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)

A cerebral injury was induced by the bilateral common carotid artery occlusion and recirculation in spontaneously hypertensive rats (SHRs). Employing this ischemia-recirculation rat model, the effects of beraprost sodium (beraprost) on (1) lipid peroxide formation, (2) the increase in the brain water content and (3) neurological signs were examined. In a dosage of 25 micrograms kg-1 or higher, beraprost, administered orally, significantly inhibited the formation of lipid peroxides in the brain and serum induced by cerebral ischemia and subsequent recirculation in a dose-dependent manner. Beraprost also alleviated ptosis and markedly inhibited abnormal running behaviour caused by the ischemia and subsequent recirculation. In addition, although administration of beraprost did not cause marked inhibition of the increase in the brain water content (used as an index of cerebral oedema) during the first 3 h after recirculation, it restored the normal brain water content within 24 h after recirculation. Therefore, this effect was observed evidently later than the effect of inhibition of lipid peroxide formation. Moreover, administration of beraprost resulted in improvement in the symptoms accompanying the ischemic treatment. These results suggest that beraprost is potentially useful for or treatment of the pathological state accompanying cerebral infarction.
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PMID:Inhibitory effect of beraprost sodium on formation of lipid peroxides in ischemia and recirculation-induced cerebral injury. 810 15

We compared the cardioprotective effects during experimental ischemia and reperfusion of beraprost sodium (beraprost), a prostacyclin analog, with those of propranolol and diltiazem. Coronary perfused guinea-pig right ventricular free wall preparations were subjected to 30 min no-flow ischemia with or without drugs, followed by 60 min reperfusion without drugs. In control preparations, decrease in contractile force and increase in resting tension were observed during the no-flow period. On reperfusion, contractile force returned to less than 50% of preischemic values. Beraprost, at 0.1 microM, showed no inotropic effect under normoxic condition and during the no-flow period, but significantly enhanced the recovery of contractile force after reperfusion to about 80% of control values. Propranolol (30 microM) or diltiazem (10 microM) produced similar enhancement of recovery of contractile force after reperfusion, but these two drugs decreased the contractile force under normoxic conditions to less than 20% of control values. Thus, the cardioprotective effect of beraprost was different from those of propranolol and diltiazem in that it was not accompanied by cardiosuppressive effects.
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PMID:Cardioprotective effects of beraprost sodium against experimental ischemia and reperfusion as compared with propranolol and diltiazem. 959 26

Renal blood flow decreases with the progression of chronic glomerulonephritis (CGN). This disease induces medullary ischemia and further renal dysfunction in patients with chronic renal insufficiency (CRI). Prostacyclin (PGI2), with its vasodilative action, increases renal blood flow (RBF) without increasing glomerular filtration rate (GFR). We therefore examined the possibility that PGI2 would mitigate the progression of renal dysfunction by increasing RBF in patients with CRI. Sixteen patients with progressive renal insufficiency (serum creatinine: 2.14+/-0.89 mg/dl) due to CGN were prospectively chosen for this study. The blood pressure was already under control using calcium channel blockers before and during this study in nine hypertensive patients. In the first 6 months the patients received a low-protein (0.6 g/kg/day) and low-salt (5.0 g/day) diet. In the next 6 months they received 60 microg/day of PGI2 analogue (Beraprost sodium) orally. GFR was determined by 24-hour creatinine clearance, and effective renal plasma flow (ERPF) was determined by 99mTc-MAG3 scintigraphy. Glomerular capillary pressure, the resistance ratio of afferent and efferent arterioles (R(A)/R(E)), and the other hemodynamic parameters from Gomez's estimation equation were determined at the start of this study, just before the administration of Beraprost and at the end of the study. The levels of GFR and ERPF were 34.6+/-12.4 and 140.6+/-52.1 ml/min at the start of this study respectively, and decreased to 28.0+/- 12.0 and 115.6+/-45.3 ml/min after the first 6 months without Beraprost. The levels of GFR and ERPF stayed at 28.1+/-15.7 and 119.2+/-57.6 ml/min after the next 6 months with Beraprost in the same patients. R(A)/R(E) increased in the first 6 months from 7.9+/-3.6 to 10.8+/-8.6, but remained constant during 6 months of Beraprost administration, at 10.5+/-8.0. These data indicate that PGI2 analogue diminishes the vascular resistance of glomerular afferent and efferent arterioles regulating the decrease of renal blood flow without glomerular hyperfiltration, thus mitigating the progression rate of renal dysfunction.
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PMID:PGl2 analogue mitigates the progression rate of renal dysfunction improving renal blood flow without glomerular hyperfiltration in patients with chronic renal insufficiency. 1172 76