جستجوی مقالات مرتبط با کلیدواژه "l-name" در نشریات گروه "پزشکی"

Paraxanthine is the major metabolite of caffeine in humans. There is no definitive proof that paraxanthine affects seizures. Nitric oxide (NO) contributes to the central effects of paraxanthine.

In this study, we examined the effect of acute paraxanthine administration on the pentylenetetrazole (PTZ)-induced seizure threshold, focusing on the NO-cyclic guanosine monophosphate (cGMP) signaling pathway.

Naval Medical Research Institute (NMRI) male mice (25 - 30 g) received paraxanthine (5, 10, 50, and 100 mg/kg) alone. L-arginine [a substrate for NO synthase (NOS)] (50 mg/kg) or L-NAME [a non-selective NOS inhibitor] (5 mg/kg) was administered alone or as pretreatment before the ineffective or effective doses of paraxanthine, respectively. The intravenous PTZ seizure threshold test was used to determine the thresholds for the onset of myoclonic twitch (MCT), generalized clonus (GNC), and forelimb tonus (FLT). Nitric oxide metabolites (NOx) were measured using the Griess method.

Paraxanthine administered at doses of 10 and 50 mg/kg significantly reduced the threshold for FLT (P < 0.05 for both). At a dose of 100 mg/kg, paraxanthine significantly reduced the thresholds for the onset of MCT (P < 0.001), GNC (P < 0.01), and FLT (P < 0.001). L-arginine (50 mg/kg), either alone or as pretreatment before paraxanthine (5 mg/kg), did not significantly change the seizure threshold. L-NAME (5 mg/kg) alone had no effect, but L-NAME pretreatment before paraxanthine (100 mg/kg) significantly increased the thresholds for the onset of MCT (P < 0.001), GNC (P < 0.001), and FLT (P < 0.001). Only paraxanthine at a dose of 100 mg/kg significantly increased NOx levels in brain tissues (P < 0.05). Pretreatment with L-arginine further increased the NOx level (P < 0.001), whereas pretreatment with L-NAME decreased it (P < 0.001) compared to the paraxanthine groups.

Our results show that paraxanthine has a proconvulsant effect. The results of L-arginine or L-NAME pretreatment before paraxanthine support the possible interaction of the NO-cGMP pathway in the proconvulsant effect of paraxanthine.

Preeclampsia is the principal cause of maternal morbidity and is characterized by hypertension, proteinuria, and edema. It is believed that oxidative stress plays an essential role in the pathophysiology of preeclampsia. This study was conducted to determine the effect of tempol on fetal limb hemorrhage, malformations, and oxidative stress in an N-nitro-L-arginine methyl ester (L-NAME)-induced preeclamptic rat model.

To induce preeclampsia, L-NAME (50 mg/kg/day, oral) was administered from day 11 of pregnancy to day 22. Four preeclamptic groups received L-NAME alone, L-NAME+tempol (20, 60, 180 mg/kg/day; L-NAME, L-T20, L-T60, L-T180 groups, respectively). The control group (normal pregnant) received only tap water, and the T60 group received tempol (60 mg/Kg) alone (without L-NAME). The concentration of 8-isoprostane in plasma and placenta, number and weight of the fetuses, and the limb defects were measured on the 22nd day of the pregnancy.

L-NAME administration caused placental oxidative stress, limb defects and hemorrhage, and low fetal weight. Administration of tempol at 20 and 60 mg/kg/day reduced limb defects (10.5 and 7.2 percent versus 24.7 percent) and limb hemorrhage (14.5 and 9.5 percent versus 23 percent) induced by L-NAME. After administration of tempol (20 and 60 mg/kg), fetal weight increased (5.14±0.08 and 5.44±0.15 versus 4.27± 0.11 g). Administration of tempol at the high dose (180 mg/kg/day) did not produce any significant effects on the measured parameters.

Tempol with certain doses improves fetal outcomes in an experimental rat model of preeclampsia. These may be the results of its antioxidant action.

Acmella oleracea has been used as a traditional medicine for the treatment of asthma, sore throat, haemorrhoids and toothache. However, whether A. oleracea has gastrointestinal functions, such as regulation of intestinal contractions, has not been fully elucidated. Therefore, the aim of the present study was to investigate the effect of A. oleracea flowers extract (AFE) on rat ileum contractions and the possible mechanism(s) of its action.

