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Biomedical subjects

S Ercan

Publications and source records attributed to S Ercan.

32 records · Page 2Linked to original sources
PubMed1994

The role of plasma arachidonic acid metabolites in the pathogenesis and the prognosis of Henoch-Schönlein purpura.

Henoch-Schönlein Purpura (HSP) involve small vessel inflammation. Arachidonate biochemical pathways play an important role in the pathogenesis of vascular inflammation. The aim of this study was to investigate the change in the ratio of plasma arachidonic acid metabolites in the patients with HSP and evaluate the association between clinical activity and prostanoid activity in the acute phase of HSP. Plasma prostaglandin E2 (PGE2)-like activities were found to be 7.2 +/- 0.8 ng/ml in control group (n = 12) while it was 5.3 +/- 0.6 ng/ml in the patients with HSP (n = 12). Plasma leukotriene C4 (LTC4)-like activities were found to be 16.0 +/- 1.1 ng/ml in control while it was 30.9 +/- 4.3 ng/ml in the patients. The differences of LTC4-like activities and the LTC4/PGE2 ratios between the HSP patients and the controls were significant (p < 0.01, p < 0.001 respectively), but no significant difference was found in PGE2-like activities. Plasma LTC4-like activity and LTC4/PGE2 ratio were also significantly increased in the patients with high clinical score (p < 0.05, p < 0.02 respectively). These results suggested that not only cyclooxygenase products but also LTs may play an important role in vascular inflammation. Therefore LTC4/PGE2 ratio must be taken into consideration in the pathogenesis and the prognosis of HSP.

Adolescent↗
PubMed1994

Effect of verapamil and iloprost (ZK 36374) on endothelin release after mesenteric ischemia-reperfusion injury.

In this experimental study we studied the effect of verapamil and iloprost on endothelin release in ischemia/reperfusion (IR) injury of the rat intestine. Endothelin levels in the portal blood and malondialdehyde (MDA), PGE2, and LTC4 levels in the intestinal tissue were determined. The MDA levels increased in the control group and this increase was reversed with iloprost, verapamil and both. The change in the LTC4 levels was insignificant between the groups. Iloprost reduced PGE2 and endothelin release, but verapamil was not as effective and no synergistic effect was encountered. The increased PGE2/LTC4 ratio was also reversed in the experimental groups, verapamil being less effective. Endothelin release seems to be related to both PGE2 levels and the PGE2/LTC4 ratio after mesenteric IR injury.

Animals↗
PubMed1993

The cytoprotective effects of verapamil and iloprost (ZK 36374) on ischemia/reperfusion injury of kidneys.

We investigated the cytoprotective effects of verapamil, a Ca channel blocker, and of iloprost (ZK 36374), a stable prostacyclin analogue, on ischemia/reperfusion (I/R) injury in Wistar albino rat kidneys that were subjected to 60 min of warm ischemia and reperfusion. The groups included sham, ischemia-untreated (ISCH), verapamil-treated (VER), iloprost-treated (ILO), and verapamil + iloprost (VER + ILO)-treated rats. The 7-day survival of all the treated groups was better than that of the ISCH group. The creatinine concentration on the 3rd day was significantly lower in the VER + ILO group than in the ISCH group. Serum creatinine on day 3 was also low in the VER + ILO groups compared to the ISCH group, although the differences were not significant. The creatinine values on day 7 were significantly lower in the VER and ILO group than in the control, VER, or ILO groups. The malondialdehyde (MDA) concentrations of the kidney cortex tissue after reperfusion in all groups were higher than normal. The tissue-reduced glutathione (GSH) concentrations of the kidneys sampled immediately after reperfusion were significantly lower in the ISCH group than in all of the other treated groups. These results indicate that although verapamil and iloprost have independent cytoprotective effects on 60-min warm ischemia/reperfusion injury of rat kidneys, the protection afforded when both drugs are combined is synergistic. The mechanism of cytoprotection is not limited to the suppression of lipid peroxidation, and a nearly complete protection of reperfusion injury can be obtained by such an intervention.

Animals↗
PubMed1993

The effect of nordihydroguaiaretic acid on leukotriene C4 and prostaglandin E2 production following different reperfusion periods in rat brain after forebrain ischemia correlated with morphological changes.

