scholarly journals Prevention of radiocontrast-induced nephropathy by adenosine antagonists in rats with chronic nitric oxide deficiency.

1997 ◽  
Vol 8 (7) ◽  
pp. 1125-1132
Author(s):  
C M Erley ◽  
N Heyne ◽  
K Burgert ◽  
J Langanke ◽  
T Risler ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Control Group ◽  
Adenosine Antagonists ◽  
Radiocontrast Media ◽  
Suitable Animal Model ◽  
Adenosine Antagonist ◽  
Nitric Oxide Deficiency ◽  
A1 Receptor ◽  
And Control

To evaluate therapeutic options for the prevention of radiocontrast media (RCM)-induced nephropathy, a model was developed in which rats received NG-nitro-L-arginine methyl ester (L-NAME) for 10 wk in order to inhibit nitric oxide (NO) synthetase. This study tests the hypothesis that infusion of an adenosine antagonist before RCM application may avoid the vasoconstrictive response in NO-depleted rats. Rats received L-NAME for 10 wk orally (50 mg/L drinking water) to achieve NO depletion. Renal function was determined by [3H]inulin clearance for analysis of the GFR and by flowmetry for assessing renal blood flow (RBF). After a control clearance period (baseline clearance period), the renal response to RCM application (sodium diatrizoate, 2 ml/kg body wt) was measured two times every 30 min starting 30 min after RCM application (clearance periods 1 and 2). L-NAME rats and control rats received two adenosine antagonists. The nonselective adenosine antagonist theophylline was given as an initial bolus of 50 mumol/kg body wt within 10 min, followed by continuous infusion of 100 mumol/kg body wt per h, and the specific adenosine A1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) was given as a bolus of 100 micrograms/kg body wt before RCM application. Results were compared with vehicle infusion. In the control group, no significant change of GFR or RBF could be detected after application of RCM with or without prior infusion of DPCPX or theophylline. In L-NAME rats, RBF decreased significantly after RCM application (baseline, 5.6 +/- 0.2 ml/min; first clearance period, 4.6 +/- 0.3 ml/min [P < 0.05]; second clearance period, 4.3 +/- 0.3 [P < 0.01]). GFR was also reduced in L-NAME rats without previous infusion of theophylline or DPCPX (baseline, 0.95 +/- 0.1 ml/min; first clearance period, 0.83 +/- 0.1 ml/min; second clearance period, 0.69 +/- 0.1 ml/min [P = 0.058]). Prior treatment with either theophylline or DPCPX resulted in complete protection against a decline of RBF and GFR induced by RCM in L-NAME rats. Rats with chronic NO blockade showed a significant increase of the renal vasoconstrictive effect of contrast media. Application of L-NAME in rats seems to constitute a suitable animal model to study the pathophysiology of radiocontrast media-induced nephropathy. In this animal model, administration of adenosine antagonists prevented the decline of GFR and RBF.

scholarly journals Role of insulin during the development of oligofructose (OF)-induced equine laminitis

2015 ◽  
Vol 59 (2) ◽  
pp. 303-309
Author(s):  
Renli Jiang ◽  
Li Gao ◽  
Guanying Wang ◽  
Xinran Li ◽  
Yue Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glucose Oxidase ◽  
Negative Correlation ◽  
Significant Negative Correlation ◽  
Control Group ◽  
Endothelin 1 ◽  
Limulus Amoebocyte Lysate ◽  
And Control ◽  
Over Time

Abstract Horses (n = 20) were divided into 2 groups: oligofructose (OF)-induced equine laminitis group (group OF; n = 11) which received 10 g/kg b.w. of OF dissolved in 4 L water via nasogastric intubation, and control group (NS; n = 9) which received 4 L of saline. Blood was collected at 4 h intervals over 72 h study period and analysed by ELISA, kinetic limulus amoebocyte lysate assay, and glucose-oxidase methods. The level of insulin changed significantly in horses which received OF (P < 0.01); there was a significant negative correlation between the level of adiponectin and insulin over time. The results suggested that insulin may play an important role in the development of OF-induced equine laminitis by altering the level of endothelin-1 and nitric oxide.

