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Biomedical subjects

G Oner

Publications and source records attributed to G Oner.

31 records · Page 2Linked to original sources
PubMed1983

Reversal of 6-hydroxydopamine-induced hypotension in Long Evans and diabetes insipidus (Brattleboro) rats.

Brattleboro (diabetes insipidus) rats showed a delayed recovery from 6-hydroxydopamine (6-OHDA) hypotension as compared to Long Evans controls. A slight increase in circulating arginine vasopressin was noted in the 6-OHDA-treated Long Evans rats but no change in circulating oxytocin was apparent in either species. The haematocrit and plasma potassium suggested haemodilution in Long Evans rats following 6-OHDA treatment but no such changes were apparent in similarly treated Brattleboro rats. Since the major difference in Long Evans and Brattleboro rats is the latter's inability to synthesize arginine vasopressin (AVP), it is suggested that AVP may have a role in the restoration of homeostasis following 6-OHDA-induced hypotension. This conclusion is supported by (a) a delayed recovery from hypotension and (b) no change in blood concentration parameters, in the Brattleboro rat.

Animals↗
PubMed1981

The role of zinc ion in the development of gastric ulcers in rats.

The properties of the gastric mucosal barrier and acid output were investigated in zinc deficient rats. A decline in total acid output, a significant diminution in hydrogen and sodium ion fluxes and an increase in gastric lesions suggest a marked breakdown of the gastric mucosal barrier in zinc deficient rats.

Animals↗
PubMed1980

Pancreatic blood flow in hemorrhagic shock.

Pancretic blood flow rates were determined using a 133Xe washout technique in a total of 40 dogs, 14 of which were used as a control group and the remaining 26 as the experimental group. The initial pancreatic blood flow rates of control group and of the experimerntal group were 85.1 +/- 10.1 ml/100 g/min of pancreas/min and 81.1 +/- 5.4 ml/100 g/min respectively. These values were not significantly different from each other (P > 0.05). In the control group the blood flow was determined 3 times at 30 min intervals. These mean values were 73.0 +/- 9.4, 74.6 +/- 8.7, and 79.4 +/- 10.4 m/100 g/min respectively (P > 0.05). The dogs in the experimental group were bled and the peripheral arterial blood pressure was reduced stepwise to 80, 50, and 30 mm Hg. At each level at 30 min of stabilization period the pancreatic blood flow rates were 49.8 +/- 3.7, 29.3 +/- 2.3 and 20.2 +/- 2.3 ml/100 g/min respectively. These mean values were very significantly reduced compared to those of the control group at 30 min (P < 0.02), at 60 and 90 min (P > 0.001). They were also very significantly different from their own initial values (P < 0.001). The metabolic consequences of this reduction in pancreatic blood flow are discussed.

Animals↗
PubMed1979

Zinc deficiency and lung converting enzyme activity in rats.

Angiotensin converting enzyme activity was found to be significantly decreased in the isolated perfused lung from zinc-deficient rats when compared with that of controls. Addition of zinc ion to the superfusion medium did not cause a recovery in this decreased activity of the enzyme. It is postulated that zinc deficiency probably produces a structural change in the lung angiotensin converting enzyme.

Angiotensin I↗
PubMedDate not supplied

The susceptibility to stress-induced gastric injury of rats exposed to cadmium.

In this experimental study, the effect of cadmium on cold and restraint stress-induced gastric lesions has been studied. Rats received 15 micrograms/mL cadmium-containing water for 30 d, and at the end of this period, they were subjected to cold and restraint stress. Cadmium accumulation in gastric mucosa was associated with increased mucosal lesions, as well as decreased mucin and PGE2 levels in rats exposed to cadmium. Stress-induced mucosal injury was more pronounced, and the hemoglobin leakage into gastric lumen owing to breakdown in the barrier was 17.30 +/- 3.45 micrograms/mL in control and 35.71 +/- 6.18 micrograms/mL in treated rats. Our data suggest that high cadmium intake facilitates the occurrence of stress-induced mucosal lesions by diminishing the mucin content and PGE2 generation in gastric mucosa.

Animals↗
PubMedDate not supplied

The effect of developmental exposure to cadmium (Cd) on visual evoked potentials (VEPs) and lipid peroxidation.

Pregnant Swiss albino rats were divided into three groups: control (C), gestational exposure of Cd (G-Cd), and gestational/postnatal exposure of Cd (GP-Cd) groups. Control animals received tap water, and the rats of GP-Cd group received Cd as CdC12 in their drinking water during the experimental period. The G-Cd group was given Cd during pregnancy, but given tap water after birth. Twenty-two days after birth, 15 rats (for each group) were taken from their mothers and continued to be treated with Cd (GP-Cd group) or tap water (C and G-Cd groups) for an additional 38 days. On postnatal day (PND) 60, flash visual evoked potentials (FVEPs) were recorded with disc electrodes attached with collodion 0.5 cm in front of and behind bregma. The mean latencies on N1, P2, and P3 were prolonged in the GP-Cd group compared with controls. The mean latency of P3 was also significantly different between G-Cd and GP-Cd groups. P1-N1 and N1-P2 amplitudes of VEPs were significantly decreased in the GP-Cd group compared with control group. N1-P2 amplitude of the G-Cd group was significantly lower than that of the control group. Thiobarbituric acid reactive substances (TBARS) were determined as an indicator of lipid peroxidation. Our data showed that pre- and postnatal Cd treatment caused a significant increase of lipid peroxidation in the brain.

Analysis of Variance↗
PubMedDate not supplied

Cadmium induced lipid peroxidation in kidney function.

Since the kidney is the main target organ for many metals including cadmium, the generation of the products of lipid peroxidation due to accumulation of these toxic metals in the kidney may have importance in the mechanism of their nephrotoxicity. In order to test this hypothesis, we carried out an experimental study in rats. The functions and the levels of tiobarbituric acid reactive substances (TBARS) of the kidney were investigated in animals receiving 15 micrograms/ml aqueous Cd solution for 30 days. Due to cadmium accumulation in kidney cortex, the ratio of Cd/Zn increased significantly and this increase was associated with elevated TBARS in both renal cortex and medulla. The content of TBARS in renal cortex rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p<0.01) and GFR decreased to 390.5 +/- 109.4 from 1008.7 +/- 4.8 microliters/min (p<0.01) in cadmium exposed animals. Daily coadministration of selenium, vitamins A, C, E did not reverse the adverse effect of cadmium on kidney function, despite the significant decrease in cortex TBARS levels (p<0.01). In conclusion, these data suggest to us that lipid peroxidation assessed by TBA test may not be the only mechanism in cadmium induced nephrotoxicity.

Animals↗