Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen mongrel dogs were chronically instrumented on the circumflex coronary artery for measurement of coronary diameter (CD; Piezoelectric crystals) and coronary blood flow (CBF: Doppler flow probe). Coronary resistance (CR) was calculated as mean arterial blood pressure (MAP)/CBF. Systemic and coronary effects of three intravenous doses of NG-nitro-L-arginine (L-NAME: 0.1; 0.3; 1 mg/kg) were recorded (n = 5). Systemic and coronary effects of two vasodilators, acetylcholine (ACH) (endothelium-dependent: 0.3 micrograms/kg) and nitroglycerin (NTG) (endothelium-independent: 1 microgram/kg) were compared before and after L-NAME (1 mg/kg) (n = 6). Finally, the effects of L-NAME (1 mg/kg) were compared one week before and three days after denudation (balloon catheter) of the circumflex coronary artery (2 cm up and downstream from the crystals attachment site). All experiments were performed in conscious dogs. L-NAME induced a dose-dependent constriction of large epicardial coronary arteries [-1.5 +/- 0.5% from 3.1 +/- 0.3 mm, p < 0.05; -4.0 +/- 0.7% from 3.2 mm, p < 0.001; -5.3 +/- 1.2% from 3.0 mm, p < 0.01; respectively]. L-NAME 0.3 and 1 mg/kg induced a significant increase in MAP [+12.5 +/- 3.0% from 90 +/- 4 mmHg, p < 0.01; +11.3 +/- 3.5% from 96 +/- 7 mmHg, p < 0.05; respectively] and CR [+18.0 +/- 8.3% from 9.8 +/- 3.0 mmHg/cm.s, p < 0.01; +18.7 +/- 8.2% from 10.4 +/- 3.0 mmHg/cm.s, p < 0.01; respectively] with a significant bradycardia, but CBF was not modified. Effects of ACH were unchanged after L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Systemic and coronary hemodynamic effects of inhibition of nitrogen monoxide synthesis in conscious dogs]. 148 63

Polygraphycal studies were carried out in order to evaluate the effects of Diltiazem (Ca-antagonist) on cerebral circulation in cats. In addition to these studies, the inhibitory effect of Diltiazem on incubated blood-, and serotonin-induced vasocontraction of basilar arteries was observed through on operating microscope. Experimental vasospasm were induced by local administration of incubated blood and 10(-5)--10(-6) M serotonin solution. The required dose of Diltiazem, 30-300 micrograms/kg, was injected by one shot intravenously. CBF slightly decreased concomitantly with transiently decreased blood pressure shortly after intravenous injection of Diltiazem. After that, CBF increased for 15-20 minutes and returned to the state similar to that before the administration of Diltiazem. The changes in reactive pattern of CBF depend on the doses of Diltiazem and related to changes of CAR and VAR which were thought to indicate the blood of cardiac output. Vasocontraction induced by incubated blood and serotonin was released 30-35 per cent for 30 minutes after intravenous injection of Diltiazem 100 micrograms/kg. However, by administration of Diltiazem before and after local application of incubated blood and serotonin on basilar arteries, vasocontraction was inhibited completely. These data suggest that administration of Diltiazem (Ca-antagonist) might be useful in the prophylaxis and treatment of vasospasm following rupture of cerebral aneurysm.
 ...
PMID:[Experimental studies of the effect of diltiazem (Ca-antagonist) on cerebral circulation and cerebral arterial spasm]. 715 44

