1. Volume 19, Issue 3, Pages 171-177 (June 2012)
Blockades of ATP-sensitive potassium channels and L-type calcium channels improve analgesic effect of morphine in alloxan-induced diabetic mice 
Shamseddin Ahmadi, Sayede Shohre Ebrahimi, Shahrbanoo Oryan, Fatemeh Rafieenia 
Pathophysiology 
Volume 19, Issue 3, Pages (June 2012)
DOI: /j.pathophys
Copyright © 2012 Elsevier Ireland Ltd Terms and Conditions

2. Fig. 1
Effects of morphine on pain reaction latency in non-diabetic and diabetic mice. Five groups of non-diabetic and five groups of diabetic mice were used. The groups of both two sets received saline or morphine at the different doses (5, 7.5, 10 and 15mg/kg), 30min before the hot-plate test. Each bar represents mean±SEM of pain reaction latencies related to ten mice per each group. *P<0.05, **P<0.01 and ***P<0.001 compared to saline group in non-diabetic animals. +++P<0.001 compared to saline group in diabetic animals. #P<0.05 and ##P<0.01 compared to the same treatments in non-diabetic mice.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2012 Elsevier Ireland Ltd Terms and Conditions

3. Fig. 2
Effects of glibenclamide on pain reaction latency. Five groups of non-diabetic and five groups of diabetic mice were examined. The groups of both two sets received either vehicle or glibenclamide at the different doses (4, 8, 12 and 20mg/kg), 45min before the hot-plate test. Each bar represents mean±SEM of pain reaction latencies related to ten mice per each group. +P<0.05 and ++P<0.01 compared to vehicle group in diabetic animals. **P<0.01 compared to the same treatment group of non-diabetic animals.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2012 Elsevier Ireland Ltd Terms and Conditions

4. Fig. 3
Effects of nimodipine on pain reaction latency. Five groups of non-diabetic and five groups of diabetic mice were used. Groups of both two sets received either vehicle or nimodipine at the different doses (2.5, 5, 10 and 20mg/kg), 45min before the hot-plate test. Each bar represents mean±SEM of pain reaction latencies related to ten mice per each group. +P<0.05 compared to vehicle control group in diabetic animals. **P<0.01 compared to the same treated group of non-diabetic animals.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2012 Elsevier Ireland Ltd Terms and Conditions

5. Fig. 4
Interaction between glibenclamide or nimodipine with morphine on pain reaction latency in diabetic mice. Eight groups of animals were used. First, four groups of the animals received glibnclamide (20mg/kg) plus saline or different doses of morphine (5, 7.5 and 10mg/kg). Second, other four groups of the animals received nimpodipine (20mg/kg) plus saline or different doses of morphine (5, 7.5 and 10mg/kg). All of the animals were tested 30min after the last injection. Each bar represents mean±SEM of pain reaction latencies related to ten mice per each group. **P<0.01 and ***P<0.001 compared to glibnclamide+saline group. ++P<0.01 and +++P<0.001 compared to nimodipine+saline group.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2012 Elsevier Ireland Ltd Terms and Conditions