To study the therapeutic effect and possible mechanism of icariin on myocardial ischemia-reperfusion injury ( MIRI) model in diabetes rats. The model of diabetic rats were induced by Streptozotocin (STZ), then the model of MIRI was established by ligating the reversible left anterior descending coronary artery for 30 min, and then reperfusing for 120 min. totally 40 male SD were randomly divided into five groups: the control group (NS), the ischemia reperfusion group (NIR), the diabetes control group (MS), the diabetic ischemia reperfusion group (MIR) and the diabetic ischemia reperfusion with icariin group (MIRI). The changes in blood glucose, body weight and living status were observed; the enzyme activity of serum CK-MB, LDH, GSH-Px and myocardium SOD and the content MDA and NO in myocardium were detected; the myocardial pathological changes were observed by HE staining; the myocardial Caspase-3, the Bcl-2, Bax protein expressions were detected by Western blot. The result showed that the diabetes model was successfully replicated; myocardial ischemia-reperfusion injury was more serious in diabetes rats; icariin can increase NO, SOD, GSH-Px, Bcl-2 protein expression, decrease MDA formation, CK-MB and LDH activities and Caspase-3 and Bcl-2 protein expressions and myocardial damage. The result suggested that icariin may play a protective role against ischemia reperfusion myocardial injury in diabetes rats by resisting oxidative stress and inhibiting cell apoptosis.
Animals ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Creatine Kinase ; metabolism ; Diabetes Mellitus, Type 2 ; complications ; Drugs, Chinese Herbal ; administration & dosage ; Flavonoids ; administration & dosage ; Humans ; Ischemia ; drug therapy ; etiology ; physiopathology ; Male ; Malondialdehyde ; metabolism ; Myocardial Reperfusion Injury ; drug therapy ; etiology ; metabolism ; physiopathology ; Myocardium ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; bcl-2-Associated X Protein ; metabolism

No abstract available.
Angiogenesis Inhibitors/*therapeutic use ; Bevacizumab/*therapeutic use ; Choroid/*blood supply ; Ciliary Arteries/pathology ; Fluorescein Angiography ; Humans ; Intravitreal Injections ; Ischemia/*drug therapy/etiology/physiopathology ; Male ; Meningeal Neoplasms/surgery ; Meningioma/surgery ; Neurosurgical Procedures/*adverse effects ; Retinal Detachment/*drug therapy/etiology/physiopathology ; Subretinal Fluid ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Visual Acuity/physiology ; Young Adult

OBJECTIVEBased on the observation that coagulation necrosis occurs in the majority of neonatal necrotizing enterocolitis (NEC) patients, it is clear that intestinal ischemia is a contributing factor to the pathogenesis of NEC. However, the published studies regarding the role of intestinal ischemia in NEC are controversial. The aim of this paper is to review the current studies regarding intestinal microcirculatory dysfunction and NEC, and try to elucidate the exact role of intestinal microcirculatory dysfunction in NEC.

DATA SOURCESThe studies cited in this review were mainly obtained from articles listed in Medline and PubMed. The search terms used were "intestinal microcirculatory dysfunction" and "neonatal necrotizing enterocolitis".

STUDY SELECTIONMainly original milestone articles and critical reviews written by major pioneer investigators in the field were selected.

RESULTSImmature regulatory control of mesentery circulation makes the neonatal intestinal microvasculature vulnerable. When neonates are subjected to stress, endothelial cell dysfunction occurs and results in vasoconstriction of arterioles, inflammatory cell infiltration and activation in venules, and endothelial barrier disruption in capillaries. The compromised vasculature increases circulation resistance and therefore decreases intestinal perfusion, and may eventually progress to intestinal necrosis.

CONCLUSIONIntestinal ischemia plays an important role through the whole course of NEC. New therapeutic agents targeting intestinal ischemia, like HB-EGF, are promising therapeutic agents for the treatment of NEC.

