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Biomedical subjects

R Onur

Publications and source records attributed to R Onur.

At least 37 records · Page 2Linked to original sources
PubMed1999

Seminal vesicle sperm aspiration in the diagnosis of ejaculatory duct obstruction.

OBJECTIVE: To determine the effectiveness of seminal vesicle aspiration in the diagnosis and treatment of patients with ejaculatory duct obstruction. PATIENTS, SUBJECTS AND METHODS: Between March 1998 and February 1999, 10 infertile men with ejaculatory duct obstruction (EDO, mean age 32.7 years, range 25-47) and 10 fertile volunteers (mean age 33.2 years, range 25-42) underwent transrectal ultrasonography (TRUS) and TRUS-guided seminal vesicle aspiration. The volume of and presence of motile sperm in the aspirate was compared with the TRUS findings for both groups. RESULTS: From TRUS of the patients with EDO, the mean (sd, range) transverse diameter of the right and left seminal vesicles were 1.97 (0.54, 0.8-2.6) cm and 1.93 (0.53, 0.9-2.6) cm; the corresponding values in the control group were 1.03 (0.15, 0.8-1.3) cm and 1.0 (0. 12, 0.8-1.4) cm, respectively (P<0.001). In all, 20 aspirate samples were obtained from the patients with EDO by bilateral seminal vesicle aspiration and only one (10%) had no sperm within the aspirate fluid. Of these 10 patients, two had immotile sperm and the remaining seven (14 samples) had a mean motile sperm count of 0.63 (0.45, 0.1-1.0)x106 /mL, whereas seven of eight men assessed in the control group had no motile sperm (one patient had immotile sperm within the aspirate fluid); this difference was significant (P<0.01). CONCLUSIONS: The aspiration of significant numbers of motile sperm from the seminal vesicles suggests the presence of distal obstructions of the ejaculatory duct and enables infertile couples to be candidates for assisted reproduction. However, there is a need for further research to determine the use of this technique in the diagnosis of partial EDO.

Adult↗
PubMed1998

Contractility and electrophysiological parameters of cremaster muscles of boys with a hernia or undescended testis.

BACKGROUND/PURPOSE: The cremaster muscle (CM) has been considered to participate in regulation of blood flow and temperature of the testis. Its contribution to testicular descent has been suggested. However, there is limited information about the CM in physiological and pathological states. Therefore, an experimental study has been conducted to evaluate and compare the contractile and electrophysiological properties of CM in boys with descended or undescended testes. METHODS: Identical CM strips were obtained from eight boys who underwent orchidopexy with a mean age of 3+/-2.2 years and from eight boys who underwent herniorrhaphy with a mean age of 4+/-1.3 years. Muscle strips of 3 x 8 mm were vertically attached to an isometric force displacement transducer, and direct muscle contractions were elicited by rectangular electrical pulses. Direct isometric muscle contractions were recorded in an organ bath containing mammalian Ringer's solution. In electrophysiological experiments, conventional microelectrode techniques were used. RESULTS: Direct electrical stimulation of CM strips obtained from patients with descended and undescended testes elicited muscle twitches and frequency-dependent contractile responses. Tetanic contractions of undescended testes at 100 Hz were 67% greater in amplitude than that of descended testes (P< .002). Muscle strips of both groups exhibited increased twitch amplitudes by 105%+/-37% when the temperature of the bathing solution was increased from 22 degrees to 37 degrees C (P< .001). The electrophysiological findings were similar. CONCLUSIONS: Contrary to other striated muscles, elevated temperature increases the contractility of CM. If the increased contractility by an increase in temperature is a property unique for CM, it should reflect the attempts at regulating testicular blood flow or temperature. The increased amplitude of contractions encountered among the CM of boys with undescended testis suggests the CM to have a role on the location of the testis.

Body Temperature↗
PubMed1998

Comparative neurotoxic effects of root canal filling materials on rat sciatic nerve.

The neurotoxic effects of the root canal filling materials--Endomethasone, N2 Universal, Traitement SPAD, Sealapex, and Calciobiotic Root Canal Sealer (CRCS)--were investigated on isolated rat sciatic nerves after local application. All of the canal filling materials reversibly inhibited the compound action potential (cAP) amplitudes. N2 Universal produced a 50% inhibition in 4.2 +/- 0.2 min. Traitement SPAD, Endomethasone, and CRCS produced the same inhibition in 6.4 +/- 0.3, 6.5 +/- 0.2, and 6.6 +/- 1.1 min, and Sealapex in 9.2 +/- 2.0 min. The inhibitory effect of Sealapex decreased fastest, and 43% recovery of cAP amplitude was observed in 60 to 70 min. The inhibitory effects of Endomethasone, CRCS, and N2 Universal were more pronounced, and 10 to 20% recovery in cAP amplitudes were observed in 2 h. The inhibitory effect of Traitement SPAD was more persistent with 4% recovery in 2.5 h.