Histomorphologic Analysis of the Soft Palate Musculature in Prenatal Cleft and Noncleft A/Jax Mice

1995 ◽  
Vol 32 (6) ◽  
pp. 455-462 ◽  
Author(s):  
Carroll-Ann Trotman ◽  
David Hou ◽  
Alphonse R. Burdi ◽  
Steven R. Cohen ◽  
David S. Carlson
Keyword(s):  
Animal Model ◽  
Light Microscopy ◽  
Soft Palate ◽  
Frontal Plane ◽  
Mouse Embryos ◽  
Control Groups ◽  
Structural Differences ◽  
Suitable Animal Model ◽  
And Control ◽  
Hematoxylin Eosin

The two specific aims of this study were as follows: to evaluate the appropriateness of the A/Jax mouse model in the investigation of the key cellular stages in prenatal soft palate morphogenesis and myogenesis; and to describe structural differences in the histomorphology of the soft palate anatomy from cleft and noncleft mice prior to, during, and after palatogenesis. Cleft-induced and control groups of A/Jax mouse embryos from timed pregnancies were harvested sequentially on gestational days 15 to 19. Embryos were weighed and staged for external body morphology. The heads were removed and fixed for light microscopy, sectioned serially in the frontal plane at 10 μm and stained with hematoxylin-eosin to characterize and compare the soft palate musculature. All observations were made at the head depth of the trigeminal ganglion in both age- and stage-matched embryos. The following findings were made: (1) the A/Jax mouse is a suitable animal model for the study of soft palate myogenesis; (2) there were no discernible morphologic differences between the soft palate muscles in cleft and noncleft A/Jax mice when viewed under light microscopy; (3) the soft palate and related muscles were identifiable as muscle fields, in both the cleft and noncleft fetuses, as early as gestational day 15 and as specific muscles at gestational day 18; (4) in both the cleft and noncleft A/Jax fetuses, the soft palate muscles appeared in a sequential anatomic fashion (the palatine aponeurosis appeared first, next the tensor palatini, and then the levator palatini muscles); and (5) in the cleft palate fetuses, both pterygoid plates were angulated and displaced laterally.

Antibiotics and Steroids in the Treatment of Acquired Subglottic Stenosis

1983 ◽  
Vol 92 (4) ◽  
pp. 377-382 ◽  
Author(s):  
John S. Supance
Keyword(s):  
Animal Model ◽  
Subglottic Stenosis ◽  
Control Group ◽  
Cross Sectional ◽  
Procaine Penicillin ◽  
Therapy Animals ◽  
Significant Difference ◽  
Medical Regimens ◽  
And Control ◽  
Systemic Antibiotics

The efficacy of a combination of systemic antibiotics and a steroid in the prevention of acquired subglottic stenosis (ASGS) was evaluated employing a previously developed canine animal model. Thirty-five healthy, postweanling mongrel puppies aged 5 weeks were each intubated for 14 days with an uncuffed polyvinyl endotracheal tube. Twenty puppies received intramuscular dexamethasone (1 mg) daily, and procaine penicillin (100,000 IU) and dihydrostreptomycin (0.125 g) in two divided doses on the day of intubation and each day thereafter until the completion of the study. The remaining 15 puppies served as a control group and received no medical therapy. Animals from both groups were killed at 5, 7, 12, 15, 20, 30, and 56 days following intubation. Comparative examinations of the laryngotracheal complexes of treated and control dogs showed that there was no significant difference between the two groups in the ultimate degree of ASGS attained, as determined by intraluminal cross-sectional area analysis, or in the extent of the lesion as documented by gross and microscopic histology. This investigation showed that the specific systemic combination of two antibiotics and a steroid used in the study was not efficacious in the prevention of ASGS in a canine animal model; for this reason we question the benefit of analogous medical regimens employed to prevent ASGS in infants and children who require long-term endotracheal intubation.

Effect of chronic lithium administration on endothelium-dependent relaxation of rat mesenteric bed: role of nitric oxide

2007 ◽  
Vol 85 (10) ◽  
pp. 1038-1046 ◽  
Author(s):  
Banafsheh Afsharimani ◽  
Leila Moezi ◽  
Hamed Sadeghipour ◽  
Bahareh Rahimzadeh-Rofouyi ◽  
Maliheh Nobakht ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nadph Diaphorase ◽  
Control Group ◽  
No Donor ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed ◽  
Vascular Beds ◽  
Oxide Synthase ◽  
And Control

