ischemia

Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion

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Influence of triptolide on neuronal apoptosis in rat with cerebral injury after focal ischemia reperfusion by Deng-ming Wei, Guang-zhao Huang, Yi-gu Zhang, Guang-xun Rao.

Objective: To study effect of triptolide(TL) on neuronal apoptosis in cerebral tissue rat after ischemia-reperfusion. Method: Triptolide at dose 0.2 or 0.4 mg·kg -1was intr aperitoneally injected once a day for 4 d. The focal ischemia-rep erfusion model was established with thread embolism middle artery before trip tolide injection the fourth day. Neurological deficit score rats eval uated; and immunohistochemical techniques were used to count positive cells express MPO TUNEL tissue. Result: Compare d control group, neural function significantly impr oved, number infiltrate neutrophil cere bral remarkably reduced two TL-treated groups. Conclusio n: results suggested that TL can inhibit infiltration decrease degree [

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Antifibrinolytics: ischemia may offset control

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Antifibrinolytics: ischemia may offset control by William A. Check.

Administering a compound that prevents dissolution of blood clots to patient who has had subarachnoid hemorrhage substantially reduces the risk rebleeding. But reduction in mortality from rebleeding is almost exactly offset by deaths ischemia and cerebral infarctions. These frustrating findings have been verified two independent studies using different antifibrinolytic agents. Both were reported at Ninth International Joint Conference on Stroke Cerebral Circulation Tampa, Fla. The received mixed reaction conference participants, some whom wondered whether fluid restriction might alter outcomes. Retrospective Data Discouraging Neal F. Kassell, MD, time was professor surgery University Iowa College Medicine City now neurosurgery Virginia School Charlottesville, described results an uncontrolled retrospective survey patients enrolled Cooperative

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Juxtaglomerular cell activity during hemorrhage and ischemia as revealed by quinacrine histofluorescence

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Juxtaglomerular cell activity during hemorrhage and ischemia as revealed by quinacrine histofluorescence by M. Ålund.

Quinacrine (QC) binds with high affinity to the intracellular storage granules of juxtaglomerular cells (JG-cells) in afferent arteriolus glomerulus kidney. The present study tests whether QC bound JG-cells can be released. were stimulated by renal ischemia and hemorrhagic shock combined immobilization stress. 1 h after onset QC-JGI (modified Hartroft & 1953) 14C-QC-treated rats had decreased about 40% ischemic kidney compared a not ligated control 14C-contents 33% that untouched Hemorrhagic was obtained bleeding into reservoir for 15 min or h. Rats who received 14C-QC before showed no change (15 shock) (1 as controls. This probably due formation new QC-binding granules, which took up still circulating quinacrine thereby masking release. If time between injection extended h, when amounts are very low, decrease (about 30% controls) seen kidneys shocked rats. results compatible possibility vivo could released together content following stimuli known induce renin Quinacrine-binding therefore possibly provides method endocrine way it has been used marker JG-cell activity.

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Asymptomatic myocardial ischemia in patients with stable and typical angina pectoris

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Asymptomatic myocardial ischemia in patients with stable and typical angina pectoris by G. Cocco, C. Strozzi, B. Leishman, D. Chu, N. Rochat, S. Braun.

The existence of transient myocardial ischemia (TMI) and the value serial dynamic electrocardiogram (DCG) in patients with variant or unstable angina pectoris are known. However, less information is available on frequency characteristics TMI stable pectoris. For this study, we selected 40 typical presence coronary artery disease ejection fraction were evaluated by means angiocardiography. DCG monitoring was performed bichannel portable recorders for three 24-h periods at 7-day intervals. optimal doses beta blockers isosorbidilate throughout study. We detected 788 episodes 22 patients. poorer ST-T changes than 18 without such changes. repolarization were: (1) ST elevation (55 symptomatic 87 asymptomatic episodes, (2) depression (138 236 (3) T-wave (83 164 episodes). All presented a combination above It appears, therefore, that more frequent hitherto suspected. valuable assessing these changes, especially when one considers almost twice as ones. lasted mean 1.8±1.3 min (mean±SD), while 3.8±2.7 (p <0.02, sign test). Heart rate unchanged during TMI, did not show any significant difference between episodes. Additional investigation necessary, however, to determine clinical implications findings.

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Protective Effect of TA-993, a Novel Therapeutic Agent for Peripheral Circulatory Insufficiency, on Skeletal Muscle Fatigue in a Rat Model of Hindlimb Ischemia

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Protective Effect of TA-993, a Novel Therapeutic Agent for Peripheral Circulatory Insufficiency, on Skeletal Muscle Fatigue in a Rat Model of Hindlimb Ischemia by Hisayoshi Doi, Minako Kaburaki, Hirotaka Inoue, Kuniharu Suzumura, Hiroshi Narita.

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Rat B2 Sequences Are Induced in the Hippocampal CA1 Region After Transient Global Cerebral Ischemia

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Rat B2 Sequences Are Induced in the Hippocampal CA1 Region After Transient Global Cerebral Ischemia by Xiaodong Liu, James A. Clemens, Tinggui Yin, Diane T. Stephenson, Edward M. Johnstone, Yansheng Du, Jill Ann Panetta, Steven M. Paul, Sheila P. Little.

Global brain ischemia causes cell death in the CA1 region of hippocampus 3–5 days after reperfusion. The biological pathway leading to such delayed neuronal damage has not been established. By using differential display analysis, we examined expression levels poly(A) RNAs isolated from hippocampal extracts prepared rats exposed global and found an up-regulated transcript, clone 17a. Northern blot analysis 17a showed approximately 35-fold increase ischemic at 24 h four-vessel occlusion. Rapid amplification cDNA ends revealed a family genes (160–540 base pairs) that had characteristics rodent B2 sequences. In situ hybridization demonstrated elevated this gene was localized predominantly pyramidal neurons. level decreased dramatically between 72 ischemia. observed occlusion treated with compound LY231617, antioxidant known exert neuroprotection subjected Since apoptosis, speculate may be involved apoptosis. We inin vitro models apoptosis cerebellar granule neurons were potassium removal, glutamate toxicity, or 6-hydroxydopamine treatment transcripts induced by stimulation but withdrawal.

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Role of adenosine in the electrical and contractile responses of cardiac myocytes to simulated ischemia and reperfusion*1

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Role of adenosine in the electrical and contractile responses of cardiac myocytes to simulated ischemia and reperfusion*1 by J Cordeiro.

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Factors to Consider When Analyzing 12-Lead Electrocardiograms for Evidence of Acute Myocardial Ischemia

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Factors to Consider When Analyzing 12-Lead Electrocardiograms for Evidence of Acute Myocardial Ischemia by Mary G. Adams-Hamoda, Mary A. Caldwell, Nancy A. Stotts, Barbara J. Drew.

An important factor to consider when using findings on electrocardiograms for clinical decision making is that the waveforms are influenced by normal physiological and technical factors as well pathophysiological factors. Traditionally, focus of bedside monitoring detection arrhythmia. However, continuous ST-segment myocardial ischemia now readily available. Many affect electrocardiographic may interfere with diagnosis based findings. Accordingly, a principal leadership role nurse specialists practitioners become knowledgeable about interpretation 12-lead share this knowledge staff nurses who care patients acute coronary syndromes. The alter reviewed, alterations electrocardiogram-based discussed.

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