Objective To investigate the expression of nuclear factor (NF)-κB and intercellular adhesion molecule (ICAM)-1 in rat′s retina injured by ischemia-reperfusion, and the effect of pyrrolidine dithiocarbamate (PDTC) on the expression of NF-κB and ICAM-1. Method The model of retinal ischemia-reperfusion was set up in 60 SD rats, which were divided into two groups with 30 rats in each: ischemia-reperfusion group and ischemia-reperfussion with injection of PDTC group. The left cephalic artery of each rat was ligated, and the right side was the control. Every group was subdivided into group 1 hour, 6, 12, 24, 48, and 72 hours after ischemia-reperfusion injury, and with 5 rats in each group. mRNA of NF-κB and ICAM-1 mRNA was measured by in situ hybridization (ISH) method in rat′s retina. Every rat underwent electroretinography (ERG) at the corresponding time before executed by neck breaking. Results In ischemia-reperfusion group, expression of NF-κB and ICAM-1 was detected at the 6th hour after ischemia-reperfusion, reached the highest level at the 24th hour, and weakened gradually later. In ischemia-reperfusion with injection of PDTC group, expression of NF-κB and ICAM-1 was detected at the 12th hour after ischemia-reperfusion, and reached the highest level at the 24th hour but lower than that in ischemia-reperfusion group. No expression of NF-κB and ICAM-1 was found in the control group. The relative recovery rate of ERG a and b wave amplitude in ischemia-reperfusion groups was lower than that in ischemia-reperfusion with injection of PDTC group at every stage(P＜0.01 ). The lowest relative recovery rate of ERG a and b wave amplitude in different stages in both of the 2 groups was at the 24th hour(P＜0.01). Conclusions NF-κB and ICAM-1 may play an important role in retinal ischemia-reperfusion injury, as the inhibitor of NF-κB, PDTC may relieve the retinal ischemia-reperfusion injury. (Chin J Ocul Fundus Dis，2004，20：175-178)
ObjectiveTo observe the effect of Crocin on structure and the expression of tumor necrosis factor-alpha; (TNF-alpha;) and interleukin-1beta; (IL-1beta;) in rat retina after injury by ischemia-reperfusion. Methods A total of 80 Sprague-Dawley male rats at the age of 8 -10 weeks were divided into control group, model group, low-dose Crocin group and high-dose Crocin group, with 20 rats in each group. The rats of control group were not treated. The rats in model, low-dose Crocin and high-dose Crocin group were induced with normal saline by anterior chamber perfusion creating a retinal ischemia-reperfusion (RIR) model. The rats of the low-dose Crocin and highdose Crocin group received intraperitoneal injection with different doses of Crocin solution (5 mg/kg, or 50 mg/kg) 30 minutes prior to ischemic injury and one time per day after successful RIR. Optical microscopy was used to observe the retinal structure. Enzymelinked immunosorbent assay (ELISA) was used to measure the expression of TNF-alpha; and IL-1beta; 6, 12, 24 and 48 hours after RIR. ResultsThe retinal structure of control group was normal. Pathological changes were found in the RIR model and low-dose Crocin group, such as retinal edema, disorganized structure and loosely packed cells. The degree of pathological changes in lowdose Crocin group was less than the RIR model group. The retinal structure of high-dose Crocin group was similar to the control group. The expression of TNF-alpha; was the highest at 24 hours after modeling, while the expression of IL-1beta; was the highest at 12 and 48 hours after RIR modeling. Six, 12, 24 and 48 hours after RIR modeling, compared with the control group, the TNF-alpha; expression of model (t=5.42, 7.94, 9.32, 9.18;P＜0.05 ), low-dose Crocin (t=3.94, 4.12, 4.98, 3.84;P＜0.05) and high-dose Crocin group (t=2.13, 2.34, 2.96, 2.78;P＞0.05) were increased. Compared with the RIR model group, the TNF-alpha; expression of low-dose Crocin (t=3.95, 4.56, 4.01, 5.12) and high-dose Crocin group (t=5.23, 7.65, 7.74, 7.63) was decreased. Compared with the control group, the IL-1beta; expression of model (t=7.23, 7.87, 7.15, 15.60), low-dose Crocin (t=5.65, 5.10, 5.54, 6.87;P＜0.05) and high-dose Crocin group (t=4.38, 5.21, 4.56, 4.75) was increased (P＜0.05). Compared with the model group, the IL-1beta; expression of low.dose Crocin group was decreased significantly 48 hours after RIR modeling (t=7.56,P＜0.05); but it decreased significantly at each time point in high-dose Crocin group (t=6.94, 5.36, 6.05, 10.50;P＜0.05). Conclusion Crocin can improve the retinal pathologic changes, while down-regulating TNF-alpha; and IL-1beta; expression in RIR rats.
