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Öğe The effect of bupivacaine on compound action potential parameters of sciatic nerve fibers(TAYLOR & FRANCIS LTD, 2004) Dalkilic, N; Bariskaner, H; Dogan, N; Demirel, I; Ilhan, BThe aim of this study was to document the effects of the local anesthetic agent bupivacaine on individual fibers of peripheral nerve. To accomplish this objective, compound action potentials (CAPs) were recorded from isolated frog sciatic nerves treated with bupivacaine for seven individual concentration levels. Numerical and fast Fourier transform (FFT) analysis were performed on these recordings. The areas, latency periods, maximum and minimum derivatives, and power spectrums of the CAPs were computed. The results show that the area and the absolute values of maximum and minimum derivatives decrease linearly as bupivacaine concentration increases. The power spectrum of the CAPs, which resides in the 0-1000 Hz interval, initially shifts to higher frequencies then returns to lower frequency region again with increasing bupivacaine concentration. Due to this result, it is thought that bupivacaine inhibits nerve fibers in a dose-dependent manner. It primarily affects the fibers having the least myelin sheets (motor fibers), then it begins to depress the fast conducting (neurosensorial) fibers as the bupivacaine concentration increases, and finally blocks the unmyelinated C-fibers.Öğe Effect of gamma-hydroxybutyric acid on lipid peroxidation and tissue lactate level in experimental head trauma(LIPPINCOTT WILLIAMS & WILKINS, 2004) Yosunkaya, A; Ak, A; Bariskaner, H; Ustun, ME; Tuncer, S; Gurbilek, MBackground. This study was designed to determine the effects of gammahydroxybutyric acid (GHB) on tissue lactate and malondialdehyde (MDA) levels in rabbit brain after experimental head trauma. Methods. Thirty New Zealand rabbits were divided equally into three groups: group S was the sham-operated group, group C, and group GHB received head trauma, where group C was the untreated and group GHB was the treated group. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 10 g from a height of 80 cm. GHB was administered 400 mg/kg intravenously for 10 minutes after the head trauma to group GHB. The nontraumatized side was named "1" and the traumatized side was named "2." One hour after trauma, brain cortices were resected from both sides and the concentrations of lactate and MDA were determined. Results There were significant differences between lactate and MDA levels of group S and all other groups (C-1, C-2, GHB(1), and GHB(2)) except between lactate levels of group S and group GHB(1), the nontramnatized and traumatized sides of groups C and group GHB, group C-2 versus group GHB(2), and group C-1 versus group GHB(1) (p < 0.05). Rectal temperature after the administration of GHB in group GHB was found lower than in groups S and C (p < 0.05). Conclusion. These results demonstrate that head trauma leads to an increase in brain tissue lactate and MDA levels, and GHB effectively suppresses the increase of lactate and MDA.Öğe Effect of gamma-hydroxybutyric acid on tissue Na+,K+-ATPase levels after experimental head trauma(WILEY, 2004) Yosunkaya, A; Ustun, ME; Bariskaner, H; Tavlan, A; Gurbilek, MBackground: A failure of the Na+,K+-ATPase activity (which is essential for ion flux across the cell membranes) occurs in many pathological conditions and may lead to cell dysfunction or even cell death. By altering the concentration of specific opioid peptides, gamma-hydroxybutyric acid (GHB) may change ion flux across cell membranes and produce the 'channel arrest' which we assumed will inhibit the failure of Na+,K+-ATPase activity and therefore lead to energy conservation and cell protection. Therefore we planned this study to see the effects of GHB at two different doses on Na+,K+-ATPase activity in an experimental head trauma model. Methods: Forty New Zealand rabbits were divided equally into four groups: group I was the sham-operated group, group II (untreated group), group III received head trauma and intravenous (i.v.) 500 mg/kg GHB and group IV received head trauma and i.v. 50 mg/kg GHB. