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Biomedical subjects

G Sahin

Publications and source records attributed to G Sahin.

52 records · Page 3Linked to original sources

Impairment of motor coordination in mice after ingestion of aluminum chloride.

The mechanisms of aluminum (Al) neurotoxicity is of increasing interest. Al compounds are known to produce neurological and behavioral abnormalities in some mammalian species. The present study was designed to determine the effects of Al chloride on the skilled motor performance in mice on the rota-rod treadmill. Al chloride, depending on the duration of treatment, produced an impairment of the motor coordination ability in mice.

Aluminum↗

Aluminum content of infant formulas used in Turkey.

In the past few years, there has been an upsurge of interest in aluminum (Al) and human health. The well-recognized manifestations of systemic Al toxicity include fracturing osteomalacia, dialysis encephalopathy, and microcytic hypochromic anemia. The role of Al in causing childhood diseases is also becoming clearer, but the safe plasma level still remains to be determined in newborns, especially in premature newborns, implying that it should be kept low. Premature infants receiving iv fluid therapy show evidence of Al loading. Additionally, the infant-feeding mixtures, especially the soy-based infant formulas, tested may be a significant additional source of Al in the diet of infants with low birthweights, and in infants and in young children with impaired renal function. Careful clinical and biochemical monitoring is warranted to determine whether it will be necessary to eliminate Al contamination of both oral and parenteral preparations used in infants and children who may be at risk for Al intoxication. In this present study, the Al content of infant feeds was measured by electrothermal atomic absorption spectrophotometry, and also compared with those of breast milk, cow's milk, milk powder, and some starches that are commonly used for preparation of infant feed in Turkey. Our results show that Al content of commercially available powdered infant formulas, most of which are imported from Europe, ranged from 1.211 to 10.925 micrograms/g. The mean value was higher than that of breast milk. It was also found that the Al content of cow's milk in various containers was higher than that of breast milk. The highest Al level among cow's milk samples was in the aluminized carton box.

Aluminum↗

Asymmetric reflex responses of the nasal and tracheal vasculatures of the dog.

Both sides of the nasal vasculature of the dog in vivo were perfused separately, with measurement of vascular resistance responses to stimulation of various nerves. Stimulation of the central end of a cut superior laryngeal nerve caused an ipsilateral vasodilation (-4.98%) and a contralateral vasoconstriction (+3.96%), the difference being statistically significant (P < 0.01). Stimulation of a glossopharyngeal nerve caused vasodilation on both sides, the ipsilateral (-17.52%) being greater than the contralateral (-6.33%) response (P < 0.05). Mechanical stimulation of the nasal mucosa caused little ipsilateral change (+0.47%) and a weak contralateral vasoconstriction (+3.78%; P < 0.01). Stimulation of the central end of a cervical vagus nerve caused vasodilations on both sides, the ipsilateral (-9.75%) being greater than the contralateral (-5.73%) change (P < 0.05). With bilateral perfusions of the cervical tracheal arteries, stimulation of a superior laryngeal nerve caused vasodilation on both sides, the ipsilateral (-10.1%) being greater than the contralateral (-7.4%) response (P < 0.05). Stimulation of the central end of a vagus nerve caused vasoconstrictions on both the sides, the ipsilateral (+37.4%) being greater than the contralateral (+10.8%) change (P < 0.05). Thus various nervous inputs from the nose, pharynx, larynx, and vagal distribution cause asymmetric vascular responses both in the nose and in the cervical trachea.

Animals↗

Formate metabolism in young swine.

Formate generated from methanol metabolism in vivo is the chemical entity responsible for the development of the methanol toxicity syndrome in the monkey. Compared to rats, monkeys are in a state of folate deficiency. This leads to a decreased ability to dispose of formate generated leading to its accumulation and the subsequent development of the classic symptoms of methanol toxicity. Rats possess a more efficient folate system; therefore, they metabolize formate very readily and do not exhibit methanol toxicity symptoms. In this report, the hepatic folate content and the ability to handle a formate "load" were evaluated in another animal species, the pig. The results obtained indicate that the pig, compared to all other species studied, has extremely low levels of folates and very low levels of a key enzyme in the folate pathway, namely 10-formyl H4folate dehydrogenase. Also the pig's ability to dispose of formate was extremely limited and slower than that observed in rats or monkeys. These results suggest that the pig may be a suitable animal model for studying formate metabolism and possibly methanol toxicity.

Animals↗

Lung and cardiac reflex actions on the tracheal vasculature in anaesthetized dogs.

1. With pentobarbitone-anaesthetized dogs, the cranial tracheal arteries have been independently perfused on both sides, to measure vascular resistance. Blood pressure and contractions of tracheal muscle were also measured. 2. Capsaicin was injected intravenously to stimulate lung C-fibre receptors. In breathing and in paralysed artificially ventilated dogs it decreased tracheal vascular resistance and blood pressure, and contracted tracheal muscle. The effects were abolished or far smaller after bilateral cervical vagosympathectomy. 3. Veratrine was injected intravenously to stimulate slowly adapting pulmonary stretch receptors and cardiac receptors. In breathing and in artificially ventilated dogs it lowered tracheal vascular resistance and blood pressure, and had variable effects on tracheal muscle tone. The vascular effects were prevented by vagotomy. 4. Veratrine injected into the left atrium caused similar vascular changes to intravenous administration. The changes were prevented by vagotomy. Veratrine causes a tracheal vasodilatation by action on cardiac receptors. 5. Inflation of the lungs in artificially ventilated dogs, to stimulate slowly adapting pulmonary stretch receptors, had no effect on tracheal vascular resistance but decreased blood pressure and tracheal muscle tone, the latter being prevented by vagotomy. 6. Bilateral carotid arterial occlusion, to decrease the discharge in carotid sinus baroreceptors, had no effect on tracheal vascular resistance but increased blood pressure and contracted tracheal muscle, the last two responses being greatly reduced by cutting the sinus nerves. 7. It is concluded that stimulation of lung C-fibre and cardiac receptors causes a reflex tracheal vasodilatation, but that no changes in the tracheal vascular bed occur with stimulation of slowly adapting pulmonary stretch receptors or inhibition of carotid sinus baroreceptors.

