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ObjectiveTo evaluate the effect of aminoguanidine on expression of inducible nitric oxide synthase (iNOS) in neurons in the small intestinal nerve plexus of starved rats.MethodsNinety male SD rats weighing 230-270 g were randomly divided into 3 groups:group normal control (group C,n =10) ; group starvation (group S,n=40) and group starvation + aminoguanidine (group A,n =40).The animals were allowed free access to water but no food during starvation in S and A groups.In group A the animals were given aminoguanidine 150 mg·kg-1 ·d-1 intraperitoneally during starvation.Ten animals were sacrificed at 3,5,7 and 9 d of starvation respectively and intestine specimens were taken for determination of ratio of intestinal transit using dextran blue-2000 as indicator.Then the specimens of intestinal myenteric nerve plexus of ileum were collected and stained by histochemistry with nicotinamide-adenine dinucleotide phosphate-d for determination of iNOS expression.ResultsStarvation significantly reduced the small intestinal transit and increased iNOS expression in neurons in the myenteric nerve plexus of small intestine in proportion to days of starvation in group S compared with group C.Intraperitoneal aminoguanidine significantly attenuated the starvation-induced changes in intestinal transit and iNOS expression.ConclusionAminoguanidine can attenuate the up-regulation of the expression of iNOS in neurons in the myenteric nerve plexus of small intestine induced by starvation and is helpful in promoting the intestinal transit in starved rats.
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@#Objective To investigate the possible protective effect of neurotropin on the corresponding spinal cord motoneuron after sciatic nerve injury early in rats.Methods 108 male Sprague Dawley rats were divided randomly into Groups A,B and C with 36 animals in each group,and all animals were cut both side of sciatic nerve,instantly make the operation of end-to-end anastomose of epineurium for abscised sciatic nerve.Group A was control group.Group B was treated with neurotropin and Group C was treated with normal saline after operation.The rats were sacrificed on 1st d,4th d,9th d,14th d,21st d and 28th d after operation.The corresponding spinal cord segments(L4～L6)were gotten to make Bcl-2 and Bax immunohistochemical staining and TUNEL staining.Results The values of Bcl-2/Bax on 9th d,14th d and 21st d after operation of Group B were different from that of Group A and Group C.The number of positive cells stained by TUNEL staining on 9th d was significantly different among Group A,Group B and Group C(v<0.05).The expression of positive TUNEL staining cells reached a peak on 14th d after operation,the number of Group B was less than that of Group A and Group C.Conclusion After instantly make the operation of end-to-end anastomose of epineurium for abscised sciatic nerve,neurotropin can protect the spinal cord motoneurons to avoid apoptosis excessively in some extent.
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Objective To observe the effect of hyperglycemia on intracranial pressure (ICP) and neurological outcome following severe brain injury. Methods A retrospective review was done on 79 cases with severe traumatic brain injury (with no history of diabetes or important extracranial complications) who underwent craniotomy for evacuation of intracranial hematoma and were divided into two groups based on Glasgow outcome scales (GOS) score, ie, favorable group with GOS of 5 or 4 and unfavorable group with GOS less than 3. Statistical analysis of data was accomplished by using SPSS 11.5 software. The outcome was assessed at the 6th month after injury. Results A significant correlation was found between ICP levels and admission or postoperative glucose values. The unfavorable group had significantly higher glucose levels both on admission and after operation compared with the favorable group, with statistical difference (P
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<p><b>OBJECTIVE</b>To observe the effect of nitric oxide (NO) on the survival of a random pattern skin flap.</p><p><b>METHODS</b>Caudal based random skin flaps (9 cm x 3 cm) were raised on the back of Wistar rats. Six methods were used in the experiment to observe the effect of NO synthase inhibitor L-NAME and NO synthase substrate L-arginine on flaps: image analysis technology; light and electron microscopic studies; enzyme histochemistry of NOS in flaps; concentration of NO2-/NO3- in plasma and wet/dry ratio of the flap tissue.</p><p><b>RESULTS</b>Survival area of flap in the L-arginine-treated group significantly increased (67.06 +/- 5.65)% (p < 0.01) whereas the area in the L-NAME-treated group significantly decreased (35.17 +/- 1.87)% (p < 0.01) compared with the control group (53.25 +/- 3.24)% at seven days after the operation. General and microscopic observations showed that pathological changes in the L-arginine-treated group were fewer. Abundant capillaries and fewer inflammatory cells were noticed in the L-arginine-treated group. Transmission Electron Microscopy (TEM) studies find endothelial swelling, thrombosis-formation and endothelial loss of contact with the basement membrane in the L-NAME treated group. Before operation, the serum NO concentrations were not significantly different in three groups (p > 0.05). After operation, NO concentration of the control group began to increase and reached to the top at the third day. L-Arg kept serum NO concentration in a higher level than the control. Enzyme histochemistry of NOS in flaps: microvessel intima in dermis, hair follicles, sweat glands and inflammatory cells showed oxford blue, more positive in flaps of the L-Arg treated group than the control group at the third day after operation. The flaps of L-NAME-treated group demonstrated negative or weak positive. Wet/dry ratio: twenty-four hours after flap elevation wet/dry weight ratios increased significantly in all regions of the flap of the L-arginine-treated rats compared with saline-treated rats. The ratios of the flaps of L-NAME-treated rats were reduced compared with saline-treated rats.</p><p><b>CONCLUSION</b>NO could improve microcirculation of the flap and increase its survival rates. The mechanism might be that NO could accelerate flap vascularization and protect flaps from ischemia-reperfusion injury.</p>