Objective:To observe the effect of beta;estradiol on gluta mate concentration in rabbitsprime; retinae injured by ischemic reperfusion. Methods:Twenty r abbits ware randomly divided into two groups, the control group and the treatmen t group, with 10 rabbits in each group. Before examined by binocular flash elect roretinography (FERG), retinal ischemic reperfusion (RIR) model was induced in t h e right eyes of all the rabbits by increasing intraocular pressure to 120 mm Hg for 60 minutes; the left eyes were as the control eyes. The rabbits were hypoder mically injected with beta;estradiol (0.1 mg/kg) in treatment group and with phys i ological saline in the control group 2 hours before ischemia. The results of FER G of the right eyes in both of the 2 groups 0, 4, 8, and 24 hours after reperfus ion were record respectively and were compared with the results of FERG before r eperfusion. The retina tissue was collected after the last time of FERG. The con c entration of glutamate was detected by Hitachi L8800 amino acid analyzer. Results:In the right eyes in both of the 2 groups, the result of F ERG showed a beeli ne just after reperfusion. There was no significant difference of awave amplit u de between the 2 groups (t=1.357, 0.798, 0.835; Pgt;0.05); the b wave amplitudes i n experimental group were much higher than those in the control group (t=4.447, 2.188, 3.106; Plt;0.01). The concentration of glutamate in retina was (0.265plusmn;0.014) g/L in the right eyes and (0.207plusmn;0.013) g/L in the left eyes in the control group, and (0.231plusmn;0.007) g/L in the right eyes and (0.203plusmn;0 .014) g/L in the le ft eyes in the treatment group; the difference between the 2 groups was signific ant (F=50.807, P=0.000). There was statistical difference between righ t and left eyes both in the 2 groups and the significant difference of the right eyes betw een the two groups was also found (P=0.000); there was no statistical diffe rence of the left eyes between the 2 groups (P＝0.505). Conclusion:beta;-estradiol may prevent the increase of the concentration of glutamate in retina induced by RIR to protect retinal tissue.
Objective To observe the effect of melatonin (MT) on retinal apoptosis in rats with ischemia-reperfusion injury (RIRI). Methods A total of 54 male healthy Sprague-Dawley adult rats were randomly divided into the normal control (CON) group (6 rats), RIRI group (24 rats) and MT group (24 rats). The rats of RIRI and MT group were induced using suture-occluded methods to establish RIRI model. The rats of MT group were injected with MT in the left carotid artery 30 minutes after RIRI, and RIRI group was injected with the same amount of saline. On 6, 24 hours and 3, 7 days after RIRI, the morphological changes of retina were evaluated by hematoxylin and eosin (HE) staining; the effects of MT on retinal cell apoptosis and Nrf2, HO-1 proteins were examined by immunohistochemistry staining. The correlation between active Caspase-3 and Nrf2 protein, active Caspase-3 and HO-1 protein in MT group were analyzed by linear regression analysis. Results HE staining results showed that the morphology of retinal cells was regular and retinal cells were well arranged in the CON and MT group. In the RIRI group, both the thickness of inner retinal layer and the number of retinal ganglion cells (RGC) were decreased. On 6, 24 hours and 3, 7 days after RIRI, the thickness of inner retinal layer (F=16.710, 62.303, 68.389, 57.132; P＜0.01) and RGC number (F=24.250, 11.624, 14.155, 32.442; P＜0.05) in MT group were more than those in RIRI group. Immunohistochemistry staining results showed that less active Caspase-3+ cells were observed in MT group as compared with those in RIRI group at each time points (F=49.118, 134.173, 76.225, 18.385; P＜0.01). There were more Nrf2+ (F=11.041, 31.480, 59.246, 6.740; P＜0.05) and HO-1+ cells (F=128.993, 21.606, 51.349, 8.244; P＜0.05) in MT group as compared with those in RIRI group at each time points. Linear regression analysis results showed that the difference of active Caspase-3+ cells were all linearly correlated with the Nrf2+ cells and HO-1+cells in the MT group (r2=0.810, 0.730; P＜0.01). Conclusion MT could reduce retinal cell apoptosis in RIRI rats, and its mechanism may be associated with increased Nrf2 and HO-1 expression, reduced active Caspase-3 expression.