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 10 g from a height of 80 cm. The non-traumatized (left) side was named as 'a' and the traumatized (right) side as 'b'. One hour after the trauma in groups II and III and craniotomy in group I, brain cortices were resected from both sides and in group I only from the right side was the tissue Na-K-ATPase activity determined. Results: The mean +/- SD of Na+,K+-ATPase levels of each group are as follows: group I - 5.97 +/- 0.55; group IIa - 3.90 +/- 1.08; group IIb - 3.58 +/- 0.90; group IIIa - 5.53 +/- 0.60; group IIIb - 5.33 +/- 0.88; group IVa - 5.05 +/- 0.72; group IVb - 4.93 +/- 0.67. The Na+,K+-ATPase levels of group IIa, IIb, IVa and IVb were significantly different from group S (P < 0.05). There were also significant differences between group IIa and groups IIIa and IVa; group IIb and groups IIIb and IVb (P < 0.05). Conclusions: We conclude that GHB is effective in suppressing the decrease in Na+,K+-ATPase levels in brain tissue at two different dose schedules after head trauma.Öğe Effects of magnesium sulfate on Na+,K+-ATPase and intracranial pressure level after cerebral ischemia(JOHN LIBBEY EUROTEXT LTD, 2004) Ustun, ME; Bariskaner, H; Yosunkaya, A; Gurbilek, M; Dogan, NIn the present study, the effects of magnesium sulfate on Na+,K+-ATPase levels and intracranial pressure (ICP) after cerebral ischemia in rabbits were studied. Thirty New Zealand rabbits were divided into three groups. Group I was the control group. In group 2 (untreated group) cerebral ischemia was produced by clamping bilateral common carotid arteries for 60 min but in group 3 magnesium sulfate was administered 100 mg/kg i.v. 10 min after opening the clamps. In group 1, ICP recordings were obtained 5, 60 and 120 min after craniectomy. In groups 2 and 3, ICP recordings were obtained 5 min after craniectomy but before clamping, 60 min after clamping and 60 min after opening the clamps. After taking ICP recordings, brain cortices were resected and Na+,K+-ATPase activity was determined by subtracting the enzyme activity in the presence of ouabain from the total activity in the absence of ouabain method. There was a significant difference between Na+,K+-ATPase levels of ;group 1 and group 2 (P < 0.05). There was no significant difference in Na+,K+-ATPase levels between group 1 and 3 (P > 0.05), also preischemic ICP values were same in all groups (P > 0.05). Preischemic and postischemic ICP values were significantly different between groups 1 and 2 (P < 0.05), also postischemic (120 min) ICP values were significantly different between group 2 and group 3 (P < 0.05). ICP values correlate well with Na+,K+-ATPase level. These results demonstrate that cerebral ischemia leads to a decrease of ATPase level in the brain and magnesium sulfate suppresses the decrease of Na+,K+-ATPase, also magnesium sulfate treatment improves the ICP changes.Öğe The relaxant effects of alfentanil and remifentanil on noradrenaline-treated rat aorta(VSP BV, 2003) Tuncer, S; Bariskaner, H; Dogan, NBackground and objective: In this in vitro study on rat thoracic aorta, the effects of indomethacin (a prostaglandin synthesis inhibitor), propranolol (a beta adrenergic receptor blocker), tetraethylammonium (TEA) (a calcium-actived potassium channel blocker), glibenclamide (an ATP-dependent potassium channel blocker) and naloxone (an opioid receptor antagonist) on the responses induced by alfentanil and rernifentanil were investigated. Methods: Aortas isolated from rats were cut into spiral strips 12 mm in length, 3 mm wide. Strips were mounted in organ baths at 37degreesC continuously gassed with 95% and 5% CO2. The responses of the drugs were recorded isometrically on polygraph. Results: In both groups, strips were precontracted with 10(-6) M noradrenaline (NA). Then alfentanil or remifentanil (10(-8) to 10(-5) M) was administered cumulatively. Both alfentanil and rernifentanil significantly produced relaxation (p < 0.05). Indomethacin, propranolol, TEA, glibenclamide and naloxone did not significantly modify responses of the opioids. The rank order of potencies of these drugs was alfentanil > remifentanil. Conclusion: Prostaglandins, beta adrenergic receptors, potassium channels and opioid receptors have no role in the responses induced by alfentanil and remifentanil.
