BACKGROUND AND OBJECTIVES: The duration of nerve block is longer in streptozotocin (STZ)-induced diabetic rats for all local anesthetics (with and without adjuvants) compared with normal rats. Perioperative glycemic control is currently practiced to reduce adverse events in many at-risk patients, especially in diabetic patients, to prevent neuropathy, poor wound healing, and greater incidence of infection. The aim of this study was to investigate in diabetic rats the importance of glycemic control before peripheral nerve block. METHODS: To induce diabetes, rats were intravenously injected with a single dose of 50 mg/kg STZ to destroy pancreatic beta cells. Tactile allodynia in response to von Frey filament stimulation of the plantar hind paws was used as the criterion for diabetic neuropathy. Diabetic rats were randomly divided into experimental treatment groups. The continuous glycemic control experiment compared: 3 U/d insulin implant for 14 days, 1.5 U/d insulin implant for 14 days, and placebo treatment. The acute glycemic control experiment compared a single 6U Human Insulin Isophane Suspension (NPH) injection and placebo treatment. Nondiabetic rats received placebo implants or injections. Following treatment, 0.1 mL of 1% lidocaine hydrochloride with 5 μg/mL epinephrine hydrochloride was injected into the left sciatic notch. Animals were then reevaluated at 10-minute intervals for the absence or presence of sensory and motor response. RESULTS: All STZ-injected rats had blood glucose levels greater than 350 mg/dL and tactile allodynia. After insulin implants or injections, diabetic rats had much lower blood glucose levels than diabetic rats with placebo treatment. With both 3 and 1.5 U/d continuous glycemic control, the local anesthetic solution produced a shorter duration of sensory and motor nerve block in insulin-treated diabetic rats compared with placebo-treated diabetic rats, and shorter duration was similar to nondiabetic rats. With 6 U acute glycemic control in diabetic rats, there was no reduction in nerve block duration compared with placebo-treated diabetic rats. CONCLUSIONS: With continuous glycemic control in diabetic rats, the duration of sensory and motor nerve block was about 40 minutes shorter than that in the untreated diabetic rats and similar to that of normal rats. However, acute glycemic control did not affect nerve block duration, suggesting that this neuropathy cannot be rapidly reversed.
BACKGROUND AND OBJECTIVES: The duration of nerve block is longer in streptozotocin (STZ)-induced diabeticrats for all local anesthetics (with and without adjuvants) compared with normal rats. Perioperative glycemic control is currently practiced to reduce adverse events in many at-risk patients, especially in diabeticpatients, to prevent neuropathy, poor wound healing, and greater incidence of infection. The aim of this study was to investigate in diabeticrats the importance of glycemic control before peripheral nerve block. METHODS: To induce diabetes, rats were intravenously injected with a single dose of 50 mg/kg STZ to destroy pancreatic beta cells. Tactile allodynia in response to von Frey filament stimulation of the plantar hind paws was used as the criterion for diabetic neuropathy. Diabeticrats were randomly divided into experimental treatment groups. The continuous glycemic control experiment compared: 3 U/d insulin implant for 14 days, 1.5 U/d insulin implant for 14 days, and placebo treatment. The acute glycemic control experiment compared a single 6U Human Insulin Isophane Suspension (NPH) injection and placebo treatment. Nondiabetic rats received placebo implants or injections. Following treatment, 0.1 mL of 1% lidocaine hydrochloride with 5 μg/mL epinephrine hydrochloride was injected into the left sciatic notch. Animals were then reevaluated at 10-minute intervals for the absence or presence of sensory and motor response. RESULTS: All STZ-injected rats had blood glucose levels greater than 350 mg/dL and tactile allodynia. After insulin implants or injections, diabeticrats had much lower blood glucose levels than diabeticrats with placebo treatment. With both 3 and 1.5 U/d continuous glycemic control, the local anesthetic solution produced a shorter duration of sensory and motor nerve block in insulin-treated diabeticrats compared with placebo-treated diabeticrats, and shorter duration was similar to nondiabetic rats. With 6 U acute glycemic control in diabeticrats, there was no reduction in nerve block duration compared with placebo-treated diabeticrats. CONCLUSIONS: With continuous glycemic control in diabeticrats, the duration of sensory and motor nerve block was about 40 minutes shorter than that in the untreated diabeticrats and similar to that of normal rats. However, acute glycemic control did not affect nerve block duration, suggesting that this neuropathy cannot be rapidly reversed.
Authors: Michael R Fettiplace; Katarzyna Kowal; Richard Ripper; Alexandria Young; Kinga Lis; Israel Rubinstein; Marcelo Bonini; Richard Minshall; Guy Weinberg Journal: Anesthesiology Date: 2016-02 Impact factor: 7.892
Authors: S Heschl; B Hallmann; T Zilke; G Gemes; M Schoerghuber; M Auer-Grumbach; F Quehenberger; P Lirk; Q Hogan; M Rigaud Journal: Br J Anaesth Date: 2016-04 Impact factor: 9.166