PURPOSE: The purpose of this study was to determine the effect of DHEA on hindlimb muscles(soleus, plantaris and gastrocnemius) in a focal brain ischemia model rat. METHOD: Twenty-seven male Sprague-Dawley rats were randomly divided into three groups: CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), or SHNS(sham + normal saline). Both the CINS and CIDH groups underwent a transient right middle cerebral artery occlusion operation. In the SHNS group, a sham operation was done. 0.34mmol/kg DHEA was administered daily by an intraperitoneal injection for 7days. RESULT: The muscle weight, muscle fiber cross-sectional area of the Type I muscle fiber of soleus and Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of gastrocnemius, and muscle strength in the CINS group decreased compared with the SHNS group. The muscle weight, muscle fiber cross-sectional area of the Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of soleus, and muscle strength in the CIDH group increased compared with the CINS group. CONCLUSION: It was identified that muscle atrophy could be induced during 7 days after a cerebral infarction, and DHEA administration during the early stages of a cerebral infarction might attenuate muscle atrophy.
Animals ; Brain Ischemia/*pathology ; Dehydroepiandrosterone/*pharmacology ; Hindlimb ; Male ; Muscle, Skeletal/*drug effects/pathology ; Muscular Atrophy/chemically induced ; Rats ; Rats, Sprague-Dawley

AIMTo determine the protective effect of ONO-1078, a leukotriene receptor antagonist, on focal cerebral ischemia induced by endothelin-1 in rats.

METHODSSlow microinjection of endothelin-1 (120 pmol in 6 microL, for > 6 min) into the region near the middle cerebral artery was used to induce focal cerebral ischemia. ONO-1078 (0.1 mg.kg-1) was i.p. injected 1 h before endothelin-1 injection. Neurological symptoms, brain edema, brain infarction size, and the survival neurons in cortex and striatum were observed 24 h after ischemia.

RESULTSIntracerebral microinjection of endothelin-1 induced remarkable neurological symptoms, brain infarction, brain edema, and decrease of survival neurons in the cortex and striatum. In rats pretreated with ONO-1078, endothelin-1-induced brain edema and brain infarction size were decreased. The numbers of survival neurons in striatum and cortex were increased significantly. The neurological symptoms were improved but not significantly.

CONCLUSIONONO-1078 possesses neuroprotective effect against cerebral ischemic injury induced by endothelin-1, therefore, leukotrienes may play a role in the injury of cerebral ischemia.

Animals ; Behavior, Animal ; drug effects ; Brain Edema ; pathology ; Brain Ischemia ; chemically induced ; pathology ; Cerebral Cortex ; pathology ; Cerebral Infarction ; pathology ; Chromones ; pharmacology ; Corpus Striatum ; pathology ; Endothelin-1 ; Leukotriene Antagonists ; pharmacology ; Male ; Neurons ; drug effects ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the molecular mechanism of Wenxin Capsule (WXC, an effective Chinese composite drug) in preventing and treating myocardial ischemia of coronary heart disease.

METHODSRat model of myocardial ischemia was established by subcutaneous multi-point injecting isoproterenol. Effect of WXC on cell apoptosis was observed by transmission electron microscopy and TUNEL method, and its effect on apoptotic related gene Bcl-2 and Fas gene protein expression was observed by immunohistochemical method.

RESULTSIsoproterenol induced myocardial ischemic injury could cause evident cardial cell apoptosis, obvious enhance Fas gene protein expression and mild enhance Bcl-2 gene protein expression. WXC could significantly down-regulate Fas, up-regulate Bcl-2 gene protein expression, significantly inhibit and block the myocardial cell apoptosis.

CONCLUSIONSTo inhibit and block the event of cell apoptosis through regulating Bcl-2 and Fas gene protein expression in ischemic myocardium might be one of the mechanisms of WXT in preventing and treating myocardial ischemic injury of coronary heart disease.

Animals ; Apoptosis ; drug effects ; Drug Combinations ; Drugs, Chinese Herbal ; pharmacology ; Isoproterenol ; Male ; Myocardial Ischemia ; chemically induced ; metabolism ; pathology ; Myocytes, Cardiac ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; biosynthesis ; genetics ; Rats ; Rats, Wistar ; fas Receptor ; biosynthesis ; genetics

The hemorrhagic side effects associated with the use of clopidogrel are within the acceptable range and occur mainly at skin or gastrointestinal sites. We report a case of spontaneous spinal epidural hematoma (SSEH) in a 60-yr-old woman who was treated with clopidogrel for frequent transient ischemic attacks. To our knowledge, this is the second reported case of clopidogrel-induced SSEH. The patient's symptoms and past history of clopidogrel use suggested the diagnosis and made the procedure proceed quickly to operate SSEH 9 hr after the onset of paraplegia. The outcome was excellent. Therefore, with the popularity of antiplatelet prescription, physicians should keep in mind and urgently treat this unusual but critical side effect.
Aged ; Brain/pathology ; Cerebral Angiography ; Female ; Hematoma, Epidural, Spinal/*chemically induced ; Humans ; Ischemia/drug therapy ; Magnetic Resonance Imaging ; Platelet Aggregation Inhibitors/*adverse effects ; Ticlopidine/adverse effects/*analogs & derivatives ; Time Factors ; Treatment Outcome

