Objective To analyze the protective effects of heat-shock response on the retinae of the rats after retinal ischemic reperfusion injury.Method Twenty Wistar rats (20 eyes) were divided into 4 groups: intracameral perfusion group (group P), intracameral perfusion after quercetin injection group (group P+Q), intracameral perfusion after heat shock group (group P+H), and in tracameral perfusion after quercetin injection and heat shock group (group P+Q+H ). According to the standard program established by International Society for Clinical Visual Electrophysiology, we recorded the results of the dark-adapted electroretinogram (D-ERG ),oscillatory potentials (OPs),and light-adapted ERG (L-ERG) of the rats with intraocular hypertension after induced by heat shock response. The expressions of HSP 70 of the rats in all groups were observed by Western blotting.Results The expression of HSP 70 of the rats in group P+H was the highest in all groups, but the expressions of HSP70 in group P+Q and P+Q+H were inhibited significantly. The amplitudes of a and b wave of ERG and O2 wave of OPs decreased, and the delitescence of them were delayed significantly in rats after intracameral perfusion. The amplitude of b wave of D-ERG and O2 wave of OPs in group P+H were higher than which in group P. Zero hour after perfusion, the amplitudes of all waves in group P+H increased significantly (Plt;0.05). Twenty-four hours after perfusion, the retinal functional resumption of the rats in group P+H was better than which in group P. In group P+Q and P+Q+H, the delitescences of all waves of ERG and O2 wave of OPs were the longest and the amplitudes were the lowest, and some waves even disappeared.Conclusions The heat-shock response may improve the recovery ability of the retinal cells after injury of ischemic reperfusion.(Chin J Ocul Fundus Dis,2003,19:117-120)
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 study the efect of IH764-3 on ischemia-reperfusion (I/R) injury in rat liver. Methods Rats were divided into 3 groups, the control group was not subjected to ischemia and no treatment was given. I/R injury group was subjected to 40 minutes ischemia followed by reperfusion for 120 minutes. The IH7643 group (40mg/kg) was administred at ischemia and reperfusion. Results In the IH764-3 group, sereum levels of ALT, AST, AKP and γ-GT were significantly lower than those in the I/R group. Energy charge level recovery was significantly higher with IH7643 (P<0.05), hepatic ultrastructure was better preserved with IH764-3. Conclusion IH764-3 may be useful in the treatment of hepatic ischemia reperfusion injury
Objective To study the interaction and mechanism of prostaglandin I2 (PGI2) receptor/thromboxane A2 (TxA2) receptor (IP/TP) and cyclooxygenase-2 (COX-2) in ischemia reperfusion injury after liver transplantation of rat. Methods Rats were randomly divided into three groups: control group (n=16), orthotropic liver transplantation group (n=32) and nimesulide intervention group (n=32). The samples were obtained at 3 h, 6 h, 12 h and 24 h after operation. The expressions of COX-2, IP and TP mRNA were detected by RT-PCR. Immunohistochemistry was used to detect the localization and expression of COX-2. Hematoxylin Eosin staining was used to classify the injury extent of liver. Serum ALT and AST levels were detected to evaluate the changes of liver enzyme. Results COX-2 protein expression detected by immunohistochemistry in orthotropic liver transplantation group mainly distributed in the district of liver sinusoidal endothelial cells, liver cells and macrophage cells, which was significantly higher than control group and nimesulide intervention group. Expressions of IP mRNA, TP mRNA and COX-2 mRNA in the orthotropic liver transplantation group were significantly increased than those in control group (P<0.05), and the ratio of IP/TP increased (P<0.05). Expressions of IP mRNA and TP mRNA in nimesulide intervention group were significantly lower than that in the orthotropic liver transplantation group at 6 h and 12 h after operation (P<0.05), and the ratio of IP/TP decreased at 3 h, 6 h and 24 h after operation (P<0.05). The expression of COX-2 mRNA in nimesulide intervention group was significantly lower than that in the orthotropic liver transplantation group at 6 h, 12 h and 24 h after operation. In orthotropic liver transplantation group liver injury was obvious by HE staining, and more severve than that in nimesulide intervention group. Serum AST (each time) and ALT (3 h, 6 h and 12 h) levels in the orthotropic liver transplantation group were significantly higher than that in control group and nimesulide intervention group (P<0.05) and peaked at 6 h after operation. Conclusion The balance of IP/TP takes part in and plays an important role in the ischemia reperfusion injury of liver transplantation. Changing imbalance of IP/TP may reduce liver transplantation ischemia reperfusion injury by inhibiting COX-2 expression.
