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 evaluate the phenomena of apoptosis and its relevant mechanism during ischemia-reperfusion period. Methods The published papers to explore the apoptotic phenomena and its mechanism in organs or tissues which experienced ischemia-reperfusion injury were reviewed. Results Apoptosis was common in ischemia-reperfusioned organ or tissue. The severity of apoptosis was influenced by many factors such as ischemia, hypoxia, oxygen free radials, intracellular free calcium ion overloading, various cytokines, et al; and also was regulated by bcl-2 family, caspase family and NF-κB，et al. Conclusion Apoptosis is a common phenomenum in ischemiareperfusioned organ or tissue which is affected and regulated by various factors.
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)
Objective To investigate the effects of different reperfusion sequence on hepatic warm ischemia-reperfusion injury and its related mechanisms. Methods Ninety-six healthy male Sprague Dawley rats were randomly divided into 6 groups by using random digits method (n=16, each)： Sham operation group, only shammed operation for negative control; the other 5 groups were all experimental groups, which were divided according to different reperfusion sequences of portal vein and hepatic artery: reperfusion first through the portal vein for 1 min with subsequent full reperfusion group, reperfusion first through the portal vein for 2 min with subsequent full reperfusion group, reperfusion first through the hepatic artery for 1 min with subsequent full reperfusion group, reperfusion first through the hepatic artery for 2 min with subsequent full reperfusion group, simultaneous reperfusion through the portal vein and hepatic artery group. Each group was further randomly divided into two subgroups (n=8, each) for sample collection at 2, 4 hours after reperfusion respectively. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA), superoxide dismutase (SOD) and glutathion (GSH) in hepatic tissue were detected respectively. HE staining of histopathologic slides was used to observe the morphological changes of hepatic tissue. TUNEL method was used to assess the apoptosis index (AI) of hepatocytes. Results The liver of rat was approximately normal in the sham operation group with lower levels of ALT, AST, MDA and AI, and higher levels of SOD and GSH as compared with all the experimental groups (P＜0.01). Less hepatic ischemia-reperfusion injury was found in reperfusion first through the portal vein for 1 min with subsequent full reperfusion group, whose ALT, AST, MDA and AI levels were significantly lower than those of the other experimental groups (P＜0.05 or P＜0.01), and its SOD and GSH levels were higher than those of the other experimental groups (P＜0.05 or P＜0.01). HE staining also showed milder hepatic injury in reperfusion first through the portal vein for 1 min with subsequent full reperfusion group as compared with the other experimental groups. Conclusion Hepatic reperfusion first through portal vein for short time with subsequent full reperfusion could depress the synthesis of free oxygen radicals and suppress apoptosis of hepatocytes, thus relieving hepatic ischemia-reperfusion injury.
Objective To systematically review the effectiveness of amiodarone in treating repurfusion arrhythmia (RA) after thrombolytic therapy for acute myocardial infarction (AMI), so as to provide high quality evidence for formulating the rational thrombolytic therapy for AMI. Methods Randomized controlled trails (RCTs) on amiodarone in treating RA after thrombolytic therapy for AMI were electronically retrieved in PubMed, EMbase, The Cochrane Library (Issue 3, 2012), CBM, CNKI, VIP and WanFang Data from inception to January, 2013. According to the inclusion and exclusion criteria, two reviewers independently screened literature, extracted data, and assessed quality. Then RevMan 5.1 software was used for meta-analysis. Results A total of 5 RCTs involving 440 patients were included. The results of meta-analysis suggested that, compared with the blank control, amiodarone reduced the incidence of RA after thrombolytic therapy in treating AMI (RR=0.60, 95%CI 0.48 to 0.74, Plt;0.000 01) and the incidence of ventricular fibrillation (RR=0.47, 95%CI 0.26 to 0.85, P=0.01). It neither affected the recanalization rate of occluded arteries after thrombolytic therapy (RR=1.00, 95%CI 0.88 to 1.15, P=0.94) nor decreased the mortality after surgery (RR=0.33, 95%CI 0.10 to 1.09, P=0.07). Conclusion Current evidence indicated that, amiodarone can decrease the incidence of RA. Unfortunately, the mortality rate can’t be reduced by amiodarone. Due to the limited quality and quantity of the included studies, more high quality studies are needed to verify the above conclusion
Objective To elucidate the protective effect of leukocyte depletion on the myocardium during the settings of myocardial reperfusion injury. Methods Twenty patients undergoing cardiopulmonary bypass with continuous infusion of blood cardioplegia were randomized into two groups:the control group (n=10) with no leukocyte depletion filter used, and the experimental group (n=10) with the use of leukocyte depletion filter on the bypass circuit. The blood cells count before and after the filtration were measure...
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.
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)
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.