The extract was prepared using the Soxhlet apparatus with 95% ethanol. Ileum was removed from male Wistar rats and mounted in an organ bath containing Krebs solution. The tissue contractions were recorded by an isotonic transducer under 1 g tension.

The cumulative concentrations of the AFE (0.01–1 mg/mL) reduced the ileum contractions induced by KCl (80 mM) (n = 6, P < 0.05). AFE (1 mg/mL) attenuated the contractions induced by cumulative concentrations of CaCl2 (1–20 mM), while the spasmolytic effects of the extract were not reduced after tissue incubation with N (ω)-nitro-L-arginine methyl ester (L-NAME) (100 μM, 20 minutes).

These results suggest that AFE inhibits ileum contractions without involving the nitric oxide pathway, which is possibly mediated via blockade of voltage-dependent calcium channels. A. oleracea may be useful in gastrointestinal disorders such as diarrhoea.

Some studies have shown therapeutic properties of Prangos ferulacea, but its effect on blood pressure (BP) is unidentified.

So acute and chronic feeding effects of P. ferulacea on BP and its mechanism were evaluated in male rats.

Hydroalcoholic extract of P. ferulacea (12.5, 25, and 50 mg/kg) was injected intravenously and mean arterial BP and heart rate were measured. The mechanism of effect of the extract on BP was evaluated by intraperitoneal administration of L-NAME, atropine or indomethacin (4, 1, and 5 mg/kg, respectively) and then intravenous injection of extract (50 mg/kg). In addition, the extract (500 mg/kg/day) was given orally in L-NAME (40 mg/kg/day)-induced hypertensive rats during 4 weeks. Then anxiety behaviors and BP were assessed.

Intravenous P. ferulacea reduced BP significantly (P < 0.01). There was a significant difference between the effect of 12.5 and 50 mg/kg of extract (P < 0.001). The effect of hypotension of the extract was eliminated by atropine and decreased by L-NAME. Chronic administration of L-NAME increased BP from 112 mmHg in the control group to 149 in hypertensive rats (P < 0.01), while the oral extract in these rats reduced BP to 119 mmHg (P < 0.01). The P. ferulacea had no effect on heart rate and anxiety behaviors in normal and hypertensive rats.

Intravenous P. ferulacea reduces BP, which may be via the muscarinic receptor. Oral P. ferulacea prevents BP augmentation induced by L-NAME. The P. ferulacea seems to be useful for prophylaxis of hypertension.

In this study we investigated the effects of endothelium removal and L-NAME on responses to α-adrenoceptor agonists. Male Wistar rats were killed by overdose with pentobarbitone sodium, after which the left and right common carotid arteries were removed. Rings of arteries 3-4 mm in length were cut from each vessel and then mounted in 10 mL isolated organ bath, bathed in Krebs maintained at 37°C and gassed with 95% 02 plus 5% CO2, The preparations were allowed to equilibrate for an hour. L-NAME was added approximately 10-15 min prior to the onset of cumulative concentration-response curves (CCRC) to an agonist. In some preparations the endothelial layer was removed mechanically by gently rolling the tissue around a thin wire. Removal of the endothelium was confirmed pharmacologically by a lack of relaxant response to the potent endotheliumdependent vasodilator acetylcholine. Inhibition of NO synthesis by L-NAME results in significant vasoconstriction. L-NAME prevented the relaxation of rat carotid artery by acetylcholine, suggesting that both basal and stimulated release of nitric oxide can regulate vascular tone in this artery. Mechanical disruption of the vascular endothelium reduced, but did not abolish, the ability of L-NAME to produce contraction. This suggests an extra-endothelial site for nitric oxide synthesis in rat common carotid artery. Inhibition of nitric oxide synthase with LNAME potentiated responses to phenylephrine and UK-14304 but not to noradrenaline. Mechanical disruption of the vascular endothelium potentiated responses to UK-14304, phenylephrine and noradrenaline. We suggest that constitutive NO activity has substantial inhibitory influence on vasoconstrictor responses to phenylephrine and UK-14304 but not to noradrenaline.