Ischemic postconditioning: brief ischemia during reperfusion converts persistent ventricular fibrillation into regular rhythm

Objectives: Brief episodes of myocardial ischemia-reperfusion employed during reperfusion after a prolonged ischemic insult may attenuate the total ischemia-reperfusion injury. This phenomenon has been termed ischemic postconditioning. In the present study, we studied the possible effect of postconditioning on persistent reperfusion-induced ventricular fibrillation (VF) in the isolated rat heart model. Methods: Isolated Langendorff-perfused rat hearts (n=46) were subjected to 30 min of regional ischemia and reperfusion. The hearts with persistent VF (n=11) present after 15 min of reperfusion were then randomly assigned into one of the two groups: (1) control hearts (n=6), in which perfusion was continued without intervention; (2) postconditioned hearts (n=5) subjected to 2 min of global ischemia followed by reperfusion. Left ventricular pressures, heart rate, coronary flow, and electrogram were monitored throughout the experiment. Results: Conversion of VF into regular rhythm was observed in all hearts subjected to postconditioning. Regular beating was maintained by all postconditioned hearts during the subsequent reperfusion. None of the hearts in the control group had normal rhythm at the end of the experiment. At the end of reperfusion, the left ventricular developed pressure was lower in beating postconditioned hearts compared to the hearts that did not develop persistent VF. Conclusions: Ischemic postconditioning possesses strong antiarrhythmic effect against persistent reperfusion-induced tachyarrhythmias. Postconditioning may be an interesting, novel adjunct strategy to protect the heart.     

硫酸锌对大鼠移植胰腺再灌注损伤的保护作用

Objective:To study the protective effects of the heat shock protein 70 （HSP70）induced by zinc sulfate on reperfusion injury following pancreaticoduodenal transplantation in rats.Methods :The homologous male Wistar rat model of heterotopic total pancreaticoduodenal transplantation was used. The ZnSO4 treated rats received the intravenous injection of Zn2+5 mins before and after operation at a dose of 5 mg/kg (Zn 1 group),10 mg/kg(Zn 2 group) and 15 mg/kg(Zn 3 group), and the control group with the same volume of saline. The tissue concentration of HSP70 was determined using Western Blot. In addition，blood sugar (BG) and serum concentration of amylase and lipase were examined 24h after transplantation, and the activity of myeloperoxidase (MPO) in the pancrease graft was measured at the same time. Histological observation was performed.Results:Light microscopic studies showed that histomorphological changes of pancreas in Zn 2 group and Zn 1 group were much less than those in control group and Zn 3 group. The value of BG and serum lipase and MPO in Zn 2 group ＜ Zn 1 group 相似文献   

Pharmacologic preconditioning effects: Prostaglandin E1 induces heat-shock proteins immediately after ischemia/reperfusion of the mouse liver

Prostaglandin E1 (PGE1) has several potential therapeutic effects, including cytoprotection, vasodilation, and inhibition of platelet aggregation. This study investigates the protective action of PGE1 against hepatic ischemia/reperfusion injury in vivo using a complementary DNA microarray. PGE1 or saline was continuously administered intravenously to mice in which the left lobe of the liver was made ischemic for 30 minutes and then reperfused. Livers were harvested 0, 10, and 30 minutes postreperfusion. Messenger RNA was extracted, and the samples were labeled with two different fluorescent dyes and hybridized to the RIKEN set of 18,816 full-length enriched mouse complementary DNA microarrays. Serum alanine aminotransferase and aspartate aminotransferase levels at 180 minutes postreperfusion were significantly lower in the PGE1-treated group than in the saline-treated group. The cDNA microarray analysis revealed that the genes encoding heat-shock protein (HSP) 70, glucose-regulated protein 78, HSP86, and glutathione S-transferase were upregulated at the end of the ischemic period (0 minutes postreperfusion) in the PGE1 group. Our results suggested that PGE1 induces HSPs immediately after ischemia reperfusion. HSPs might therefore play an important role in the protective effects of PGE1 against ischemia/reperfusion injury of the liver.     

