Protective effects of morphine preconditioning in delayed phase on myocardial ischemia-reperfusion injury in rabbits.

The aim of this study was to investigate the protective mechanisms of delayed-phase morphine preconditioning on myocardial ischemia-reperfusion injury. Thirty healthy male New Zealand white rabbits were randomly divided into three groups: a sham operation group (C), ischemia-reperfusion group (I/R), and delayed-phase morphine preconditioning group (M) (N = 10/group). Rabbits in the C group received thoracotomy for 160 min. Rabbits in the I/R group received left artery blockage for 40 min and reperfusion for 120 min. Rabbits in the M group received 1.0 mg/kg intravenous morphine 24 h prior to the identical treatment as the rabbits in the I/R group. In each group, the interleukin (IL)-10 and tumor necrosis factor (TNF)-α levels were detected at five time points: 20 min before the left coronary artery blockage (T1), 20 and 40 min after the left coronary artery blockage (T2 and T3, respectively), and 1 and 2 h after the myocardial reperfusion (T4 and T5, respectively). After reperfusion, the infarction size was measured with Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. Compared with the C group, serum IL-10 and TNF-α concentrations increased in the I/R and M groups; the difference was significant (P < 0.05). When compared with the I/R group, the IL-10 concentrations in the M group were significantly increased (P < 0.05), but the infarction size and TNF-α concentrations were significantly decreased (P < 0.05). These results suggested that delayed-phase morphine preconditioning might achieve myocardial protection through the regulation and balance of inflammatory cytokines.

Effect of morphine preconditioning in the delayed phase on the expression of p38 mitogen-activated protein kinase in a rabbit model of myocardial ischemia-reperfusion injury.

This study aimed to investigate the protective effects of delayed morphine preconditioning on myocardial ischemia-reperfusion injury. We randomly divided 30 rabbits into three groups with 10 rab-bits in each group as follows: sham operation group (C group), isch-emia-reperfusion group (I/R group), and morphine pretreatment group (M group). Rabbits in C Group received left coronary without blocking for 160 min. The left descending artery of rabbits in the I/R group was blocked for 40 min and reperfused for 120 min. Rabbits in the M group received intravenous administration of 1.0 mg/kg morphine; after 24 h, rabbits in this group received the same treatment as that administered to the I/R group. We determined tumor necrosis factor alpha (TNF-α) levels in blood samples from the internal carotid artery of rabbits in each group 20 min before occlusion of the left descending coronary artery, 20 and 40 min after occlusion of the left descending coronary artery, and 1 and 2 h after myocardial reperfusion. After 120 min of reperfusion, immunoblotting was used to measure the activity levels of myocardial p38 mitogen-activated protein kinase (MAPK); in addition, the infarct size was measured. Compared to the I/R group, the M group showed a significant decrease in TNF-α levels, p38 MAPK activity, and the myocardial infarct size (I/R group 37.8% ± 1.7% vs 21.5% ± 2.4%; P < 0.05). Thus, morphine preconditioning in the delayed phase may exert protective effects on myocardial I/R injury by inhibiting myocar-dial p38 MAPK activity and decreasing TNF-α production.

Effects of goal-directed fluid therapy with different lactated Ringer's: hydroxyethyl starch ratios in hemorrhagic shock dogs.

The effects of goal-directed fluid therapy, with lactated Ringer's (LR) and 6% hydroxyethyl starch (HES) solution, on hemorrhagic shock dogs are unknown. We aimed to determine the optimal LR: HES ratio for the resuscitation of hemorrhagic shock dogs. Hemorrhagic shock was induced in 40 ventilated dogs by drawing an estimated 60% blood volume. The animals were randomly divided into five groups (N = 8) according to the LR: HES ratio of the resuscitation fluid (3:1, 2:1, 1:1, 1:2, and 1:3), and were then resuscitated for 24 h to reach the stroke volume variation (SVV) and hemoglobin (Hb) goals by fluid infusion and autologous blood perfusion. The extravascular lung water index (EVLWI), pH, partial pressure of oxygen (PaO2), base excess (BE), sodium, chloride, Hb and creatinine clearance (Clearcrea) were checked after 24 h (R24). The EVLWI of the 3:1 group at R24 were higher than that of the 1:3 group and the baseline value (P < 0.05), whereas the PaO2 was lower (P < 0.05). In contrast to the 3:1 group at R24 and baseline, plasma chloride and sodium in the 1:3 and 1:2 groups increased; however, pH, BE, and Clearcrea decreased (P < 0.05). No significant differences were found in the 1:1 and 2:1 groups at R24 compared with baseline (P > 0.05). Resuscitation with LR and HES at 2:1 and 1:1 ratios are superior in maintaining the acid-base, electrolyte, and lung water balances as well as renal function in hemorrhagic shock dogs than at ratios of 3:l, 1:2, and1:3.

Effects of isoflurane preconditioning in the delayed phase on myocardial tumor necrosis factor alpha levels and caspase-3 protein expression in a rabbit model of ischemia-reperfusion injury.