Objective To establish a new model on isolated human cadaver testes with ischemiareperfusion (I/R). MethodsThirteen isolated cadaver testes contributed by 13 persons were preserved under 0℃-4℃ hypothermia and then reperfused under 37℃. Histological and histochemical changes were observed. Results4℃ cold ischemia in 12 hours induced only trivial swelling and vascular degeneration of endothelial cells (ECs), obvious pathologic changes occurred after 24 hours, including detachment of ECs, separation between basement membrane and seminiferous epithelium, degeneration and detachment of spermatogenous cell and edema of mesenchyme. Injury was worse along with the prolongation of cold preservation time. Changes of LDH and SDH activities were found by histochemical staining. Reperfusion following 6 hours ischemia induced tissue injury and unusual enzyme activity. All changes were more obvious after reperfusion following 12,18,24 or 36 hours cold ischemia.Conclusion This new model on isolated cadaver testes with ischemiareperfusion is successful, it can substitute other solid organs of human beings for I/R injury study.
Objective To determine whether the different durations and times of the ischemic preconditioning affect the effectiveness of the ischemic preconditioning. Methods Ninety male Wistar rats were randomly divided into the control group and the eight preconditioned groups of 10 rats each. A transverse rectus abdominis musculocutaneous flap (TRAM) was elevated in each rat. The flaps were preconditioned by clamping the pedicle and reperfusing for 5 or 10 minutes per cycle. This was repeated for one or two cycles. The controls were simply perfused for 30 minutes. Each flap was then subjected to 4 hours of the global ischemia. Three rats in each group were killed for anestimate of the water content in the muscle and for observation on the muscularstructure under microscope. The flap surface survival areas of the other rats were calculated on the 7th postoperative day by the computerized video planimetry. Results The water content in the muscle was evidently reduced. The mean survival area of the flap in every preconditioned group increased by2-3 times compared with that of the controls(P<0.001). The different proceduresof the ischemic preconditioning produced different protective effects. Conclusion The ischemic preconditioning is an available means to alleviate an ischemiareperfusion injury to the transverse rectus abdominis musculocutaneous flap in rats. The effect of the ischemic preconditioning is affected by the duration and time of the ischemic preconditioning.
Objective To investigate the maximum tolerance limit of rats to hepatic inflow occlusion with portal vein blood bypss (PBB) in normothermia. Methods First. A new animal model was established, the animal survival rate were calculated following 7 days of reperfusion after hepatic inflow occlusion of 30, 60, 90, 100, 110, 120 min or portal triad clamping (PTC) of 30 min. And then, the hepatic energy metabolism (RCR, P/O, ATP, AKBR) was studied following 30, 90, 120 min of ischemia or 1, 6, and 24 hours of reperfusion after the ischemia. According to the reversibility of the hepatic motochondrial function injury and maximum as long as a period of liver warm ischemia of all animal postoperative 7 days survial, the safe limit of rat to hepatic inflow occlusion was evaluated. Results The survival rate on postoperative 7 days was one hundred percent subjected to 30, 60 and 90 min of hepatic inflow occlusion, and 50, 30, 20 percent in 100, 110, 120 min, respectively, the survival rate in rats with 30 min of portal triad champing was about 40 percent. The parameters of hepatic motochondrial function reflecting the degree of liver damage to ischemia showed significantly different as compared to sham group. The functional lesion was exacerbated during inital reperfusion, then was restored progressively in PBB-30 min and PBB-90 min groups, but was maintained low level in PBB-120 min and PTC-30 min groups.Conclusion The 90 minutes is the maximum limit of rats to hepatic inflow occlusion in normothermia.
This prospective animal study was designed to investigate the changes of plasma endothelin (ET) levels in acute necrotizing pancreatitis (ANP). Sprague-Dawley rats were randomly devided into 3 groups: acute necrotizing pancreatitis (ANP) group in which ANP was induced by infusion of 5% sodium taurocholate (STC) into biliopancreatic duct, sham operation (SO) group and platelet activating factor antagonist BN50739 (BN) group. Blood levels of ET and platelet activating factor (PAF) were detected. Pancreatic microcirculatory blood flow was measured and pancreatic histological scores were evaluated. Results showed that the pancreatic microcirculatory blood flow in ANP group was decreased to a great extent immediatly after induction of ANP and soon began to rise slowly for 3 hours and again decreased steadily after that. The blood levels of ET, PAF and histological scores in ANP group were significantly higher than those in SO group. In BN group, the blood flow was significantly improved and the levels of blood ET, PAF and histological scores were all significantly lower as compared to those in ANP group. It is concluded that ischemia/ reperfusion is present in the initiation of acute necrotizing pancreatitis induced by STC in the rat. This leads to injuries of endothelial cells and increase in the production of ET and PAF. I/R lesions,and interaction of ET and PAF lead to a vicious circle, thus augmenting the pathological changes in the pancreas.