医源性桡神经损伤46例分析

目的阐述医源性桡神经损伤的伤因、治疗和预防措施。方法分析1991年～2003年间收治的46例医源性桡神经损伤的病例。结果伤因分为上肢手术误伤，肱骨干和桡骨上端闭合性骨折复位手法不当，头静脉穿刺致桡神经浅支损伤。本组21例保守治疗，22例手术治疗，3例行肌腱转位功能重建。结论手术误伤是医源性桡神经损伤的首要原因；临床医生丰富的解剖知识和细致、轻柔的操作是预防医源性桡神经损伤的关键。     

肌病肾病代谢综合征治疗进展

肌病肾病代谢综合征是急性动脉阻塞致骨骼肌溶解的严重并发症。积极治疗原发病，及早补液扩容、碱化尿液、早期血液净化治疗是降低截肢率、病死率的关键。本文就肌病肾病代谢综合征治疗进展作一综述。     

Use of epr oximetry with india ink to measure the po2 in the liver in vivo in mice

The partial pressure of oxygen (pO₂) of the liver in vivo in unanesthetized mice was determined using electron paramagnetic resonance (EPR) oximetry with India ink. The EPR spectra were obtained using a low-frequency (1.2 GHz) EPR spectrometer with a loop gap cavity resonator. The line width of the India ink used in this experiment was reversibly broadened by oxygen and was particularly sensitive to pO₂ below 30 torr. After the administration of India ink into the tail vein, the India ink particles were taken up mainly by Kupffer cells in the liver and in part by phagocytes in the spleen. The pO₂ measured in the normal liver was about 14 torr and was constant for the 2-week experimental period. The pO₂ decreased when measured at 1, 2, and 6 days after treatment with a hepatotoxin (carbon tetrachloride (CCI₄)); within 2 weeks, it returned almost to the initial level. Measurements by EPR at sacrifice of controls and CCI₄-treated mice indicated that more than 90% of the India ink went to the liver; the spleen contained 4.7% of total amount in control mice and 8.8% in CCI₄-treated mice when measured 2 weeks after the treatment. These data indicate the usefulness of India ink for measuring the pO₂ of the liver in vivo and that the pO₂ in the Kupffer cells is decreased when the liver is damaged by CCI₄.     

Minor,moderate and severe head injury

Summary The future role of the neurosurgeon in the management of head injury is reviewed in terms of the care of patients with minor, moderate and severe head injuries. In minor head injury it is predicted that there will be increasing pressure on the neurosurgeon to undertake the management and follow-up of all patients who have sustained head injury, and this will place a considerable additional load on each neurosurgical unit. This is based on a survey of 1919 head injuries admitted in one calendar year (1981), consisting of 93 severe injuries (GCS < 8), 210 moderate injuries (GCS 8–12), and 1616 minor injuries (GCS 13/14). In moderate injuries CT will assume a major role in detecting hematoma early and identifying contusions. There may yet be a role for steroids in these cases and there should be a greater use of neurorehabilitation, instead of the current overemphasis on the severely injured. In severe injury future efforts will be to prevent early secondary insults and to find better methods of controlling raised intracranial pressure.     

实验冻伤大鼠神经纤维的超微结构改变

为探讨冷冻损伤发生、发展及转归的规律，采用健康Ｗｉｓｔａｒ大鼠，分为冻伤组（２０只）和对照组（５只）。电镜下观察大鼠后肢冷冻至－２０℃后即刻、４小时、２４小时及７２小时时周围神经的超微结构改变。冻后即刻，神经髓鞘即出现轻度变性；冻后１～２４小时，有髓神经雪旺细胞及轴突严重变性，而无髓神经变性较轻；冻后７２小时，神经溃变及修复并存，无髓神经较有髓神经易于修复。