Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bilateral Clamping of both Carotid Arteries (BCCA) in normotensive rats is known to cause a transient reduction in cerebral blood flow. Using in vivo trans-striatal microdialysis and HPLC/ECD we measured the release of dopamine and DA-metabolites under these oligemic conditions. BCCA caused a substantial stimulation of striatal DA-release (40-fold) and a decrease of the outflow of DA-metabolites. The elevated DA-release returned to baseline levels before the onset of reperfusion. Upon reperfusion, DA-metabolites rose above their initial baseline values. Trans-striatal administration of glutamate-diethylester (GDEE, 10 mM) attenuated the oligemia-induced DA-release. A sudden reduction of blood flow appears to disrupt the compartmentation of dopamine in striatal dopaminergic nerve endings in a similar but more moderate manner as compared to ischemia.
J Neural Transm Gen Sect 1993
PMID:Effect of transient reduction of cerebral blood flow in normotensive rats on striatal dopamine-release. 769 Feb 31

1. The antiischemic properties of the flavonoids acetylvitexin-rhamnoside (AVR) and luteolin-7-glucoside-(LUT), combining phosphodiesterase (PDE)-inhibitory and antioxidant properties, were studied in comparison to amrinone (AMR) or superoxide dismutase (SOD). The effects of the new dihydropyridine-type calcium-agonist Bay T 5006 were studied in comparison to Bay K 8644. 2. In isolated Langendorff-rabbit hearts perfused at constant pressure, acute regional ischemia (MI) was induced by coronary artery occlusion (CAO) and quantitated from epicardial NADH-fluorescence photography. Drugs were applied either before or after CAO (pre-treatment or treatment) to permit distinguishing the influence of functional and direct cytoprotective actions in the poorly collateralized rabbit hearts. 3. SOD did not affect left ventricular pressure (LVP) or coronary flow (CF) and reduced MI only if applied before CAO. LVP and CF were enhanced by LUT or AMR but not by AVR. MI was reduced to a similar extent in hearts treated with either drug. Cardioprotection by LUT was not improved by starting drug application before CAO. 4. Bay K 8644 reduced LVP and particularly CF, whereas Bay T 5006 did not affect functional parameters. MI was enlarged by Bay K 8644 and remained unaffected by treatment or pretreatment with Bay T 5006. 5. AMR, LUT and AVR possess antiischemic properties related to an improvement of myocardial perfusion. Although oxygen free radicals contribute to ischemic tissue injury, as shown by the cardioprotective effectiveness of SOD, antioxidant properties of the flavonoids LUT and AVR do not seem to be relevant for the antiischemic effects. Our findings also give no evidence for antioxidant properties of dihydropyridines relevant for cardioprotection.
Gen Pharmacol 1995 May
PMID:Effects of different inotropes with antioxidant properties on acute regional myocardial ischemia in isolated rabbit hearts. 778 35

Oxygen radicals accumulated during ischemia and reperfusion may affect coronary contractility by endothelium dependent and independent pathways one of which may involve Na(+)-pump. Here we report a contractility assay for Na(+)-pump in pig coronary artery and use it to examine the effects of hydrogen peroxide and superoxide. Coronary artery rings contracted in a K(+)-free Krebs solution and relaxed upon subsequent exposure to K+. The relaxation approximated a single exponential decay whose rate constant depended on [K+]2. This K(+)-induced relaxation was abolished by ouabain and was attributed to Na(+)-pump. In tissues pretreated with peroxide, the rate of relaxation of the K(+)-free contracted arteries decreased with an IC50 = 1.6 +/- 0.6 mmol/l for peroxide. Another set of tissues was pretreated with the superoxide generating system containing 0.3 mmol/l xanthine + varying concentrations of xanthine oxidase (XO) and precontracted in K(+)-free Krebs solution. The rate of the K(+)-induced relaxation decreased with IC50 = 24 +/- 8 mU/ml for XO. Thus, using the relaxation assay we conclude that exposing coronary arteries to oxygen radicals can damage Na(+)-pumps.
Gen Physiol Biophys 1994 Jun
PMID:Coronary artery contractility, Na(+)-pump and oxygen radicals. 783 85

1. We investigated the effect of efonidipine hydrochloride (NZ-105) against acute renal failure (ARF) in male Wistar rats. ARF was produced by ischemia or glycerol. 2. Ischemia-induced ARF was produced by right nephrectomy and clamping of the left renal artery for 60 min, followed by reperfusion. NZ-105 (20 mg/kg) was orally administered twice a day for 3 days before ARF. The plasma creatinine and urea nitrogen concentrations were markedly elevated in the ischemia ARF group on the 1st day, but the elevation was significantly suppressed by NZ-105 treatment. 3. Glycerol-induced ARF was produced by intramuscular injection of 50% (v/v) glycerol (10 ml/kg) in rats which were restricted to drinking water for 24 hr. NZ-105 (20 mg/kg) was orally administered twice a day for 3 days before ARF. NZ-105 significantly attenuated the severe impairment of creatinine and urea nitrogen clearances and the elevated fractional sodium excretion (FENa) caused by ARF. 4. In the kidney homogenate, NZ-105 (10(-6)-10(-4) M) inhibited lipid peroxidation induced by ascorbic acid and Fe or by NADPH and the inhibitory effect of NZ-105 was stronger than alpha-tocopherol, an antioxidant agent. NZ-105 (10(-5)-10(-3) M) showed radical scavenging action against diphenyl-p-picrylhydrazyl and galvinoxyl induced radicals. 5. These findings suggest that NZ-105 prevents the renal damage caused by the two kinds of ARF. Moreover, the inhibitory effects of NZ-105 against lipid peroxidation and radical formation may be one of the mechanisms involved in the prevention of ARF.
Gen Pharmacol 1994 Nov
PMID:Effects of efonidipine hydrochloride (NZ-105), a new calcium antagonist, against acute renal failure in rats. 789 60