The mechanism of action of lithium, an effective treatment for bipolar disease, is still unknown. In this study, the mesenteric vascular beds of control rats and rats that were chronically treated with lithium were prepared by the McGregor method, and the mesenteric vascular bed vasorelaxation responses were examined. NADPH-diaphorase histochemistry was used to determine the activity of NOS (nitric oxide synthase) in mesenteric vascular beds. We demonstrated that ACh-induced vasorelaxation increased in the mesenteric vascular bed of rats treated with lithium. Acute Nο-nitro-l-arginine methyl ester (l-NAME) administration in the medium blocked ACh-induced vasorelaxation in the control group more effectively than in lithium-treated rats, while the vasorelaxant response to sodium nitroprusside, a NO donor, was not different between lithium-treated and control groups. Acute aminoguanidine administration blocked ACh-induced vasorelaxation of lithium-treated rats, but had no effect in the control rats. Furthermore, NOS activity, determined by NADPH-diaphorase staining, was significantly greater in the mesenteric vascular beds from chronic lithium-treated rats than in those from control rats. These data suggest that the enhanced ACh-induced endothelium-derived vasorelaxation in rat mesenteric bed from chronic lithium-treated rats might be associated with increased NOS activity, likely via iNOS. Simultaneous acute l-NAME and indomethacin administration suggests the possible upregulation of EDHF (endothelium-derived hyperpolarizing factor) in lithium-treated rats.

scholarly journals The Role of Nitric Oxide in Resolution of Vasospasam Corresponding with Cerebral Vasospasms after Subarachnoid Haemorrhage: Animal Model

2008 ◽  
Vol 8 (2) ◽  
pp. 177-182
Author(s):  
Kemal Dizdarević
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Control Group ◽  
Blood Products

Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

2004 ◽  
Vol 287 (3) ◽  
pp. H1225-H1231 ◽  
Author(s):  
Lucilla D. Monti ◽  
Claudio Landoni ◽  
Emanuela Setola ◽  
Elena Galluccio ◽  
Pietro Lucotti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Control Group ◽  
Diabetic Patients ◽  
Control Groups ◽  
Type 2 Diabetic Patients ◽  
Myocardial Insulin Resistance ◽  
And Control ◽  
Type 2 Diabetic

We evaluated the influence of chronic hypertriglyceridemia and endothelial dysfunction on myocardial glucose uptake (MGU) in Type 2 diabetic patients without coronary heart disease. Patients were divided into two groups according to fasting triglyceride (TG) levels: 5.4 ± 1.1 and 1.5 ± 0.3 mmol/l for high- and normal-TG groups, respectively. Five subjects were assigned to the high-TG group and 11 to the normal-TG group. Age, gender, body mass index, systolic and diastolic blood pressure, glucose, insulin, HbA1c, cholesterol, and HDL cholesterol were similar in the two groups, whereas free fatty acid (FFA) levels were higher in the high-TG group basally and at the end of the clamp. Furthermore, five healthy subjects were subjected to the same protocol and used as the control group. MGU was assessed by using 18F-labeled 2-fluoro-2-deoxy-d-glucose under hyperglycemic-hyperinsulinemic conditions. Basal endothelin-1 and nitric oxide levels were significantly higher in the high-TG group than in the normal-TG and control groups, and cGMP and maximal postischemic vasodilation were significantly decreased in the high-TG group compared with the normal-TG and control groups. However, significant alterations were found in the same parameters in the normal-TG group compared with the control group. By the end of the hyperglycemic clamp, in the high-TG group, MGU was ∼40 and 65% of that in the normal-TG and control groups. MGU negatively correlated with TG, FFA, and endothelin-1, whereas a positive correlation was found with cGMP and maximal postischemic vasodilation. In conclusion, increased TG and FFA levels are risks, in addition to Type 2 diabetes mellitus, for myocardial insulin resistance, endothelial dysfunction, and alteration of nitric oxide/cGMP levels.

Roles of Free Radicals, Nitric Oxide, and Scavenging Enzymes in Nasal Polyp Development

2005 ◽  
Vol 114 (2) ◽  
pp. 122-126 ◽  
Author(s):  
Turgut Karlidaǧ ◽  
Erol Keles ◽  
Nevin İlhan ◽  
Sinasi Yakclin ◽  
İrfan Kaygusuz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nasal Polyp ◽  
Inferior Turbinate ◽  
Control Group ◽  
Free Oxygen Radicals ◽  
Control Groups ◽  
Free Radical Damage ◽  
Scavenging Enzymes ◽  
And Control