This study aimed to characterize and MRI track the mesenchymal stem cells labeled with chitosan-coated superparamagnetic iron oxide (Chitosan-SPIO). Chitosan-SPIO was synthesized from a mixture of FeCl2 and FeCl3. The human bone marrow derived mesenchymal stem cells (hBM-MSC) were labeled with 50 microg Fe/mL chitosan-SPIO and Resovist. The labeling efficiency was assessed by iron content, Prussian blue staining, electron microscopy and in vitro MR imaging. The labeled cells were also analyzed for cytotoxicity, phenotype and differentiation potential. Electron microscopic observations and Prussian blue staining revealed 100% of cells were labeled with iron particles. MR imaging was able to detect the labeled MSC successfully. Chitosan-SPIO did not show any cytotoxicity up to 200 microgram Fe/mL concentration. The labeled stem cells did not exhibit any significant alterations in the surface markers expression or adipo/osteo/chondrogenic differentiation potential when compared to unlabeled control cells. After contralateral injection into rabbit ischemic brain, the iron labeled stem cells were tracked by periodical in vivo MR images. The migration of cells was also confirmed by histological studies. The novel chitosan-SPIO enables to label and track MSC for in vivo MRI without cellular alteration.
Animals ; Brain Ischemia/chemically induced/pathology/therapy ; Cell Differentiation ; Chitosan/*chemistry ; Coordination Complexes/*chemistry/toxicity ; Ferric Compounds/*chemistry ; Humans ; Magnetic Resonance Imaging ; Magnetics ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells/*chemistry/cytology ; Metal Nanoparticles/*chemistry ; Phenotype ; Rabbits

This study is to investigate the protective effect of urantide against myocardial ischemia injury in mice and its mechanism. The ischemic model was made by using subcutaneous injection of isoproterenol (Iso) in mice, the change of ST segment of electrocardiogram (ECG) was observed, and the activitise of lactate dehydrogenase (LDH) and nitric oxide synthetase (NOS), the contents of malonaldehyde (MDA) and nitric oxide (NO) in serum were measured. The histopathological changes of myocardium were observed by using HE staining. The anoxia/reoxygenation (A/R) model of myocardial cells on neonatal Sprague-Dawley rats was established. Methyl thiazolyl tetrazolium (MTT) assay and confocal microscopy were respectively used to measure the viability and intracellular Ca2+ concentration in myocardial cells exposed to A/R. LDH activity and cTnI content in the cell culture medium were assayed for the evaluation of myocardial cells injury. The results revealed that urantide in the range of 3 - 30 microg kg(-1) iv markedly inhibited Iso-induced raise of the ST segment of ECG; 10 and 30 microg kg(-1) significantly reduced the increases of MDA content and LDH activity in mice serum, remarkably raised the activity of NOS and the content of NO. Urantide (10 and 30 microg kg(-1)) also significantly ameliorated myocardial ischemic injury. On the A/R model of myocardial cells, urantide (1 x 10(-6) - 1 x 10(-9) mol L(-1)) could evidently inhibit the increases of cTnI content, reduce the rise of intracellular Ca2+ concentration. Urantide (1 x 10(-6) - 1 x 10(-7)) mol L(-1) increased the viability of myocardial cells injured by A/R and cut down LDH activity in the cell culture medium. Therefore urantide has significant protective effect against myocardial ischemia or A/R injury via the inhibition of Ca2+ overload and the augmentation of NO synthesis.
Animals ; Calcium ; metabolism ; Cardiotonic Agents ; pharmacology ; Cells, Cultured ; Electrocardiography ; Female ; Isoproterenol ; L-Lactate Dehydrogenase ; blood ; Male ; Malondialdehyde ; blood ; Mice ; Myocardial Ischemia ; blood ; chemically induced ; pathology ; Myocardium ; pathology ; Myocytes, Cardiac ; metabolism ; pathology ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; blood ; Peptide Fragments ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Troponin I ; metabolism ; Urotensins ; pharmacology

OBJECTIVETo study the protective effect of Naomaitong on inflammatory cascade response after focal cerebral ischemia reperfusion in aged rats.

METHODWe duplicated focal cerebral ischemia model with MCAO, with ischemia 3 h and I/R 1, 3, 6, 12 d points. The effect of Naomaitong on the nervous dysfunction score, the water content of cerebral constitution and the expression of TNF-alpha, VCAM-1, ICAM-1 and its mRNA were observed, and the group with nimodipine was as control.