Anesthesia, General↗

Chemical control of tracheal vascular resistance in dogs.

With anesthetized dogs we have measured upper tracheal vascular resistance on both sides of the trachea simultaneously by perfusing the cranial tracheal arteries and measuring inflow pressures at constant flows. The ratio of pressure to flow gave vascular resistance (Rtv). Lung airflow, blood pressure (BP), heart rate, and pressure in a cervical tracheal balloon (Ptr) were also measured. In paralyzed dogs, systemic hypoxia due to artificial ventilation with 10% O2-90% N2 increased Rtv by +8.1 +/- 1.0% (SE), Ptr by +76 +/- 22.8%, and BP by +18.9 +/- 24%. After bilateral cervical vagosympathectomy the increases in Rtv and BP were present (+8.8 +/- 0.9 and +22.3 +/- 0.3%, respectively). After carotid body denervation Rtv, Ptr, and BP increased (+6.4 +/- 1.3, +58.6 +/- 31.6, and +14.6 +/- 3.3%, respectively). After vagotomy Rtv and BP increased (+14.1 +/- 1.7 and +22.4 +/- 10.1%, respectively). Tracheal perfusion with hypoxic blood caused a small vasodilation (-2.2 +/- 1.1%). Systemic hypercapnia due to artificial ventilation with 8% CO2-92% air increased Rtv by +16.7 +/- 3.8%, Ptr by +67 +/- 2.0%, and BP by +12.9 +/- 9.9%. Tracheal perfusion with hypercapnic blood caused a small vasodilation (-2.5 +/- 1.2%). Stimulation of the carotid body chemoreceptors with KCN caused a small increase in Rtv (+1.2 +/- 0.5%) and increases in Ptr (+49.8 +/- 13.6%) and BP (+11.1 +/- 2.1%). Systemic hypoxia and hypercapnia caused tracheal vasoconstriction mainly by an action on the central nervous system.

Animals↗

[Aflatoxin B1 in flours (author's transl)].

Inadequate storage conditions may cause growth of fungi on foodstuffs. Most well known fungi are Aspergillus species, which produce a number of toxins known as aflatoxins, destructive to human health. Several health organisations consider these aflatoxins and their metabolites as toxic and cancerogenic and state limitations on their amount in foodstuffs. In ninety three flour samples screened for aflatoxins, three were found to contain aflatoxin B1 over the limits or very close to it.

Aflatoxins↗

Determination of aluminum levels in the kidney, liver, and brain of mice treated with aluminum hydroxide.

In the present study, aluminum (Al) accumulation has been examined after aluminum loading in mice. The kidney, liver, and brain aluminum levels for mice that had been treated orally with aluminum hydroxide for 105 d and for the control group were determined using graphite furnace atomic absorption spectrophotometry (GFAAS) following an acid digestion. Matrix modifier consisted of 2% Triton X-100 and 2% Mg (NO3)2. Al loaded mice showed a significant increase in tissue aluminum levels, relative to the control group.

Aluminum↗

Effects of intravenous and intracerebroventricular theophylline on hypoxic ventilatory depression in anesthetized cats.

OBJECTIVE: The present study was undertaken to investigate the ventilatory response due to sustained isocapnic moderate hypoxia and the possible role of adenosine in hypoxic depression in anesthetized cats. MATERIALS AND METHODS: Cats anesthetized with pentothal sodium (30 mg kg(-1) i.p.) were divided into two groups: treated (n = 11) and control (n = 15). Respiratory frequency (f), tidal volume (VT), minute volume (VE) and systemic arterial blood pressure were recorded during air and 20 min of breathing hypoxic gas mixture (14% O2-86% N2). Isocapnia was maintained by adding fractions of 1% CO2 to the inspired hypoxic gas mixture. The PaO2 and PaCO2 were determined. RESULTS: On hypoxic gas mixture breathing, VT and VE values of the control animals increased significantly, at 5 min to 50 +/- 6 and 53 +/- 6%, respectively, above the prehypoxic air phase value (p < 0.001). After that, the magnitude of increase in VT and VE declined gradually. At 20 min of hypoxia, VT and VE were less than those in prehypoxic air phase (17 +/- 7, 16 +/- 7%, respectively). In cats injected with an adenosine antagonist (theophylline 13.6 mg kg(-1) i.v.), f, VT and VE increased significantly at 5 min of hypoxia (p < 0.001). At 20 min of hypoxia, f, VT and VE were 8 +/- 2, 30 +/- 8, and 39 +/- 8%, respectively, higher than corresponding values of the prehypoxic stage. In cats injected with theophylline (0.5 mg kg(-1)) by cisternal puncture VT and VE increased significantly at 5 min of hypoxia. At 20 min of hypoxia, VT and VE were 27 +/- 7 and 31 +/- 8% higher than those in the prehypoxic air phase. CONCLUSION: The results of this study show that accumulation of adenosine in the brain during hypoxia seems to reduce the response of the central mechanisms to chemoreceptor impulses.

Anesthesia, General↗