Abstract: Objective To invest igate the early and m iddle2long term clinical outcome of surgical t reatment for pulmonary th romboembo lism (PTE). Methods The data of 57 cases of surgical t reatment fo r pulmonary embolism from O ctober 1994 to O ctober 2007 in A nzhen Ho sp italw ere analyzed ret ro spect ively, of w h ich 47 casesw ere ch ronic PTE done w ith pulmonary th romboendarterectomy, and 10 w ere acute PTE done w ith pulmonary embo lectomy. Results There w ere 6 (12. 8%) perioperat ive death s in ch ronic PTE and 4 (40. 0%) death s in acute PTE (P =0.030). F ifteen cases suffered w ith residual pulmonary hypertension and 25 casesw ith severe pulmonary reperfusion injury. The pulmonary artery systo lic p ressure (PA SP) and the pulmonary vascular resistance (PVR ) of 41 cases with ch ronic PTE at 72 hours after surgery w ere low ered significant ly than tho se befo re surgery (52. 9±26. 1 mmHg vs. 91. 2±37. 4 mmHg; 410. 3±345. 6 dyn?s/ cm5 vs. 921. 3±497. 8 dyn?s/ cm5). The arterial oxygen saturat ion (SaO 2) and the arterial part ial p ressure of oxygen (PaO 2 ) at 72 hours after surgery w ere h igher significant ly than tho se befo re surgery (94.8% ±2.7% vs. 86.7% ±4.3%; 84. 4±5. 4 mmHg vs. 51. 8±6. 4 mmHg, P lt; 0. 05). With the fo llow -up of 44. 6±39. 3 month s (cumulat ive fo llow -up w as 160. 1 pat ient-years) of the 47 perioperative survivo rs, there w ere 5 late death s, of w h ich 4 ch ronic PTE and 1 acute PTE. A cco rding to Kap lan-Meier survival curve, the 5 years survival rate w as 89. 43%±5. 80% fo r ch ronic PTE and 83. 33%±15. 21% fo r acute PTE (Log rank test= 1.57, P = 0. 2103). The lineal bleeding rate related to ant icoagulat ion w as 1. 25% pat ient-years, and the lineal th romboembo lic rate related to ant icoagulat ion w as 0. 62% pat ient-years. A nd of the 42 mid-long term survivo r, the heart funct ion in 29 cases w as N ew Yo rk Heart A ssociat ion (NYHA ) class I , 10 cases NYHA class II , 3 cases N YHA class III. A cco rding to logist ic regression, the risk facto rs fo r the early death w ere acute PTE (OR = 3.28, peripheral type of PTE (OR = 2. 45) , unadop t ive of deep hypertherm ia and circulato ry arrest (OR = 2.86) ; and the risk facto rs fo r late death w ere peripheral type of PTE (OR = 2. 69) , lower limb edema p rep rocedure (OR = 2.79). Conclus ion The operat ive mo rtality in acute PTE is significant ly h igher than that in ch ronic PTE, and the mid-long term survival rate is agreeable in bo th acute and ch ronic PTE, and the comp licat ions rate related to ant icoagulat ion is relat ively accep table.
Objective To explore the effect of ischemia-reperfusion injury on the retinal functions of rats. Methods Seventy Wistar rats were selected, 20 of which were selected randomly and divided into two groups (control group and single-irrigated group). The rats were anesthetized and their anterior chambers of the right eyes were cannulated with a 7-gauge needle connected to a reservoir containing ringers balanced salt solution, which was maintained at the same level o f the eye for 1 hour. After that, ERG was recorded in both eyes of all rats. All the left rats were divided randomly into 10 groups and they were treated as the single-irrigated group. Retinal ischemia was induced by raising the reservoir to a height of 150 mm Hg. One hour later except the single ischemia group, all o f t he groups resumed perfusion after 3,6,12,and 24 hours and 3,5,7,14,and 21 days s eparately. ERG was recorded in both eyes of all rats.Results There was no difference in the results of ERG between left and right eyes in either the control group or the single-irrigated group. All the waves of ERG vanished in the single-ischemia group after 1 hour. In the ischemia-reperfusion groups, the waves of ERG partly recovered and the amplitude reduced persistently and progressively.Conclusion Ischemia-reperfusion injury may affect the function of the retina persistently and progressively. (Chin J Ocul Fundus Dis，2003，19：201-268)
rough the ultramicroscopic observation on muscle and microcirculation, Group A,where a largeamount of DXM combined with heporin was given svstematically and locally into the femoral artery of the severed limb before replantation, and in Group B only heporin was given, and Group C and D ascontrol.The results showed that if the hormone and heparin were administred in large dosage, it wasadvantageous to reduce the tissues from reperfusion injury during delayed replantation.