Administration, Topical↗
PubMed1997

Monitoring cellular edema at single-neuron level by electrical resistance measurements.

Electrical resistance measurements have been used for investigating extracellular volume fraction (EVF) of brain tissue. Conventional techniques using multiple metal electrodes are limited in their spatial resolution, and thus not suitable for detecting local EVF changes at cellular level. We used a multibarrelled glass microelectrode to monitor cellular swelling locally at single-neuron level. The microelectrode was placed in CA1 region of the rat hippocampus, in situ. A constant current pulse was applied between one of the barrels and a reference electrode placed in the neck. The resultant voltage drop, which was directly proportional to the resistance of the immediate environment surrounding the tip of the microelectrode, was recorded through another barrel. A third barrel was used for iontophoretic injection of N-methyl-D-aspartate (NMDA) for inducing local cellular edema. The effect of diffuse edema induced by bilateral carotid artery ligation on EVF was also investigated. NMDA application increased the local tissue resistance by 2.0-, and ischemia, by 3.4-folds. We conclude that the method described can detect changes in EVF of minute volumes of brain tissue, and is suitable for monitoring very local effects of drugs or changes in the metabolism on cell volume.

Animals↗
PubMed1996

Effects of Androctonus crassicauda scorpion venom on endothelium-dependent and -independent vascular responses of rabbit aorta.

The effects of Androctonus crassicauda scorpion venom on acetycholine (ACh)-induced relaxations and contractions of rabbit thoracic aorta were studied. Endothelium-dependent relaxations induced by ACh in phenylephrine-precontracted arteries were enhanced by the scorpion venom. ACh-induced contractions in endothelium-intact open aortic rings were less than those obtained in denuded preparations (n = 6, P < 0.05, ANOVA). Venom (5, 10 and 30 micrograms/ml) potentiated ACh-induced contractions in intact and denuded segments. In the denuded segments, this potentiation was inhibited by indomethacin (10 microM). Thromboxane synthase inhibitor, BW 149H (100 microM) and thromboxane A2 (TXA2) receptor antagonist, R 68070 (10 microM) partly inhibited venom-induced potentiation. NG-nitro-L-arginine (100 microM) increased venom-potentiated ACh responses in intact arterial segments. Venom increased the basal tone by 25-35% at 30 micrograms/ml. These results suggest that A. crassicauda venom may release a relaxing factor from endothelium and contracting factor from the smooth muscle of rabbit isolated thoracic aorta. The contracting factor may be a cyclooxygenase-like product, most likely TXA2. The increase in basal tone by 30 micrograms/ml venom was inhibited by phentolamine (10 microM) and guanethidine (10 microM), indicating a venom-induced release of a neurotransmitter from adrenergic nerve endings.

Acetylcholine↗
PubMed1996

Effects of cerebral ischemia on N-methyl-D-aspartate and dihydropyridine-sensitive calcium currents. An electrophysiological study in the rat hippocampus in situ.

BACKGROUND AND PURPOSE: During cerebral ischemia, both promoting and limiting factors are present for activation of the N-methyl-D-aspartate (NMDA) receptor ion channel and the dihydropyridine (DHP)-sensitive Ca2+ channels. We investigated the activity of these channels during ischemia and reperfusion in the rat hippocampus in situ. METHODS: Reversible ischemia was induced by bilateral carotid artery ligation. NMDA and BAY K8644 were applied by iontophoresis or pneumatic ejection, and extracellular field potential and resistance changes were recorded from the CA1 region of the rat hippocampus. Resting membrane potentials of the CA1 neurons were also recorded. RESULTS: DC potential shifts produced by NMDA and BAY K8644 were reduced when ischemia depressed the evoked activity more than 50%. They disappeared on total failure of synaptic transmission and recovered during reperfusion. When the evoked activity was depressed less than 50%, DC shifts were greater than their preischemic values; however, BAY K8644-induced potentiation did not reach statistical significance. CA1 neurons were depolarized during ischemia. CONCLUSIONS: These data suggest that ischemia severe enough to cause transmission failure inactivates NMDA and DHP-sensitive Ca2+ currents. During less intense ischemia and reperfusion, NMDA and DHP-sensitive Ca2+ channels are functional, and their overactivation may lead to neurotoxicity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Effects of aconitine on neurotransmitter release in the rat neuromuscular junction.

