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 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 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)
ObjectiveTo investigate the effect of basic fibroblast growth factor (bFGF) on expression of apoptosisrelated genes in retinal ischemiareperfusion injury (RIRI).MethodsTwentyeight rats were divided into normal, ischemia and treatment group randomly; and the latter two groups were subdivided into 6 subgroups according to different time points: 1 hour, 6, 12, 24, 48, and 72 hours after reperfusion. The rats′ model of experimental RIRI was established. After intravitreously injected with bFGF (treatment group) or balanced saline solution (ischemia group), the expressions of wide type p53 (WTp53)，c-fos, and c-jun in each subgroups were detected by streptavidinbiotin complex of immunohistochemistry.ResultIn ischemia group, the expression of WTp53,c-fos and c-jun was found 6 hours after reperfusion, reached the peak at the 24th hour after reperfusion, kept expressing bly at the 48th hour, and decreased obviously at the 72nd hour. In treatment group, the rule of changes of expression of WTp53, c-fos and c-jun was similar to which in ischemia group, except that the expression amount was obvious decreased. There was statistical significance of the expression of WTp53, c-fos and c-jun between the ischemia and treatment group 6-48 hours after reperfusion (P＜0.05）. ConclusionThe expression of WTp53,c-fos,and c-jun in retinal ganglion cell layer and inner nuclear layer may increase led by RIRI；WTp53,c-fos,and c-jun may be involved in the generant mechanisms of RIRI by playing parts in apoptosis；bFGF can inhibit the increase of expression of WTp53,c-fos,and c-jun in RIRI.Thus, which may has therapeutic effect on RIRI.( Chin J Ocul Fundus Dis,2005,21:310-313)
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.
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 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)
【Abstract】ObjectiveTo explore the protective effect of ligustrazine on the ischemia-reperfusion injury of rat liver. MethodsNinety-six healthy SD rats were divided randomly into three groups: sham operation group, ischemiareperfusion group（I/R group) and ischemia plus ligustrazine reperfusion group(therapy group).The plasm ALT,AST and LDH were measured before operation,at thirty minutes,six hours and twentyfour hours after operation. One week survival and liver pathological change of every group were observed, and the hepatocyte apoptosis index was measured simultaneously.ResultsOne week survival of therapy group was higher than that of I/R group (P＜0.05). The plasm ALT,AST and LDH of therapy group and I/R group were higher than those of the sham operation group significantly (P＜0.05), and those of therapy group were lower than those of the I/R group (P＜0.05). Light microscopy indicated that the liver sinusoid and central veins were congested remarkably after operation, the hepatocyte necrosis in I/R group was more severe than that in therapy group, and the hepatocyte apoptosis index of I/R group was higher than that of therapy group (P＜0.05). ConclusionThe protective effect of ligustrazine on ischemia-reperfusion injury of rat liver is obvious.
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 dynamically observe the effect of N-acetylserotonin (NAS) on the expression of tumor necrosis factor-α (TNF-α) protein in retina of retinal ischemia reperfusion injury (RIRI) rats, and to explore the mechanism.MethodsBy using random number table method, 90 healthy male Sprague-Dawley rats were divided into sham operation group (n=10), RIRI group (n=40), and NAS group (n=40). The right eye was as the experimental eye. In the RIRI group and NAS group, the anterior chamber high intraocular pressure method was used to establish the RIRI model. In the NAS group, 10 mg/kg NAS was injected intraperitoneally before modeling and 30 minutes after modeling. At 6, 12, 24, 72 h after modeling, hematoxylin-eosin staining was used to observe the pathological changes of the retina, and the retinal ganglion cells (RGC) were counted. Each group was detected by immunohistochemical staining and Western blot about the relative expression of TNF-α, nuclear factor E2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) protein in the rat retina. One-way analysis of variance was used for differences between groups. The general linear regression method was used to analyze the correlation between the relative expression changes of TNF-α protein and the changes of Nrf2 and HO-1 protein expression after NAS intervention.ResultsOptical microscope observation revealed that the retinal edema of rats in the RIRI group was observed at 6, 12, and 24 h after modeling; the thickness of the retina in the NAS group was significantly thinner than that in the RIRI group, and the difference was statistically significant (F=9.645, 477.150, 2.432; P＜0.01). At 6, 12, 24, and 72 h after modeling, the retinal RGC counts in the NAS group were significantly higher than those in the RIRI group, and the difference was statistically significant (F=12.225, 12.848, 117.655, 306.394; P＜0.05). The results of immunohistochemical staining and Western blot showed that 6 h after modeling, the relative expression of TNF-α protein in the retina of the RIRI group increased significantly compared with that in the sham operation group, reaching a higher level at 12 h, and decreased at 24 and 72 h. But all were significantly higher than the sham operation group, the difference was statistically significant (immunohistochemical staining: F=105.893, 1 356.076, 434.026, 337.351; P＜0.01; Western blot: F=92.906, 534.948, 327.600, 385.324; P＜0.01). At different time points after modeling, the relative expression of TNF-α protein in the retina of the NAS group was significantly lower than that of the RIRI group (immunohistochemical staining: F=15.408, 570.482, 21.070, 13.767; P＜0.05; Western blot: F=12.618, 115.735, 13.176, 111.108; P＜0.05), but still higher than the sham operation group (immunohistochemical staining: F=40.709, 151.032, 156.321, 216.035; P＜0.01; Western blot: F=33.943, 79.729, 74.057, 64.488; P＜0.01), the difference was statistically significant; 12 h after modeling, Nrf2 in the retina of the NAS group (immunohistochemical staining: F=51.122, P＜0.05; Western blot: F=33.972, P＜0.05), HO-1 (immunohistochemical staining: F=30.750, P＜0.05; Western blot: F=18.283, P＜0.05) protein relative expression was significantly higher than that of RIRI group, and the differences were statistically significant. The results of linear regression analysis showed that the difference in the number of TNF-α+ cells in the RIRI group and the NAS group was negatively correlated with the difference in the number of Nrf2+ and HO-1+ cells (r2=0.923, 0.936; P＜0.01).ConclusionsNAS can inhibit the expression of TNF-α protein in the retina of RIRI rats and reduce RIRI. The mechanism may be related to the Nrf2/HO-1 pathway.
