Changes in nasal flora one year after endoscopic dacryocystorhinostomy.

PURPOSE: This study investigated changes in patient nasal and conjunctival flora one year after endoscopic dacryocystorhinostomy (EDSR). METHODS: The prospective study included 20 patients that underwent EDSR due to chronic dacryocystitis. Conjunctival and nasal cultures were obtained one year after EDSR from both study and control groups. Patient characteristics, chronic illnesses, the severity and duration of complaints, culture results, and the stent removal time were recorded and analyzed. RESULTS: In the study group, the most commonly isolated microorganism in the nasal cultures was coagulase-negative staphylococcus (n = 11), and the second most commonly isolated microorganism was Staphylococcus aureus (n = 7). A total of 11 (55%) of the nasal cultures in the study group showed the presence of multi-drug resistant (MDR) bacteria, as did 2 (10%) of the nasal cultures in the control group (p = 0.007). CONCLUSIONS: One year after EDSR surgery with silicon stent placement, we detected changes in the nasal flora in the operated side compared with the non-operated side. Even though more than half of the nasal cultures in the study group were positive for MDR bacteria, these microorganisms did not cause attacks of dacryocystitis or affect surgical success.

A central link between angiotensinergic and cholinergic systems; role of vasopressin.

Participation of central cholinergic system in the effects of intracerebroventricular (i.c.v.) injection of angiotensin II (Ang II) on blood pressure and heart rate was studied in conscious, freely moving rats. Ang II dose-dependently increased blood pressure and decreased heart rate. Both atropine and mecamylamine (i.c.v.) pretreatments prevented the cardiovascular effects of Ang II. Pretreatment with a vasopressin V1 antagonist also prevented the cardiovascular responses to Ang II. Our data suggest that the central pressor effect of Ang II is mediated in part by central acetylcholine via both muscarinic and nicotinic receptors, and vasopressin participates in this effect through V1 receptors.

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline

In the present study, we investigated the involvement of the brain renin-angiotensin system in the effects of central cholinergic stimulation on blood pressure in conscious, freely moving normotensive rats. In the first step, we determined the effects of intracerebroventricular (icv) choline (50, 100 and 150 µg) on blood pressure. Choline increased blood pressure in a dose-dependent manner. In order to investigate the effects of brain renin-angiotensin system blockade on blood pressure increase induced by choline (150 µg, icv), an angiotensin-converting enzyme inhibitor, captopril (25 and 50 µg, icv), was administered 3 min before choline. Twenty-five µg captopril did not block the pressor effect of choline, while 50 µg captopril blocked it significantly. Our results suggest that the central renin-angiotensin system may participate in the increase in blood pressure induced by icv choline in normotensive rats.

Central injection of captopril inhibits the blood pressure response to intracerebroventricular choline.

In the present study, we investigated the involvement of the brain renin-angiotensin system in the effects of central cholinergic stimulation on blood pressure in conscious, freely moving normotensive rats. In the first step, we determined the effects of intracerebroventricular (icv) choline (50, 100 and 150 microg) on blood pressure. Choline increased blood pressure in a dose-dependent manner. In order to investigate the effects of brain renin-angiotensin system blockade on blood pressure increase induced by choline (150 microg, icv), an angiotensin-converting enzyme inhibitor, captopril (25 and 50 microg, icv), was administered 3 min before choline. Twenty-five microg captopril did not block the pressor effect of choline, while 50 microg captopril blocked it significantly. Our results suggest that the central renin-angiotensin system may participate in the increase in blood pressure induced by icv choline in normotensive rats.

Do recurrent febrile convulsions decrease the threshold for pilocarpine-induced seizures? Effects of nitric oxide.

The aim of the study was to determine whether (1) number of febrile convulsions is a predictor of development of temporal lobe epilepsy, (2) the susceptibility of rats to pilocarpine-induced seizures is increased due to febrile convulsions and (3) nitric oxide is a mediator in the pathogenesis of febrile convulsions. Rat pups were exposed to single or multiple hyperthermic seizures. Subconvulsant doses of pilocarpine (100 mg/kg and 150 mg/kg) were injected intraperitoneally to these rats at 60--70 days of age. Also L-arginine was applied to some rats before a single hyperthermic seizure. We found that risk of future epilepsy increases parallel to the number of febrile convulsions and nitric oxide does not have a pathogenetic role at given doses.

Effects of L-arginine on prevention and treatment of lithium-pilocarpine-induced status epilepticus.

The effects of various doses of L-arginine, a nitric oxide substrate, on lithium-pilocarpine-induced seizures were studied in rats. Rats were implanted with chronic, stainless steel screw electrodes epidurally for electrocortical recordings. A control group received 3 mEq/kg LiCl (i.p.) and 24 h later 45 mg/kg pilocarpine HCl (i.p.). Two different experimental procedures were followed: (1) L-arginine was applied in doses of 100 mg/kg, 300 mg/kg or 500 mg/kg (i.p.), 30 min before pilocarpine injection; (2) 300 mg/kg, 500 mg/kg or 1000 mg/kg (i.p.) L-arginine was injected either 5 min or 30 min after the onset of status epilepticus (SE). L-arginine (300 mg/kg) injected 30 min before pilocarpine significantly reduced the percentage of SE, but did not change the latency to SE or 24-hour survival. These parameters were not significantly affected by the 100 mg/kg or 500 mg/kg dose of L-arginine. On the other hand, no dose of L-arginine that was applied after SE had begun, had any significant influence on the seizures. We concluded that L-arginine may prevent seizure activity in some but not all doses, and does not have any effect on the ongoing seizure activity.