Aconitine (ACO), A Na+ channel activator, induces depolarization in skeletal muscle and blocks neuromuscular transmission. We investigated the effects of ACO on neurotransmitter release in the rat isolated phrenic nerve-diaphragm preparation at 24 +/- 1 degrees C. ACO inhibited the twitch responses to nerve stimulation but did not affect direct muscle contractions. ACO, without causing excessive membrane depolarization, increased the frequency of miniature end-plate potential (MEPP)s, but did not alter their amplitude or time course. The increase in MEPP frequency started about 60, 30 and 15 min after the application of 6, 20 and 60 microM ACO, respectively. MEPP frequency reached its maximum (250-400 sec-1), within 10-15 min after it began to increase. ACO, without altering direct muscle action potentials decreased the amplitude and blocked end-plate potential (EPP)s and nerve action potential (NAP)s simultaneously, before the increase in MEPP frequency became evident. ACO did not increase MEPP frequency in Ca(2+)-free media. Prior application of tetrodotoxin (1 microM) inhibited the ACO-induced MEPP frequency increase. Carbamazepine (120 microM) and amiloride (100 microM) did not completely inhibit the MEPP frequency increase but prolonged the latency. ACO-induced alterations in the neuromuscular transmission exhibited minimal recovery upon washing for 2-3 hr. These results indicate that ACO-induced neuromuscular blockade is mainly due to presynaptic mechanisms and can be explained by excessive presynaptic depolarization which leads to the blockade of NAPs and EPPs. Depolarization in turn increases intraterminal Ca2+ concentration and results in an excessive increase in MEPP frequency.

Aconitine↗
PubMed1993

Arterial bridging for repair of peripheral nerve gap: a comparative study.

A new experimental model was designed in which the regeneration of rat femoral nerve across a 8 mm excised gap was investigated after insertion of the distal and proximal stumps into the anatomically and functionally intact femoral artery (AIAB). This model was compared with groups of free artery and autologous nerve grafting. After a period of 12 weeks, a histological and electrophysiological analysis was carried out, which demonstrated that the AIAB and autologous nerve grafting group had a significantly higher percentage of regeneration compared with the free artery-graft group. The nerve regeneration and intraneural vascular reconstruction that occurred within AIAB group were more successful than those that occurred in the artery and nerve-grafting groups.

Anastomosis, Surgical↗
PubMed1992

Glycine is required for NMDA receptor activation: electrophysiological evidence from intact rat hippocampus.

Fimbrial/commissural stimulation evokes a prolonged negative field potential in stratum radiatum of CA1 region of the rat hippocampus, in situ, upon activation of N-methyl-D-aspartate (NMDA) receptors. This activity can be induced by iontophoresis of NMDLA (50 nA) or glycine (50-100 nA) during low-frequency stimulation. 7-Cl-Kynurenate (10-30 nA) fully antagonized the NMDA receptor-mediated negative wave induced not only by glycine (N = 3) but also by NMDLA (N = 9), suggesting that activation of NMDA receptors is not possible without glycine binding. 7-Cl-Kynurenate also depressed the extracellular negative d.c. potential shifts appearing during iontophoresis of NMDLA. Stimulation with brief, high-frequency trains evoked a negative wave of 2.1 +/- 0.2 mV and 176 +/- 4 ms (N = 20) on the hippocampal field response following the last stimulus. Ketamine (100-200 nA, N = 6) and MK-801 (50-200 nA, N = 7) blocked the negative wave by 74 +/- 13 and 62 +/- 8%, respectively, while glycine (100 nA) potentiated it by 35 +/- 2% (N = 6), indicating that it had a component mediated by NMDA receptors. 7-Cl-Kynurenate (100 nA) antagonized this activity at a comparable rate to the NMDA receptor antagonists (67 +/- 8%, N = 4). A similar negative wave of 0.9 +/- 0.2 mV and 41 +/- 3 ms (N = 12) was evoked in hippocampal slices by high-frequency orthodromic stimulation. Potentiation of this activity upon lowering Mg2+ in ACSF from 1.3 to 0.5 mM further supported that it had an NMDA-mediated component.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Electrophysiological evidence for activation of NMDA receptors and its antagonism by MK-801 in cerebral ischemia.