OBJECTIVE To determine the role of endogenous carbon monoxide(CO) in oxidant-mediated organ injury following limb ischemia-reperfusion (I/R) in rats. METHODS: Sixty-four SD rats were divided into 4 groups: Sham group, Sham + zinc protoporphyrin (ZnPP, an inhibitor of heme oxygenase activity), 2-hour ischemia followed by 4-hour reperfusion (I/R) group and I/R + ZnPP group. Carboxyhemoglobin (COHb) level in the artery blood, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the lung, heart, liver and kidney were detected. The 24-hour survival rate of rats was studied. RESULTS: Compared with the sham group, the COHb level and MDA content significantly increased, while the SOD activity and the survival rate significantly decreased in I/R group (P lt; 0.05). Compared with the I/R group, MDA content significantly increased, while the SOD activity, the 24-hour survival rate and COHb level significantly decreased in I/R + ZnPP group (P lt; 0.05, respectively). CONCLUSION: Limb I/R could lead to the oxidant-mediated multiple organ injury accompanied by the increase of CO level which play an important role in the defense against I/R-induced remote multiple organ injury in rats.
Objective To investigate the damage to the retinal cells and apoptosis of retinal cells of rats after ischemia-reperfusion insult. Methods The retinal ischemia-reperfusion model was developed by increasing intraocular pressure to 109725 mm Hg in rat eyes. Morphological changes of the rat eyes were observed by means of routine histopathology with HE staining. Apoptosis of the retina was assayed by both DNA fragmentation gel-electrophoresis and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL). Results Compared with the normal control, no histopathological changes were revealed in the rat retinas 30 min after the ischemia and then reperfued for 24 h or 48 h. Retinal ganglion cell layer (RGL) and inner plaxiform layer (IPL) of the retina were observed, however, to become significantly thinner 60 min after the ischemia and then reperfued for 24 h or 48 h. Together with the pathological changes DNA ladder pattern was detected in the same group of the rats. Further, immunochemical stain of the eye demonstrated that TUNEL positive cells were localized in RGL and IPL of the retina. Conclusion Ischemia-reperfusion insult of the eye may remarkably damage the retina of the rat eye. The damage to the retinal cells is mainly localized within RGL and IPL and apoptosis is the important mechanism of the retinal disorder. (Chin J Ocul Fundus Dis, 2002, 18: 296-298)
Objective To study the protective effects of pre-storing glycogen on warm ischemia reperfusion injury during partial hepatectomy. Methods Thirty-eight patients were randomly divided into a trial group (n=19) and a control group (n=19). In the trial group, patients were given high concentration glucose intravenously during the 24 hours before the operation. The hepatic lesion was resected after portal triad clamping in the two groups. Liver function of all patients was measured before the operation and the first and fifth days after the operation. Normal hepatic tissue was biopsied to measured hepatic tissue glycogen contents before the operation and the change of superoxide dismutase (SOD) at the point of pre-ischemia, post-ischemia, and reperfusion 2 hour. Bcl-2 mRNA, a well known anti-apoptotic factor, was also detected using quantitative polymerase chain reaction. Results The hepatic tissue glycogen content of the trial group was significantly higher than that of the control group before the operation (Plt;0.01). Liver function of the trial group was significantly better than that of the control group on the first and fifth day after operation (Plt;0.05). There was significant difference in SOD activity between the two groups at the end of hepatic vascular occlusion and at the point of 2-hour reperfusion (Plt;0.05). Furthermore Bcl-2 mRNA expression of the trial group was notably up-regulated at the point of 2-hour reperfusion compared to the control group. Conclusion Pre-store storing glycogen might protect liver ischemia reperfusion injury caused by hepatic vascular occlusion during partial hepatectomy. The potential mechanism might be that pre-storing glycogen enhances Bcl-2 expression.