Leukotriene C4 (LTC4) and prostaglandin E2 (PGE2) are the 5-lipoxygenase and cyclooxygenase metabolites of arachidonic acid (AA). They constrict blood vessels and enhance vascular permeability inducing vasogenic edema that may hurt the ischemic penumbra after cerebral ischemia and reperfusion. Nordihydroguaiaretic acid (NDGA) is known as the most potent inhibitor of 5-lipoxygenase in different tissues. Furthermore, it has considerable inhibitory activity against cyclooxygenase. In this study, after developing a global ischemic model in the rat, the levels of LTC4 and PGE2 in the forebrain were measured, following different reperfusion periods after 10 min ischemia including 8 rats for each reperfused group. Sham operations were performed for each corresponding control group (n = 8). AA metabolites were then correlated with neuropathological findings. In the combined reperfused groups both metabolites increased significantly when compared with 10 min, ischemic group (P < 0.05). In the 8 min reperfused group, PGE2 and LTC4 increased significantly compared with each corresponding control group (P < 0.005). These mediators also increased to high levels compared with the 4 min reperfused group (P < 0.05, P < 0.005). PGE2 and LTC4 were reduced significantly at the 15th and 60th min of reperfusion compared with the 8 min reperfused group (P < 0.05, P < 0.005). NDGA (0.1 mg/kg) reduced both metabolites in the 8 min reperfused group significantly (P < 0.05). Brain cortex specimens were taken for light and electromicroscopical investigations. No significant differences were noted between the structural changes in the 4, 8 and 15 min of reperfusion and NDGA administered groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of preoperative i.m. administration of diclofenac on suxamethonium-induced myalgia.

We have studied the effects of preoperative administration of diclofenac on suxamethonium-induced myalgia, plasma met-enkephalin-like activity (E-LA), prostaglandin E2-like activity (PGE2-LA), leukotriene C4-like activity (LTC4-LA) and histamine-like activity (H-LA). Thirty-four ASA I patients undergoing elective ophthalmic surgery were allocated randomly to two groups to receive either saline placebo or diclofenac 75 mg i.m. 20 min before operation, in a double-blind design. Anaesthesia was induced with thiopentone 5-7 mg kg-1 followed by suxamethonium 1.5 mg kg-1 and maintained with 67% nitrous oxide and halothane in oxygen. Plasma PGE2-LA, LTC4-LA, H-LA and E-LA were measured before premedication, 1 min after the administration of suxamethonium and 24 h after operation. Muscle fasciculations, intubation conditions and postoperative myalgia were graded numerically. Postoperative myalgia in the diclofenac group was significantly (P < 0.05) less (47.1%) than in the control group (76.5%). Post-suxamethonium and 24-h concentrations of plasma PGE2-LA and LTC4-LA were also significantly (P < 0.05) greater than baseline in the control group. Plasma H-LA was increased in both groups after suxamethonium and this increase was significant (P < 0.05) in the control group. We conclude that diclofenac reduces significantly the incidence and intensity of suxamethonium-induced myalgia.

Adult↗
PubMed1992

Prostaglandin E2 and leukotriene C4 levels following different reperfusion periods in rat brain correlated with morphological changes.

Prostaglandin E2 (PGE2) and leukotriene C4 (LTC4) are the metabolites of arachidonic acid (AA) that increase in forebrain following global ischemia and reperfusion. These mediators are highly potent vasoconstrictors of cerebral arteries leading to enhanced vascular permeability that induces the formation of vasogenic edema. In this study, after developing an experimental animal model simulating the concept of ischemic penumbra in the rat, the levels of PGE2 and LTC4 produced in the forebrain were measured and the effects of these mediators in short duration and prolonged reperfusion were investigated and then correlated with neuropathological findings. We found statistically significant reduction both in PGE2 and LTC4-like activities after just 10 min ischemia (p less than 0.05, p less than 0.05). PGE2-like activity significantly increased in the 4th and 60th min of reperfusion (p less than 0.05, p less than 0.05). In the 15th min of reperfusion, PGE2 was found to be significantly reduced (p less than 0.005) that may be due to the formation of free oxygen radicals by activation of PG hydroperoxidase reaction that inhibits PGE2 production in the cyclooxygenase pathway. LTs were not significantly increased in any reperfused group. Inhibition of the lipoxygenase pathway of AA metabolism may occur as a result of 15-HPETE (15-hydroperoxyeicosatetraenoic acid) production. Pathologically, edema and degeneration of brain tissue were seen beginning from the 4th min of reperfusion that reached a peak in the 60th min of reperfusion which is in accordance with biochemical changes in the damaged tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Nicardipine reduces the levels of leukotriene C4 and prostaglandin E2, following different ischemic periods in rat brain tissue.