We studied the effects of iontophoretically administered MK-801 (50-150 nA) on ischemic changes on the CA1 hippocampal field potential. Twenty rats under urethane anesthesia, of which the hippocampal field response was depressed or lost upon ligation of the carotid arteries, were used. MK-801 applications starting before carotid ligation, decreased the depression of the field response in 8 of 11 trials. MK-801 was applied after the appearance of ischemic changes and partly restored the deteriorated hippocampal field potential in 16 of 34 penetrations. MK-801 was ineffective in preventing or restoring the severely depressed or lost evoked activity. During ischemia a DC potential shift of -32.6 +/- 3.7 mV (n = 10) was recorded. MK-801 reduced the amplitude of the DC potential shift by 50% when applied before (n = 6) or after (n = 4) the initiation of ischemia. Activation of N-methyl-D-aspartate (NMDA) receptors by glutamate or N-methyl-DL-aspartate (NMDLA) induces a slow negative wave on the field response. During ischemia a similar negative wave spontaneously appeared in 9 trials and was also induced with low currents (5-10 nA) of NMDLA which were insufficient to evoke the NMDA-mediated wave before ischemia. These data provide electrophysiological evidence that NMDA receptors are activated during ischemia and MK-801 reduces ischemia neuronal dysfunction.

Animals↗
PubMed1990

Glutamate and glycine induce a negative wave on hippocampal field response through NMDA receptors.

In rats under urethane anesthesia, iontophoresis of large amounts (30-300 nA) of glutamate in the hippocampus induced a negative wave on the field potential evoked by stimulation of fimbria/commissura or perforant pathway. The amplitudes of the negative waves ranged between 0.2 and 9.8 mV and their mean duration was 341 +/- 12 ms. This activity was antagonized by iontophoresis of N-methyl-D-aspartate (NMDA) antagonists: Mg2+ (80-100 nA), ketamine (50-150 nA), MK-801 (50-150 nA) and by systemic ketamine (5 mg/kg, i.v.) administration. Iontophoresis of N-methyl-DL-aspartate (NMDLA) (20-40 nA) and glycine (25-100 nA) also elicited a negative wave which was blocked by NMDA antagonists. The negative waves were induced in all hippocampal layers except the dentate hilus by glutamate, NMDLA and glycine. Pyramidal regions were found to be as sensitive as dendritic layers; the mean amplitudes of glutamate-induced negative waves on the field response were 4.1 +/- 0.6 and 4.2 +/- 0.5 mV for CA1 stratum pyramidale and radiatum, respectively. These data suggest that large amounts of glutamate activate NMDA receptor/ion channels causing appearance of a long-lasting negative wave on the hippocampal field response. The data also demonstrate that glycine leads to a significant participation of NMDA receptors during glutamatergic transmission which is largely mediated through non-NMDA receptors.

Animals↗
PubMed1990

Acute idiopathic demyelinating polyneuropathy: passive transfer to mice by immunoglobulin.

Systemic administration of acute idiopathic demyelinating polyneuropathy (AIDP) immunoglobulins to mice for two weeks resulted in reduced sural nerve action potential amplitudes and reduced (rotarod) motor performance. Electron microscopic examination of the sciatic nerves of the AIDP-immunoglobulin-treated animals revealed loosening of myelin lamellae with widening of interperiod lines and multivesicular disruption of myelin. Vacuolar degeneration was detected in half of the nerves examined by light microscopy. Injection of AIDP-immunoglobulins for three days led to only minor changes, and mice receiving healthy human immunoglobulins showed no abnormalities. These data show that some features of AIDP can be transferred to mice by systemic administration of immunoglobulins and suggest that humoral factors have a pathogenic role in AIDP in addition to cellular factors.

Action Potentials↗
PubMed1989

Glutamate, without GABA antagonists, induces synchronized discharges in intact hippocampus via NMDA receptors.

In rats under urethane anesthesia, iontophoresis of high amounts of glutamate (50-150 nA) in hippocampus caused repetitive field potentials. These synchronized discharges were best recorded in the proximal part of stratum radiatum as positive waves of 10-15 ms duration and of 0.5-5 mV amplitude. A tetrodotoxin-sensitive faster component of 2-5 ms duration was frequently superimposed on the peaks of the positive waves and was followed by a negative wave of 1-6 mV and 20-30 ms. Glutamate-evoked discharges were suppressed by iontophoresis of N-methyl-D-aspartate (NMDA) antagonists, MK-801, Mg2+ and ketamine and also by ketamine injection (i.v. 5-10 mg/kg). The population spikes evoked by fimbrial stimulation were not facilitated by glutamate and the synchronized discharges were suppressed for up to 300 ms following the stimulation, suggesting the presence of an efficient inhibition during glutamate-induced synchronized activity. Glutamate also had no effect on paired-pulse inhibition. No synchronized discharges were recorded with a second electrode separated more than 150 microns from the iontophoretic electrode, suggesting that the activity was local. These data demonstrate that high amounts of glutamate evoke synchronized discharges in hippocampus, possibly through activation of NMDA receptors. The model presented may be utilized to study the mechanisms of synchronization without disinhibition.