The aim of this study was to investigate the role of nitric oxide (NO), free oxygen radicals, and scavenging enzymes in the development of nasal polyp (NP) disease. This study included 41 patients who underwent endoscopic surgery because of NPs. Control specimens were taken from the inferior turbinate of 32 patients who underwent septoplasty. The levels of malondialdehyde (MDA), NO, and superoxide dismutase (SOD) were measured in intraoperative specimens of polyp tissue and turbinate mucosa. The levels of tissue NO were 191.06 ± 26.62 μmol/mg of protein in patients with NPs and 145.30 ± 19.19 μmol/mg of protein (p < .001) in the control group. The levels of MDA in the study and control groups were 12.47 ± 2.12 nmol/mg and 8.83 ± 1.08 nmol/mg (p < .01), respectively. The levels of SOD in the study and control groups were 50.77 ± 14.74 U/mg and 77.93 ± 15.31 U/mg (p < .001), respectively. It was determined that the levels of MDA in plasma and erythrocytes were higher in the patients with NPs than in the control group (p < .05). The levels of NO in plasma and erythrocytes in both groups were similar. The levels of SOD in plasma and erythrocytes were lower in patients with NPs than in the control group (p > .05). Increases in the levels of tissue MDA and NO and decreases in scavenging enzymes in patients with NPs as compared to control groups may indicate the presence of free radical damage in patients with nasal NPs. New studies are needed to clarify the efficacy of using antioxidants in the treatment of NPs.

scholarly journals Overexpression of Nitric Oxide and Inducible Nitric Oxide Synthase in Mucous Membrane of the Maxillary Sinus Fungus Ball

2020 ◽  
Author(s):  
Hang-jin Li ◽  
Yan Guo ◽  
Bo Yu ◽  
Ling-yan Zhang ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Maxillary Sinus ◽  
Inflammatory Cells ◽  
Control Group ◽  
Fungus Ball ◽  
Spearman Correlation ◽  
Oxide Synthase ◽  
And Control ◽  
Sinus Mucosa ◽  
Better Than

Abstract Objective: We aimed to explore the expression and interplay of NO and iNOS to elucidate their roles in human maxillary sinus mucosa with maxillary sinus fungus ball (MSFB) and chronic rhinosinusitis (CRS).Methods: Fifty-one patients with MSFB, CRS and simple maxillary sinus cyst were included in this study. The NO content of the mucosa of each group was detected by Nitric acid reductase method. The expression of iNOS was tested by immunohistochemistry and Western blott. Spearman correlation analysis was used to analyze the correlation between the expression of iNOS and the occurrence of MSFB and CRS.Results: The results showed that NO and iNOS were highly expressed in the maxillary sinus mucosa of MSFB group, which were significantly different from CRS and control group (P<0.01). The expressions of NO and iNOS in the samples of CRS group were higher than that of the control group (P<0.05). Moreover, iNOS was widely presented in the cytoplasm of sinus mucosa epithelium and inflammatory cells in the maxillary sinus mucosa of MSFB patients. Furthermore, Spearman correlation coefficient indicated that the expression of iNOS was positively correlated with the incidence of MSFB (r=0.6395, P<0.05).Conclusion: NO and iNOS are overexpressed in the maxillary sinus mucosa of MSFB and CRS patients, and the increase in the MSFB patients was better than the CRS. The expressions of NO, iNOS were also correlated with the incidence of MSFB. We thus provide a new indicator to assist the diagnosis of MSFB and its distinction from CRS.

Effect of homocysteine and nitric oxide levels on specific Computed Axial Tomography measurements in Alzheimer disease

2007 ◽  
Vol 2 (1) ◽  
pp. 99-108
Author(s):  
Silvia Baiguera ◽  
Maurizio Gallucci ◽  
Andrea Zanardo ◽  
Marcella Folin
Keyword(s):  
Nitric Oxide ◽  
Alzheimer Disease ◽  
Brain Atrophy ◽  
Serum Levels ◽  
Vascular Lesion ◽  
Control Group ◽  
Axial Tomography ◽  
Computed Axial Tomography ◽  
Global Brain ◽  
And Control

AbstractThe present study was undertaken to examine the effect of Homocysteine (Hcy) and nitric oxide (NO) levels on specific Computed Axial Tomography (CAT) measurements, as global brain atrophy and brain vascular lesion in Alzheimer Disease (AD) and in Vascular Dementia (VD) patients. We have analysed serum Hcy and NO levels in AD patients and compared the findings with those in VD patients and control subjects. Moreover we have studied the correlation of Hcy and NO levels with cognitive impairment and brain atrophy determined by Computed Axial Tomography. Hcy serum levels significantly increased in all demented patients compared to control group, independently from the dementia type. On the contrary, no differences were observed in NO serum levels between groups. Moreover, we found significant correlation between Hcy and brain atrophy in both demented groups; whereas NO levels correlated only in AD, but not in VD patients. The pathogenic effect of Hcy either in AD and VD patients appears to confirm a definitive vascular component in AD. As regards NO, our results highlight the role of NO as a beneficial molecule in AD and support the use of NO mimetics as an antineurodegenerative therapy for AD patients.

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