 is also able to increase blood glucose level. For this reason, we examined whether 6% HES-130, which has a lower molecular weight and lower degree of substitution than the 6% HES-450, increase blood glucose level in non-diabetic patients undergoing lower limb surgery under spinal anesthesia. In addition, we compared the serial differences of mean blood glucose levels from baseline between 6% HES-130 and lactated Ringer’s solution. Materials and Methods After approval by the Institutional Review Board, written informed consents were obtained from all patients after the study was carefully explained. A total of 60 patients who were scheduled to undergo elective lower limb surgery with spinal anesthesia were enrolled. Only patients who belonged to the American Society of Anesthesiologists (ASA) class I or II and were aged between 30 and 80 years, with a body weight between 40 and 75 kg, were included in the study . Patients with diabetes mellitus, taking hyperglycemic drugs (acetaminophen, ascorbic acid, steroids, etc.), with possible BI6727 allergies to experimental drugs (especially with an allergy to corn), coagulation disorders, renal or cardiac dysfunctions, and suspected hypervolemia, including pulmonary BI6727 edema, were excluded from the study. Patients were divided into two groups: Group LR, administered lactated Ringer’s solution (15 ml/kg, n = 30); Group HES, administered 6% HES-130/0.4 (Volulyte 6%?, Fresenius-kabi Korea, 7.5 ml/kg, n = 28). All patients were premedicated with 0.05 mg/kg midazolam, intramuscularly, 30 min prior to the induction of anesthesia. An intravenous access was achieved with an 18 gauge intravenous cannula and the patients were transported to the operating room. Basal monitoring devices such as electrocardiogram, pulse oximetry, and non-invasive arterial BI6727 pressure were attached to the patients in.