Endothelin-1 ; physiology ; Endothelium, Vascular ; physiopathology ; Enterocolitis, Necrotizing ; drug therapy ; etiology ; pathology ; Heparin-binding EGF-like Growth Factor ; Humans ; Infant, Newborn ; Intercellular Signaling Peptides and Proteins ; therapeutic use ; Intestines ; blood supply ; Ischemia ; complications ; Microcirculation ; physiology ; Nitric Oxide ; physiology ; Splanchnic Circulation

A 60-year-old woman who had experienced two episodes of amaurosis fugax in her right eye presented with vision loss. Two weeks earlier, at a private clinic, she was diagnosed with impending central retinal vein occlusion (CRVO) of the right eye and received an intravitreal injection of bevacizumab. Two weeks after this injection she was diagnosed with ischemic CRVO. At 11-weeks post-presentation, extremely ischemic features were observed with fluorescein angiographic findings of severe vascular attenuation and extensive retinal capillary obliteration. At 22-weeks post-presentation she was diagnosed with neovascular glaucoma; she experienced no visual improvement over the following several months.
Antibodies, Monoclonal/*administration & dosage ; Disease Progression ; Female ; Fluorescein Angiography ; Glaucoma, Neovascular/complications ; Humans ; Injections, Intraocular ; Ischemia/diagnosis/*etiology/physiopathology ; Middle Aged ; Retinal Vein Occlusion/*complications/*drug therapy/physiopathology ; *Retinal Vessels ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Visual Acuity/drug effects ; Vitreous Body

OBJECTIVETo observe the development of arrhythmia induced by ischemia/reperfusion (I/R) of the right coronary artery in rabbits and the intervening effect of Chinese medicine Qiangxin Fumai Granule (QFG), a Chinese preparation for activating yang and promoting blood circulation, on it.

METHODSRabbit right coronary artery I/R model was adopted. Forty healthy adult rabbits were randomly divided into 5 groups, the sham-operation group, the model group, the atropine group, the high-dose QFG group, and the low-dose QFG group, eight in each group. The drugs were administered via duodenal perfusion 10 min after ischemia. The changes of AA interval before and after medication were observed and the scores of arrhythmia were calculated.

RESULTSDuring ischemia period, AA interval prolonged for more than 40 ms in the model group, and the scores of arrhythmia showed a rising trend along with the prolonging of ischemia, with the presence of atrial-ventricular block (AVB) and aggravating of sinus and atrial arrhythmia; during reperfusion period, the incidence of AVB decreased, and AA interval somewhat decreased. The AA intervals and scores of arrhythmia in the high and low-dose QFG groups were significantly lower than those in the model group respectively (P < 0.01 or P < 0.05).

CONCLUSIONQFG is beneficial for shortening AA interval and preventing arrhythmia induced by I/R.

Animals ; Anti-Arrhythmia Agents ; administration & dosage ; pharmacology ; therapeutic use ; Arrhythmias, Cardiac ; drug therapy ; physiopathology ; Coronary Artery Disease ; complications ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Female ; Male ; Myocardial Ischemia ; complications ; Myocardial Reperfusion Injury ; etiology ; physiopathology ; Phytotherapy ; Rabbits ; Random Allocation ; Treatment Outcome

We report on a case of ischemic dysfunction of the sinus node as a complication after percutaneous transluminal coronary angioplasty of the distal left circumflex artery. After local thrombolytic therapy in the sinus node artery, sinus node arterial flow was re-established and sinus node function normalized over the period of a week. Our experience suggests that immediate reperfusion of a totally occluded nodal artery can be re-established. Ischemic dysfunction of the sinus node, as a complication of angioplasty, is generally transient and requires a prolonged period for recovery. Therefore the decision to implant a permanent pacemaker should be delayed for at least one week after the ischemic insult.
Urinary Plasminogen Activator/administration & dosage/*therapeutic use ; Thrombolytic Therapy/*methods ; Sinoatrial Node/*physiopathology ; Myocardial Ischemia/*complications/radiography/therapy ; Middle Aged ; Male ; Infusions, Intravenous ; Humans ; Follow-Up Studies ; Fibrinolytic Agents/administration & dosage/*therapeutic use ; Electrocardiography ; Coronary Angiography ; Arrhythmia/diagnosis/*drug therapy/etiology ; Angioplasty, Transluminal, Percutaneous Coronary/adverse effects