Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the middle cerebral artery occlusion model, we studied the effects of Zuzhongping on experimental focal cerebral ischemia. Twenty-eight adult male Wistar rats were randomly divided into three groups: (1) Zuzhongping group (n = 9), (2) Saline control group (n = 10), and (3) Blank control group (n = 9). Group 1 and group 2 received via a gastric tube 1 1ml/kg/day of Zuzhongping and normal saline, respectively. The cerebral middle arteries on the right side of 28 rats were occluded with a bipolar electro-coagulater at sites 1-2 mm from the right olfactory nerve tract. Ischemic volumes were measured by an image analytic system when the cerebral ischemia had lasted 24 h. The results showed that the ischemic volume of Zuzhongping group was significantly smaller than that of group 2 and group 3, suggesting a protective effect of Zuzhongping.
Hua Xi Yi Ke Da Xue Xue Bao 1994 Mar
PMID:[Effects of zuzhongping on ischemic volume in the rat model of middle cerebral artery occlusion]. 807 Jul 59

Blood plasma thromboxane-B2 (TXB2) and 6-keto-PGF1 alpha levels were determined by radioimmunoassay technique during the first six to sixteen hours of life in 16 newborn infants with severe asphyxia, 18 newborn infants with mild asphyxia and 27 normal term neonates. Plasma lipid peroxidation (LPO) content was measured by TBA-colour-contrast method in 15 infants with severe asphyxia, 17 infants with mild asphyxia and 24 healthy term newborn infants. The results showed that blood plasma LPO, TXB2 and 6-keto-PGF1 alpha levels in infants suffering from severe asphyxia were higher than those in infants with mild asphyxia and normal infants (P < 0.01), but no significant difference was noted between the mild asphyxia group and normal control group (P > 0.01). These suggest that production of free radicals is increased and prostaglandin metabolism is triggered in the infants with severe asphyxia, that cerebral ischemia and hypoxia caused by asphyxia contributes to the augmented production of prostaglandins and free radicals, and that accumulation of free radicals and prostaglandin enhances brain damage and the metabolism of arachidonic acid appears to be an important source of the free radicals in infants with intrauterine asphyxia.
Hua Xi Yi Ke Da Xue Xue Bao 1993 Jun
PMID:[The changes in free radical and prostaglandin metabolism in newborn infants with asphyxia]. 824 9

Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. Diagnosis of SMI or SCI was based on the finding of ischemic evidence by SPECT of myocardiotomograph or cerebrotomograph. All patients ECG and blood pressure were normal, and they had no history of clinical symptoms and signs of MI or CI. The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies.
Hua Xi Yi Ke Da Xue Xue Bao 1997 Mar
PMID:[Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia]. 1068 70

Nitric oxide (NO) was speculated to play an important role in the pathophysiology of cerebral ischemia. In this study, the effect of oxygen-glucose deprivation (OGD) on the cellular production of NO was investigated in cultured hippocampal neurons. Intracellular Ca(2+) was also detected as its closely relationship with NO. The generation of NO and changes in intracellular Ca(2+) were evaluated using confocal laser scanning microscopy with diaminofluorescein diacetate (DAF-2 DA), an NO probe, and Fluo-3, a Ca(2+) probe respectively. Extracellular glutamate level was also measured by HPLC with fluorescence detection. Results showed that OGD induced an increase in NO production and intracellular Ca(2+) concentration ([Ca(2+)](i)), the rise of DAF-2 and Fluo-3 fluorescence intensity was about 160% and 270% respectively; an increase of about 100% in glutamate level was observed after 20 min of OGD. NMDA inhibitor MK-801 significantly reduced the OGD-induced elevation of [Ca(2+)](i) and NO, DAF-2 and Fluo-3 fluorescence intensity uptake was inhibited by 69% and 74% respectively. The increase in NO production was also attenuated by extracellular Ca(2+) elimination and calmodulin (CaM) antagonist trifluoperazine dose-dependently. These results indicated that NO production increased during oxygen-glucose deprivation, and was greatly modulated by glutamate release, intracellular Ca(2+) change and Ca(2+)-CaM pathway.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2003 Jun
PMID:The influence of oxygen-glucose deprivation on nitric oxide and intracellular Ca(2+) in cultured hippocampal neurons. 1279 18