This study aimed to investigate the protective effects and the mechanisms underlying these effects of isoflurane preconditioning in the delayed phase of myocardial ischemia-reperfusion injury. We randomly divided 30 healthy male New Zealand white rabbits into three groups with 10 rabbits in each group as follows: sham operation group (C group), ischemia-reperfusion group (I/R group), and 2.0% isoflurane preconditioning group (S group). Rabbits in the C group received thoracotomy for 160 min. Rabbits in the I/R group underwent left coronary artery occlusion for 40 min and reperfusion for 120 min. Rabbits in the S group received inhalation of 2.0% isoflurane and 100% oxygen for 2 h; after 24 h, rabbits in this group received the same treatment as that administered to rabbits in the I/R group. We examined the tumor necrosis factor alpha (TNF-α) levels in each group 20 min before occlusion of the left coronary, 20 and 40 min after occlusion of the left coronary artery, and 1 and 2 h after myocardial reperfusion. After reperfusion, immunoblotting was used to measure the myocardial caspase-3 expression levels, and the infarct size was measured using Evans blue and tetrazolium chloride staining. The levels of TNF-α and caspase-3 were lower in the S group than in the I/R group, and the myocardial infarct size decreased in the S group. Thus, isoflurane preconditioning in the delayed phase exerted protective effects by decreasing the myocardial caspase-3 expression and TNF-α production in a rabbit model of ischemia-reperfusion injury.

Effects of musk ketone on nerve recovery after spinal cord injury.

The present study aimed to determine the effects of musk ketone on nerve recovery in rats after spinal cord injury. A total of 105 SD female rats were used to establish the rat with dorsal spinal cord injury model (modified Allen's method). The rats weighed from 200 to 250 g and were provided by the Experimental Animal Center of Chongqing Medical University. They were randomly divided into five treatment groups: saline (NS group), methylprednisolone (MP group), and musk ketone groups (MO1, MO2, and MO3 groups). The Swash plate test and BBB behavioral score were used to determine neurological function recovery after spinal cord injury. Hematoxylin-eosin (HE) staining was used to detect general structural changes in spinal cord tissue. The enzyme-linked immunosorbent assay was used for the determination of interleukin 10 (IL-10) in spinal cord tissue. We found that compared with the NS control group, critical angle, BBB score and IL-10 levels in rat spinal cord tissue significantly increased in the MP group and MO groups 7 and 14 days after the operation. HE staining showed that in the NS group, there was hemorrhage, edema, necrosis, axonal demyelination, inflammatory cell infiltration and glial cell response in spinal cord tissue. After 7 days, spinal cord edema and inflammation were reduced and neuronal degeneration and necrosis were not evident in the MP and MO groups. We conclude that musk ketone can reduce secondary damage after spinal cord injury and promote nerve recovery in rats.

Effect of different time phases of radionuclide hepatobiliary scintigraphy on the differential diagnosis of congenital biliary atresia.

To investigate the value and essentiality of 6- and 24-h delay hepatobiliary scintigraphy in the differential diagnosis of biliary atresia (BA), we retrospectively analyzed 197 infants (121 boys/76 girls; age range, 3-205 days; average age, 63.9 days) admitted to Jiangxi Children's Hospital for persistent jaundice (> 2 weeks), hepatosplenomegaly, and abnormal liver function. After receiving anti-inflammatory treatment and cholagogic pre-treatment for 7-10 days without a clear diagnosis, the children underwent 99mTc-labeled diethylacetanilide-iminodiacetic acid hepatobiliary scintigraphy. BA and infant hepatitis syndrome were diagnosed in 107 and 90 infants, respectively after laparoscopic cholangiography, surgical pathology, or 6-month clinical follow-up. The diagnostic efficiencies of hepatobiliary scintigraphy for BA were evaluated within 50 min and at 6 and 24 h. The areas under the receiver operating characteristic curves within 50 min, at 6 and 24 h were 0.696, 0.829 , and 0.779 , suggesting poor diagnostic value within 50 min, but improvement at 6 and 24 h. The compliance rate of 6- and 24-h imaging for BA diagnosis was 89.34% (176/197; paired chi-square test Kappa value, 0.77; P > 0.05), signifying high consistency. The diagnostic efficiency values of 6-/24-h imaging for BA diagnosis were sensitivity (90.65/89.72%), specificity (74.44/78.89%), accuracy (83.25/84.77%), positive and negative predictive values (80.83/83.48% and 87.01/86.59%), with no significant difference (P > 0.05). To provide optimal treatment in early BA, the- 6-h hepatobiliary scintigraphy had practical value, especially when combined with tomographic or dynamic imaging; 24-h delay imaging was deemed unnecessary because it was not significantly superior.

Ginkgo biloba extract postconditioning reduces myocardial ischemia reperfusion injury.

We examined the protective effects of Ginkgo biloba extract (EGb761) postconditioning on myocardial ischemia reperfusion injury in rabbits. Four groups of 8 white rabbits were allocated to: pseudo surgery group: the left coronary was lined without blocking for 160 min after thoracotomy; ischemia and reperfusion group (IR): the left anterior descending coronary artery was blocked for 40 min and reperfused for 120 min; ischemic postconditioning group: the left anterior descending artery was ligated for 40 min, reopened for 30 s and ligated for 30 s, repeated three times, and then reperfused for 120 min; EGb761 postconditioning group (E): 100 mg/kg EGb761 was injected into a vein while the left coronary artery was opened for 1 min. The reperfusion took 120 min. Internal carotid arterial blood in each group was collected for cTnI measurement at five times: 20 min before occlusion of the left coronary artery, 20 min after left coronary artery occlusion, 40 min after left coronary artery occlusion, 1 h after myocardial reperfusion, and 2 h after myocardial reperfusion. Superoxide dismutase (SOD), malondialdehyde (MDA) in the centrifuged blood and myocardial infarction area were measured at the end of reperfusion. We found that the serum cTnI concentrations in the E group during reperfusion decreased significantly compared with those in the IR group. The infarction area was significantly lower in the E group than that in the IR group. The SOD activity in the E group was increased compared with that in the IR group; the MDA content decreased significantly in the E group compared with that in the IR group. We conclude that G. biloba extract postconditioning had myocardial protection effects by reducing the generation of oxygen-free radicals and increasing the antioxidant capacity of the myocardial cells.