To investigate the effect of propofol intra-aortic and intravenous infusion on the concentration of propofol for an ischemia-reperfusion spinal cord injury in rabbits. Methods Forty-six healthy adult New Zealand white rabbits were randomly divided into 3 groups: sal ine infusion group (group N, n=10), propofol intra-aortic infusion group (group A, n=16) and propofol intravenous infusion group (group V, n=16). The infrarenal abdominal aorta was occluded for 30 min during which propofol 50 mg/kg was infused continuously intra-aortic or intravenous with a pump in group A and V. In group N, the same volume of normal sal ine was infused in the same way and at the same rate as in group A. Upon reperfusion, propofol concentration of the spinal segments of L4-6 and T6-8 was examined in group A and V. At 48 hoursafter reperfusion, the neurological outcomes were recorded in each group. Results Mean blood pressure in group V from the time of 5 minutes after occlusion decreased more than in group N (P lt; 0.05) and than in group A from the time of 10 minutes after occlusion(P lt; 0.05). The mean blood pressure in group N increased more than in group A from 15 minutes after occlusion (P lt; 0.05). The heart rate increased more in group V from 10 minutes after occlusion than in group N and A (P lt; 0.05) in which no difference was observed. The propofol concentration in L4-6 of group A (26 950.5 ± 30 242.3) ng/g was higher than that in T6-8 of group A (3 587.4 ± 2 479.3) ng/g and both L4-6 (3 045.9 ± 2 252.9) ng/g and T6-8 (3 181.1 ± 1 720.9) ng/g of group V(P lt; 0.05). The paraplegia incidence was lower (30%) and the median of normal neurons was higher (8.4) in group A than in group N (80%, 2.2) and group V(100%, 1.9), (P lt; 0.05). There was no significant difference in group N and V in paraplegia incidenceand the median of normal neurons (P gt; 0.05). Conclusion Intra-aortic infusion shows a better neurological outcome than intravenous infusion and could contribute to higher concentration of propofol in the ischemia spinal cord.
Objective To study the influence of ischemia-reperfusion on the expression of the hyperpolarization activated cycl icnucleotide gated cation channel 4 (HCN4) and to discuss the mechanism of functional disturbance of sinoatrial node tissue (SANT) after ischemia reperfusion injury (IRI). Methods Eighty five healthy adult rabbits, weighing 2-3 kg, were randomly divided into 3 groups: control group [a suture passed under the root section of right coronary artery (RCA) without l igation, n=5], experimental group A (occluding the root section of RCA for 30 minutes, then loosening the root 2,4, 8 and 16 hours, n=10), experimental group B (occluding the root section of RCA for 1 hour, then loosening the root 2, 4,8 and 16 hours, n=10). At the end of the reperfusion, the SANT was cut off to do histopathological, transmission electronmicroscopical and immunohistochemical examinations and semi-quantitative analysis. Results The result of HE stainingshowed that patho-injure of sinoatrial node cell (SANC) happened in experimental groups A and B after 2 hours of reperfusion, the longer the reperfusion time was, the more serious patho-injure of SANC was after 4 and 8 hours of reperfusion, SANC reached peak of damage after 8 to 16 hours of reperfusion; patho-injure of SANC was more serious in experimental group B than in experimental group A at the same reperfusion time. Immunohistochemical staining showed that the expression of HCN4 located in cellular membrane and cytoplasm in the central area of SANC and gradually decreased from the center to borderl ine. The integral absorbance values of HCN4 expression in the control group (397.40 ± 34.11) was significantly higher than those in the experimental group A (306.20 ± 35.77, 216.60 ± 18.59, 155.40 ± 19.11 and 135.00 ± 12.30) and in the experimental group B (253.70 ± 35.66, 138.70 ± 13.28, 79.10 ± 9.60 and 69.20 ± 8.42) after 2, 4, 8 and 16 hours of reperfusion (P lt; 0.05). With reperfusion time, the expression of HCN4 of SANC decreased, which was lowest after 8 hours of reperfusion; showing significant difference among 2, 4 and 8 hours after reperfusion (P lt; 0.05) and no significant difference between 8 and 16 hours after reperfusion (P gt; 0.05). At the same reperfusion time, the expression of HCN4 was higher in the experimental group A than in the experimental group B. The result of transmission electron microscope showed that ultramicrostructure of SANC was damaged after reperfusion in experimental groups A and B. The longer the reperfusion time was, the more serious ultramicrostructure damage of SANC was, and reached the peak of damage after 8 hours of reperfusion. Ultramicrostructure of SANC was not different between 8 and 16 hours of reperfusion. At the same reperfusion time, the ultramicrostructure damage of SANC was moreserious in experimental group B than in experimental group A. Conclusion IRI is harmful to the morphous and structure ofSANC, and effects the expression of HCN4 of SANC, which is concerned with functional disturbance and arrhythmia.