Action Potentials↗
PubMed1989

Intravenously and iontophoretically administered naloxone reverses ischemic changes in rat hippocampus.

Forty rats under urethane anesthesia were subjected to cerebral ischemia by ligation of the right carotid, the right plus the left carotid, or the right carotid plus two vertebral arteries. Ischemia caused three types of changes in the field potential of the right hippocampal CA1 region evoked by fimbrial stimulation: 1) completely reversible deterioration (57% and 16% of the rats with unilateral and bilateral carotid artery ligation, respectively), 2) moderate deterioration (37% and 24% of the rats with unilateral and bilateral carotid artery ligation) and 3) irreversible loss of the evoked activity (6% and 60% of the rats with unilateral and bilateral carotid artery ligation and all the rats subjected to three-vessel occlusion). Naloxone improved the moderate deterioration in 10 of 11 rats (1-3 mg/kg i.v.) and in 15 of 16 (50-150 nA) iontophoretic applications, but naloxone did not restore the lost evoked activity. Intravenous morphine (10 mg/kg) aggravated the ischemic changes, and this effect was reversed by naloxone, while iontophoretic administration of morphine caused only excitation. These findings suggest that naloxone has a favorable effect on cerebral ischemia not severe enough to cause transmission failure. The reversal of ischemic changes by iontophoretic naloxone indicates that its site of action is at the neuronal or microcirculatory level.

Animals↗
PubMed1987

Facilitatory effects of dexamethasone on neuromuscular transmission.

The beneficial effects of glucocorticoids in myasthenia gravis are attributed to their immunosuppressive actions. There are also studies reporting direct facilitatory as well as depressant effects of glucocorticoids on neuromuscular transmission. The effects of dexamethasone on neuromuscular transmission were studied by intracellular and extracellular microelectrode recording techniques in the mouse phrenic nerve-diaphragm preparation. Creatinine had to be added to the bathing media to prevent precipitation of the glucocorticoid with Ca2+ and Mg2+; creatinine had no effect. One hour of perfusion with dexamethasone (10(-4) to 10(-3) M) increased the frequency of miniature end-plate potentials (MEPPs), as well as the amplitude and quantum content of end-plate potentials (EPPs), but did not change MEPP amplitude, suggesting an increase in acetylcholine release. Dexamethasone also enhanced presynaptic facilitation and potentiation during repetitive stimulation. It had no effect on muscle resting membrane potential but increased the amplitude, overshoot, and rate of rise of muscle action potentials. The amplitudes of nerve terminal action potentials were also enhanced by dexamethasone. These findings suggest that glucocorticoids have a direct facilitatory action on neuromuscular transmission by a presynaptic action.

Acetylcholine↗
PubMed1987

Calcium channel blockers and essential tremor.

Acute effects of two calcium blockers, nifedipine and verapamil, were investigated on the tremor activity of 8 patients with essential tremor and compared with those of propranolol and placebo. Following a single oral dose of 10 mg of nifedipine, tremor intensity of the patients was increased by 71.4 +/- 22.6%. Nifedipine also enhanced physiological tremor in 6 healthy volunteers by 56.0 +/- 21.9%. This effect of nifedipine was not correlated with the increase in heart rate or decrease in systemic blood pressure. Verapamil (80 mg) did not appreciably alter the patients' tremor activity.

Adult↗
PubMed1987

Effect of naloxone on physostigmine-induced pressor response in adrenalectomized rats.

Physostigmine-induced pressor response was studied in adrenalectomized rats. The increase in mean arterial blood pressure elicited by intravenous administration of physostigmine was not altered by adrenalectomy or sham-operation. The pressor response to intracerebroventricular administration of physostigmine was found to be partially inhibited in both acutely adrenalectomized and sham-operated rats, but not in those adrenalectomized 24 h earlier. This inhibition was completely prevented by naloxone pretreatment. The results suggest that endogenous opioid peptide release induced by surgical stress may be responsible for inhibition of the pressor effect of centrally administered physostigmine in rats.

Adrenalectomy↗