Ischemic depolarization of nerve membranes is associated with a rapid influx of calcium into the cell, resulting in production of arachidonic acid (AA) metabolites. These metabolites, particularly leukotriene C4 (LTC4) have a very potent vasoconstrictor effect on cerebral arteries inducing vasogenic edema that may damage the ischemic penumbra. Calcium antagonists are assumed to prevent or reduce metabolic disturbances associated with ischemia. In this study, after developing an experimental animal model simulating the concept of the ischemic penumbra in the rat, the levels of LTC4 and prostaglandin E2 (PGE2) produced in the forebrain following different ischemic periods, such as 4th, 15th, 60th and 240th min were measured by a bioassay method, including 6 rats for each ischemic group. Then the effect of the 1-4 dihydropyridine nicardipine (1 mg/kg) on these mediators was investigated by giving it to the rat 30 min before the development of the ischemic model in each corresponding group (n = 6). We showed that nicardipine significantly reduced the high levels of LTC4 and PGE2 in the 4th min and 4th h of cerebral ischemia (p less than 0.005, p less than 0.0005). So it may be concluded that institution of nicardipine may be helpful in protecting the ischemic penumbra during the early hours of cerebral ischemia.

Animals↗
PubMed1992

The effect of iloprost and NDGA in ischemia reperfusion injury in rat liver.

In this study, the effects of iloprost (ZK 36374) and NDGA on warm ischemia and reperfusion injury in rat liver were investigated. Rats were given isotonic saline (control group), iloprost 25 micrograms/kg i.v. (group II) just before warm ischemia or NDGA 10 micrograms/kg i.v. (group III) 5 min before reperfusion or the same drugs were given together (group IV). Serum SGOT, SGPT, and LDH values and tissue malondialdehyde (MDA), glutathione (GSH), prostaglandin (PG)E2, and leukotriene (LT)C4 levels were determined after ischemia-reperfusion injury. Histopathologic examination of the liver was carried out under the light microscope. The serum SGOT, SGPT and LDH levels improved significantly in groups II, III, and IV when compared with the control group (p < 0.05). There was a significant decrease (p < 0.05) in tissue MDA levels and significant increase (p < 0.05) in tissue GSH levels in group I, when compared with group IV and the control groups. The values did not differ significantly in group IV when compared to controls. The LTC4/PGE2 ratio was low and histologic findings were worse in group III. In conclusion, iloprost was found to be beneficial in preventing the ischemia-reperfusion injury in the rat livers. NDGA, either by direct toxic effect or by shifting the arachidonic acid metabolism to the cyclooxygenase route, was not found to be as effective. Iloprost and NDGA did not exert a synergist effect.

Alanine Transaminase↗
PubMed1991

Leukotriene C4 and prostaglandin E2 activities in the serum and cerebrospinal fluid during acute cerebral ischemia.

Lipoxygenase pathway products of arachidonic acid (AA) metabolism (known as leukotrienes, LTs) are produced in the brain during pathologic conditions such as ischemia, hemorrhage, trauma, and seizure in which the release of AA is sustained by the activation of local phospholipases. The most common type of LT in the central nervous system is an LTC4 which is a highly potent vasoconstrictor leading to increase in vascular permeability. In this study, we compared the serum (S) and cerebrospinal fluid (CSF) prostaglandin E2 (PGE2) and LTC4 levels in 13 consecutively admitted patients with acute cerebral ischemia aged 55-80 years with 10 age-matched controls. Patients with previous glucocorticosteroid and antiinflammatory drug usage were not included in the study. S and CSF samples were drawn during the first 72 h of the attack, and samples were evaluated by bioassay. There was no significant difference in S PGE2 and LTC4 values, whereas a significant difference was observed between CSF PGE2 and LTC4 values as compared with the control group. The high levels of CSF PGE2 and LTC4-like activity in acute cerebral ischemia may indicate that these mediators have a role to play in cerebral edema. The CSF PGE2/LTC4 ratio was also found to be reduced in the ischemic group implying higher LTC4 synthesis than PGE2 synthesis. In the light of these findings, we suggest that use of a selective antagonist of LTs may be helpful in reducing the ischemic penumbra during acute cerebral ischemia by controlling the vasogenic edema.

Aged↗
PubMed1991

The alterations of leukotriene C4 and prostaglandin E2 levels following different ischemic periods in rat brain tissue.