The role of nitric oxide (NO) in the mediation of cerebrovascular CO2 responsiveness was studied in 10 distinct brain and spinal cord regions of the anesthetized, ventilated, temperature-controlled, normoxic cat. Regional CBF was measured with 15-micron radiolabeled microspheres in hypocapnic, normocapnic, and hypercapnic conditions. CO2 responsiveness of each region was determined from the equation of the best-fit regression lines to the obtained flow values. The effect of altered endothelial and/or neuronal NO synthesis on CO2 responsiveness was studied following either selective blockade of the NO synthase enzyme by N omega-nitro-L-arginine methyl ester (L-NAME; 3 or 30 mg/kg i.v.) or simultaneous administration of L-NAME (3 mg/kg i.v.) and a large dose of the NO precursor L-arginine (30 mg/kg i.v.). Blockade of NO synthesis by 30 mg/kg L-NAME resulted in a significant reduction of the steady-state regional blood flow values and in an almost complete abolition of the CO2 sensitivity in each region studied. Changes of the basal flow values as well as the reduction of the regional CO2 sensitivity were dose dependent. Hypothalamic, sensorimotor cortical, and cerebellar regions were the areas most sensitive to the NO blockade. Impaired CO2 responsiveness following NO synthase inhibition, however, was reversed in these regions by simultaneous administration of a large dose of intravenously injected L-arginine. These findings suggest a major role of nitric oxide in the mediation of regional cerebrovascular CO2 responsiveness in cats.
 ...
PMID:Major role of nitric oxide in the mediation of regional CO2 responsiveness of the cerebral and spinal cord vessels of the cat. 750 82

Despite the increasing number of publications devoted to the cerebrovascular role of NO, its precise influence in awake animals is still poorly characterized. The effect of nitric oxide synthase (NOS) inhibition on the cerebrovascular CO2 reactivity was therefore studied in conscious rats. Regional CBF was measured using the [14C]iodoantipyrine technique and brain tissue sampling. The CO2 reactivity was determined 60 min after administration of 30 mg kg-1 N omega-nitro-L-arginine methyl ester (L-NAME). Blockade of NOS by L-NAME significantly decreased CBF in all 11 brain regions studied (-17 to -49%) and increased arterial pressure from 117 +/- 12 to 147 +/- 11 mn Hg. In control conditions, CO2 responsiveness ranged from 1.3 +/- 0.4 in the hypophysis to 6.4 +/- 0.6 ml 100 g-1 min-1 mm Hg-1 in the parietal cortex. Following L-NAME injection, the reactivity to hypercapnia was significantly attenuated in all structures, the magnitude of the reduction ranging from 57% in the medulla to 74% in the cerebellum. This result shows that NO is an important mediator of the hypercapnic vasodilation in the conscious rat.
 ...
PMID:Widespread attenuation of the cerebrovascular reactivity to hypercapnia following inhibition of nitric oxide synthase in the conscious rat. 752 Apr 50

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-L-arginine (L-NNA) or N-nitro-L-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.
 ...
PMID:Cerebral blood flow changes during cortical spreading depression are not altered by inhibition of nitric oxide synthesis. 752 32

Nitric oxide has been implicated in N-methyl-D-aspartate (NMDA)-mediated damage in vitro; however, its role in excitotoxic damage in vivo is not clear. In the present study we evaluated the histopathological and hemodynamic consequences of intrastriatal injections of various doses of NMDA and determined the effects of nitric oxide synthase inhibition on these changes. NMDA was injected into the striatum at doses of 50, 150, and 300 nmol with or without N omega-nitro-L-arginine methyl ester (L-NAME; 100 micrograms, locally). Three days following injections histopathological assessment was performed by morphometric analysis of the lesion area in multiple sections taken from the anterior to the posterior borders of the lesion. In animals injected with 150 and 300 nmol of NMDA (+/- L-NAME), local CBF (lCBF) was determined 30 min following injections using 14C-iodoantipyrine autoradiography. All NMDA-treated animals showed a well-demarcated lesion extending beyond the injection site. The volume of the lesion correlated significantly with the NMDA dose injected. The effects of L-NAME on lesion size were dependent on the dose of the NMDA. The lesion induced by 50 nmol of NMDA was not affected by L-NAME. With a dose of 150 nmol of NMDA, L-NAME induced a 43% increase in lesion volume. In contrast, a 38% decrease in lesion size was observed in animals treated with 300 nmol of NMDA combined with L-NAME. At a dose of 150 nmol, NMDA induced a significant elevation in lCBF, which was restricted to regions close to the injection site including the center areas of the anterior and middle striatum. The increase in lCBF observed with 150 nmol of NMDA was significantly attenuated in the NMDA + L-NAME-treated group. The lCBF changes induced by 300 nmol of NMDA were not significantly different from those in the 150-nmol group; however, the extent of the regions involved was larger. The increases in lCBF were observed in all striatal regions including the central and peripheral areas. L-NAME did not have a significant effect on the lCBF changes induced by NMDA at a dose of 300 nmol. These data suggest that in vivo the involvement of nitric oxide in NMDA toxicity depends on the NMDA dose and on the participation of hemodynamic mechanisms secondary to NMDA exposure.
 ...
PMID:A dual role for nitric oxide in NMDA-mediated toxicity in vivo. 759 50