RESULTThe nervous dysfunction score (I/R1, 3, 6 d), the water content of cerebral constitution (all the time points), the expression of TNF-alpha, VCAM-1 (I 3 h, I/R 1, 3, 6 d), ICAM-1 (I 3 h,I/R 1, 3, 6 d) and its Mrna (all the time points) in model group were higher than those of the sham-operated group; The nervous dysfunction score, the water content of cerebral constitution (I/R 3, 6, 12 d), the expression of TNF-alpha, VCAM-1 (I 3 h, I/R 1, 3 d), ICAM-1 and its mRNA (I 3 h, I/R 1, 3 d) in model group were decreased compared with that of model group. The nervous dysfunction score (I/R 6, 12 d), the expression of TNF-alpha, ICAM-1 (I/R 1d) and its mRNA (I/R 1, 3 d) in Naomaitong group were higher than that of Nimodipine group.

CONCLUSIONNaomaitong could protect brain cell from damage after focal cerebral ischemia reperfusion injury by inhibiting the expression of TNF-alpha, adhesion molecule.

Animals ; Brain ; metabolism ; pathology ; Brain Ischemia ; etiology ; metabolism ; pathology ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Infarction, Middle Cerebral Artery ; chemically induced ; Intercellular Adhesion Molecule-1 ; biosynthesis ; genetics ; Male ; Neuroprotective Agents ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; RNA, Messenger ; biosynthesis ; genetics ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; etiology ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism ; Vascular Cell Adhesion Molecule-1 ; metabolism

Terlipressin is a synthetic analogue of vasopressin, which has been used in the treatment of acute variceal hemorrhage. In contrast to vasopressin, terlipressin can be administered as intermittent injections instead of continuous intravenous infusion. Thus, it has a less adverse reaction than vasopressin. We report a case of ischemic skin complication in a cirrhotic patient treated with terlipressin. A 71-year-old man with liver cirrhosis was admitted because of hematemesis and melena. He was commenced on terlipressin at a dose 1 mg every 6 hours for the treatment of varicieal bleeding. After 36 hours of treatment, skin blistering and ecchymosis was noted on the skin of his upper thigh, scrotal area and trunk. We found that terlipressin was a possible cause of ischemic skin complication based on the skin biopsy finding. Terlipressin may induce a complication of the ischemic event. In spite of rarity, special attention needs to paid on the peripheral ischemic complication of terlipressin.
Aged ; Fatal Outcome ; Hematemesis/diagnosis ; Hemorrhage/drug therapy ; Humans ; Ischemia/*chemically induced/*pathology ; Liver Cirrhosis/*complications ; Lysine Vasopressin/administration & dosage/adverse effects/*analogs & derivatives/therapeutic use ; Male ; Melena/diagnosis ; Necrosis ; Skin/*blood supply/drug effects/*pathology ; Vasoconstrictor Agents/administration & dosage/*adverse effects/therapeutic use

AIMTo determine the protective effect and influence on NOS expression of Montelukast sodium--a leukotriene antagonist on myocardial necrosis in rats.

METHODSMyocardial ischemia and necrosis were induced in rats by isoproterenol (2 mg.kg-1, s.c., qd for 2 d). Serum activity of LDH, CK, MDA, NO content in myocardium and scope of myocardial necrosis were measured. nNOS, iNOS and eNOS were investigated by immunohistochemical evaluation.

RESULTSDecreased serum level of LDH, CK, MDA and attenuated myocardial necrosis area were found in rats pretreated with Montelukast sodium 10 and 30 mg.kg-1. Montelukast sodium 30 mg.kg-1 also enhanced NO content in myocardium. Montelukast sodium activated the eNOS expression and reduced the iNOS expression.

CONCLUSIONMontelukast sodium is cardioprotective during myocardial injury in rats by halting the leukotrienes-induced inflammatory response and upregulating the eNOS expression as well as downregulating the iNOS expression. This may represent an approach to the treatment of myocardial ischemia with leukotriene antagonists.

Acetates ; pharmacology ; Animals ; Cardiotonic Agents ; pharmacology ; Female ; Isoproterenol ; Leukotriene Antagonists ; pharmacology ; Male ; Myocardial Ischemia ; chemically induced ; enzymology ; pathology ; Myocardium ; metabolism ; pathology ; Necrosis ; Nitric Oxide Synthase ; metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Quinolines ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the protective effect of Ginsenoside Rg2 on Chemical myocardial ischemia.

METHODThe models of myocardial ischemia were built in rats with isoproterenol, sodium nitrite,pituitrin. Ginsenoside Rg2 (iv 2.5, 5.0, 10.0 mg x kg(-1)) were intravenously administered.

RESULTGinsenoside Rg2 could improve the abnormal electrocardiogram (ECG), reduce the arca of myocardial ischemia and improve the abnormal zymologic value of myocardial.

CONCLUSIONGinsenoside Rg2 has inhibitory function on myocardialischemia.

Animals ; Creatine Kinase ; metabolism ; Electrocardiography ; drug effects ; Female ; Ginsenosides ; isolation & purification ; pharmacology ; Isoproterenol ; Male ; Malondialdehyde ; metabolism ; Myocardial Ischemia ; chemically induced ; pathology ; physiopathology ; Myocardium ; pathology ; Panax ; chemistry ; Pituitary Hormones, Posterior ; Plant Leaves ; chemistry ; Plants, Medicinal ; chemistry ; Rats ; Rats, Wistar ; Sodium Nitrite ; Superoxide Dismutase ; metabolism