Leukotrienes and prostaglandins are formed from arachidonic acid by activation of local phospholipases in pathological conditions such as cerebral ischemia, subarachnoid hemorrhage, cerebral tumors and seizures. These mediators, especially leukotrienes have a very potent vasoconstrictor effect on cerebral arteries. Experimental studies have shown that this effect, by increasing vascular permeability causes vasogenic edema that contributes to the ischemic penumbra. In this study, after developing an experimental animal model simulating the concept of ischemic penumbra in the rat, the levels of leukotriene C and prostaglandin E2 produced in the forebrain were measured and the effects of these mediators in prolonged ischemia were investigated. The results, in the first 4 min of ischemia, showed that the arachidonic acid metabolites, particularly, leukotriene C4, reached a peak in the ischemic cerebral tissue in association with leukocyte accumulation. Later in the 15th min, significant decreases in leukotriene C4 and prostaglandin E2 levels were seen. In the 1st and 4th h, probably due to the stimulation of the relevant enzymes by free oxygen radicals in the ischemic tissue; the levels increase again, returning to control values by the 12th h. It is concluded that the use of lipoxygenase inhibitors and free radical scavengers may be helpful to limit the infarct area in the first 4 h of ischemia.

Animals↗
PubMed1990

The effects of prostacyclin analogue ZK 36374 and thromboxane synthetase inhibitor UK 38485 on mesenteric ischemia in guinea pigs.

The effects of ZK 36374, a prostacyclin analogue and UK 38485, a thromboxane synthetase inhibitor were studied in guinea pigs after performing mesenteric arterial occlusion. In this study, while ZK 36374 significantly lowered the alkaline phosphatase and creatine phosphokinase values two hours after mesenteric arterial occlusion when compared with the control group (p less than 0.005), UK 38485 did not induce any change. In guinea pigs, when given together, ZK 36374 and UK 38485 lowered the enzyme levels to preligation values and the difference was nonsignificant (p greater than 0.1). The histopathologic investigation of the small intestine after giving ZK 36374 and UK 38345 together revealed minimal changes. These findings stress the importance of preserving the PGI2 levels in the PGI2/TXA2 ratio in preventing the increase of lysosomal enzyme levels and histopathologic changes after mesenteric arterial occlusion in guinea pigs.

Alkaline Phosphatase↗
PubMed1989

[Leukotrienes and neurological diseases].

Assessment of Leukotriene C4 (LTC4) activity in the serum and cerebrospinal fluid (CSF) specimens of patients with multiple sclerosis (MS), Parkinson's disease, amyotrophic lateral sclerosis (ALS), Myasthenia gravis (MG), Behçet's disease and neuro-Behçet, as well as in normal controls were carried out in order to determine its role in the pathogenesis of neurologic disorders. LTC4 levels were found to be elevated in MS and Behçet patient in comparison with controls. Augmentation of LTC4 levels underlines the fact that leukotrienes may be held responsible the pathogenesis of these disorders.

Adult↗
PubMedDate not supplied

The effects of contrast media on renal function in children: comparison of ionic and non-ionic agents.

Nephrotoxicity is a common side effect of intravascular contrast media (CM). Although nephrotoxicity of ionic CM has been widely demonstrated, recent studies suggest that newer and more costly non-ionic agents are not less nephrotoxic. We studied the hemodynamic, hematologic and nephrotoxic effects of CM prospectively in 38 patients (ages six months-16 years) with or without risk factors predisposing to nephropathy and compared ionic and non-ionic CM. We performed intravenous urography (IU) with a ionic CM, sodium meglumine diatrizoate (n = 18) and a non-ionic CM, iohexol (n = 20). The patients were divided into three groups according to glomerular filtration rate (GFR) [GFR < or = 50 (n = 9), 50-80 (n = 13), > or = 80 ml/min/1.732 (n = 26)]. Eleven patients had risk factors for nephropathy. Blood pressure, heart rate, ECG, urine and blood samples were obtained 24 hours and one hour before as well as one, 24, and 48 hours after CM infusion. Although a significant increase was found in urine specific gravity, protein/creatinine ratios and serum Na and creatinine levels, the increased levels were within normal limits. We observed a significant reduction in Hb and Htc and urinary prostaglandin E1 levels. Many of the changes observed in the urine and serum values after the use of CM were minor, insignificant and transient, later returning to their initial values. The GFR levels, the presence of risk factors and the use of ionic vs. non-ionic CM had no effect on the results. The elevated urinary basal beta-2-microglobulin levels further increased after CM in patients with low GFRs. It was concluded that non-ionic CM was not superior to ionic CM in patients with GFRs greater than 50 ml/min regardless of predisposing risk factors. One of the non-invasive radiological methods is advised instead of IU in patients with low GFRs.

Adolescent↗