NOS activity has been recently described in airway epithelial cells. Because these cells are often ciliated we hypothesized that NO modulates airway ciliary beating. CBF was measured in cultured BBECs using video microscopy. L-NMMA, a NOS inhibitor, caused a 40% decrease in CBF following pre-stimulation with isoproterenol (8.5 +/- 0.3 Hz vs 14.6 +/- 0.2 Hz; p < 0.0001) which lasted approximately 60 minutes. Similar attenuation in CBF after isoproterenol pre-treatment was observed with another NOS inhibitor, L-NAME. NOS inhibitor-induced CBF slowing was also observed when cells were pre-stimulated with either bradykinin or substance P and was completely reversed by L-arginine or SNP but not by D-arginine. These observations demonstrate a novel NO-dependent mechanism that upregulates ciliary motility in response to stimulation.
 ...
PMID:Modulation of airway epithelial cell ciliary beat frequency by nitric oxide. 768 May 60

The effects of bilateral carotid artery occlusion/recirculation on cortical CBF (cCBF) were studied in rats following the intravenous administration of either the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester hydrochloride (L-NAME; 30 mg/kg) or an equivalent volume of saline (500 microliters). Induction of bilateral carotid occlusion (BCO) in L-NAME-treated animals resulted in a reduction of cCBF to 30% of baseline. During recirculation subsequent to 20 min of BCO, cCBF in L-NAME-infused animals remained at 30% of baseline. In contrast, cCBF in saline-treated control animals returned to the original baseline level following a similar reduction to 30-40% of baseline during BCO. These results indicate that inhibition of nitric oxide generation limits normalization of regional cortical perfusion following occlusion of proximal large cerebral vessels.
 ...
PMID:Effects of nitric oxide synthase inhibition on cerebral blood flow following bilateral carotid artery occlusion and recirculation in the rat. 768 75

The consequences of inhibition of nitric oxide synthesis on local CBF and glucose utilisation have been studied in the conscious rat using the specific nitric oxide synthase inhibitor Ng-nitro-L-arginine methyl ester (L-NAME; 30 mg kg-1 i.v.). Local CBF and glucose utilisation were assessed with the [14C]iodoantipyrine and the 2-deoxy-D-[14C]glucose autoradiographic techniques, respectively. L-NAME induced prolonged (> 3 h) reductions in local CBF throughout the CNS with concomitant increases in arterial blood pressure. For example, 1 h post L-NAME, CBF dropped from 79 +/- 4 to 45 +/- 1 ml 100 g-1 min-1 in cerebellum, from 76 +/- 4 to 47 +/- 2 ml 100 g-1 min-1 in medulla oblongata, and from 117 +/- 6 to 72 +/- 2 ml 100 g-1 min-1 in cortex. L-NAME produced sustained elevations (e.g., 46 +/- 2 mm Hg at 1 h after bolus administration) in mean arterial blood pressure throughout the period evaluated. Despite evidence implicating nitric oxide in neuronal signalling, L-NAME did not significantly influence CNS functional activity, as measured by local rates of glucose utilisation, in any neuroanatomical region examined. Consequently, the normal ratio of blood flow to glucose use throughout the brain was significantly reduced in the presence of L-NAME, although the hierarchy of blood flow levels in different neuroanatomical regions was preserved. These results are consistent with the involvement of nitric oxide in the tonic control of cerebral tissue perfusion.
 ...
PMID:Inhibition of nitric oxide synthesis: effects on cerebral blood flow and glucose utilisation in the rat. 769 55

The effect of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (PaCO2 approximately 60 mm Hg and PaCO2 approximately 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety-Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. L-NAME treatment did not have a significant effect on either CMRO2 or CBF under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.
 ...
PMID:Role of nitric oxide in regulating cerebrocortical oxygen consumption and blood flow during hypercapnia. 816 93


1 2 3 Next >>