1. The aim of the study was to determine the effect of selenium added cardioplegic solutions on postischemic myocardial recovery. 2. The hearts were mounted on Langendorf perfusion apparatus and perfused with Krebs-Henseleit solution. The hearts were arrested by one of the following cardioplegic solutions; (a) K+ 20 mmol/l (control group); (b) K+ 20 mmol/l+selenium 10(-3) mol/l (experimental group). After 20 min of normothermic ischemia the hearts were reperfused by the same buffer. 3. Postischemic percentage changes of heart rate, contractile force and heart work were compared between the groups. 4. Addition of selenium to the cardioplegic solution significantly decreased the postischemic myocardial injury.
Gen Pharmacol 1994 Nov
PMID:The effect of selenium added cardioplegia in guinea pigs. 789 65

1. A 6-week gliclazide treatment improved left ventricular developed pressure and left ventricular end-diastolic pressure, left ventricular pressure-rate products in isolated working hearts from streptozotocin-induced diabetic rats. 2. Post-ischemic recovery in heart rate, left ventricular developed pressure, left ventricular end-diastolic pressure, left ventricular pressure-rate products and cardiac work were also shown in gliclazide-treated diabetic rats. 3. Gliclazide treatment did not modify the degree of insulinopenia and hyperglycemia, nor the myocardial energy metabolism during ischemia-reperfusion. 4. The results suggest that the gliclazide treatment has a cardioprotective effect on basal and post-ischemic cardiac functions of chronic diabetes.
Gen Pharmacol 1994 Jul
PMID:Chronic gliclazide treatment affects basal and post-ischemic cardiac function in diabetic rats. 795 31

1. Cerebral ischemia of 5 min duration was induced in unanesthetized gerbils by bilateral occlusion of the carotid arteries. 2. The extent of cerebral damage was assessed by the elevation of motor activity in comparison with control animals and by a histological assessment of the extent of neuronal degeneration in the CA1 area of the hippocampus. 3. Atropine, an antagonist of ACh, at either a low (1 mg/kg) or a high (10 mg/kg) dose administered 15 min prior to the ischemic episode, did not confer protection against cerebral ischemic damage. 4. This finding suggests that ACh does not play a critical role in the generation of ischemia reperfusion injury.
Gen Pharmacol 1994 Jul
PMID:Atropine and cerebral ischemic injury in the Mongolian gerbil. 795 34

1. The preventive effect of allopurinol on reduced glutathione and lipid peroxide levels of the liver and the accompanying ultrastructural changes during liver ischemia was investigated in guinea pigs. 2. Liver glutathione levels decreased significantly while lipid peroxide levels increased slightly in the ischemic group. 3. Allopurinol administered before ischemia resulted in a reverse significant increase in liver glutathione levels and a significant decrease in lipid peroxide levels indicating a protective effect upon cell membrane during ischemia. 4. On the other hand, electron microscopic changes in the liver associated with ischemia could not be altered by allopurinol.
Gen Pharmacol 1994 Jul
PMID:The effect of allopurinol on the liver ultrastructure, reduced glutathione and lipid peroxide levels during liver ischemia in guinea pigs. 795 42

1. Na+K+ATPase is a membrane bound enzyme whose activity is essential for maintenance of cell viability. Lipid peroxidation changes membrane fluidity and enzyme activity. 2. The purpose of this study was to investigate the effect of allopurinol (free radical scavenger) on Na+K+ATPase activity in rabbit kidney cortex membrane. In this in vivo study we created ischemia and reperfusion in rabbit kidneys. 3. Enzyme activity were low in ischemic and reperfused kidneys, compared to the controls. In allopurinol treated ischemic and reperfused groups, the levels of Na+K+ATPase activity were high compared to the untreated group. 4. It has been concluded that allopurinol may protect this enzyme activity.
Gen Pharmacol 1994 Mar
PMID:The effect of allopurinol on Na+K+ATPase related lipid peroxidation in ischemic and reperfused rabbit kidney. 802 34

1. KRN2391 (3-30 micrograms/kg, i.v.) produced a decrease in mean blood pressure (MBP) with concomitant increase in heart rate (HR) and change in electrocardiogram (ECG) such as the shortening of PP and PQ intervals and the prolongation of QTc and these changes in HR and ECG were attenuated by pretreatment with propranolol (1 mg/kg) in normal dogs. 2. KRN2391 at 30 micrograms/kg induces neither suppression nor aggravation of ventricular arrhythmias caused by adrenaline and digitalis. 3. In two-stage coronary ligation-induced arrhythmia, KRN2391 inhibited arrhythmia at 48 hr. 4. These results suggest that KRN2391 may be effective on arrhythmia related to ischemia. In addition, it is considered that arrhythmia is not induced even by a high dose of KRN2391 in the normal condition.
Gen Pharmacol 1994 Jan
PMID:Effect of KRN2391 on canine ventricular arrhythmia models. 804 50


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