A COMPARISON STUDY BETWEEN 8-ETHYLISOTHIOUREA, A POTENT AND NON SELECTIVE INHIBITOR OF INDUCIBLE NITRIC OXIDE (NO) SYNTHASE, AND A NO DONOR IN SPLANCHNIC ARTERY OCCLUSION (SAO) SHOCK.

Shock ◽  
1996 ◽  
Vol 5 ◽  
pp. 65
Author(s):  
F. Squadrito ◽  
D. Altavilla ◽  
G. Squadrito ◽  
G. M. Campo ◽  
M. Ioculano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Artery Occlusion ◽  
Selective Inhibitor ◽  
No Synthase ◽  
Comparison Study ◽  
No Donor ◽  
Splanchnic Artery ◽  
Inducible Nitric Oxide

scholarly journals Lipopolysaccharide induces relaxation in lung pericytes by an iNOS-independent mechanism

2000 ◽  
Vol 278 (5) ◽  
pp. L880-L887 ◽  
Author(s):  
Cecilia L. Speyer ◽  
Christopher P. Steffes ◽  
James G. Tyburski ◽  
Jeffrey L. Ram
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Cell Types ◽  
Inhibitory Effect ◽  
No Synthase ◽  
No Production ◽  
No Donor ◽  
Independent Mechanism ◽  
Deficient Mice ◽  
Inducible Nitric Oxide

Lipopolysaccharide (LPS)-regulated contractility in pericytes may play an important role in mediating pulmonary microvascular fluid hemodynamics during inflammation and sepsis. LPS has been shown to regulate inducible nitric oxide (NO) synthase (iNOS) in various cell types, leading to NO generation, which is associated with vasodilatation. The purpose of this study was to test the hypothesis that LPS can regulate relaxation in lung pericytes and to determine whether this relaxation is mediated through the iNOS pathway. As predicted, LPS stimulated NO synthesis and reduced basal tension by 49% ( P < 0.001). However, the NO synthase inhibitors N ω-nitro-l-arginine methyl ester, aminoguanidine, and N ω-monomethyl-l-arginine did not block the relaxation produced by LPS. In fact, aminoguanidine and N ω-monomethyl-l-arginine potentiated the LPS response. The possibility that NO might mediate either contraction or relaxation of the pericyte was further investigated through the use of NO donor compounds; however, neither sodium nitroprusside nor S-nitroso- N-acetylpenicillamine had any significant effect on pericyte contraction. The inhibitory effect of aminoguanidine on LPS-stimulated NO production was confirmed. This ability of LPS to inhibit contractility independent of iNOS was also demonstrated in lung pericytes derived from iNOS-deficient mice. This suggests the presence of an iNOS-independent but as yet undetermined pathway by which lung pericyte contractility is regulated.

scholarly journals Inducible nitric oxide synthase inhibits oxygen consumption in collateral-dependent myocardium

2014 ◽  
Vol 306 (3) ◽  
pp. H356-H362 ◽  
Author(s):  
Yingjie Chen ◽  
Ping Zhang ◽  
Jingxin Li ◽  
Xin Xu ◽  
Robert J. Bache
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Vascular Endothelial Cells ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coordinated Expression ◽  
Collateral Vessels ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Following coronary artery occlusion growth of collateral vessels can provide an effective blood supply to the dependent myocardium. The ischemia, which results in growth of collateral vessels, recruits an inflammatory response with expression of cytokines and growth factors, upregulation of endothelial nitric oxide (NO) synthase (eNOS) in vascular endothelial cells, and expression of inducible nitric oxide synthase (iNOS) in both vessels and cardiac myocytes. Because NO is a potent collateral vessel dilator, this study examined whether NO derived from iNOS or constitutive NOS regulates myocardial blood flow (MBF) in the collateral region. Nonselective NOS inhibition with NG-nitro-l-arginine (LNA) caused vasoconstriction with a significant decrease in MBF to the collateral region during exercise. In contrast, the highly selective iNOS inhibitor 1400W caused a 21 ± 5% increase of MBF in the collateral region. This increase in MBF following selective iNOS blockade was proportionate to an increase in myocardial O2 consumption (MV̇o2). The results suggest that NO produced by iNOS inhibits MV̇o2 in the collateralized region, so that the increase in MBF following iNOS blockade was the result of metabolic vasodilation secondary to an increase in MV̇o2. Thus the coordinated expression of iNOS to restrain MV̇o2 and eNOS to maintain collateral vasodilation act to optimize the O2 supply-demand relationship and protect the collateralized myocardium from ischemia.

scholarly journals 1400W Is a Slow, Tight Binding, and Highly Selective Inhibitor of Inducible Nitric-oxide Synthasein Vitroandin Vivo

1997 ◽  
Vol 272 (8) ◽  
pp. 4959-4963 ◽  
Author(s):  
Edward P. Garvey ◽  
Jeffrey A. Oplinger ◽  
Eric S. Furfine ◽  
Rachel J. Kiff ◽  
Ferenc Laszlo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tight Binding ◽  
Selective Inhibitor ◽  
Inducible Nitric Oxide

Functional Layer-by-Layer Thin Films of Inducible Nitric Oxide (NO) Synthase Oxygenase and Polyethylenimine: Modulation of Enzyme Loading and NO-Release Activity

2018 ◽  
Vol 10 (9) ◽  
pp. 7745-7755 ◽  
Author(s):  
Bhagya Gunasekera ◽  
Charbel Abou Diwan ◽  
Ghaith Altawallbeh ◽  
Haitham Kalil ◽  
Shaimaa Maher ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Thin Films ◽  
No Synthase ◽  
Layer By Layer ◽  
Enzyme Loading ◽  
Functional Layer ◽  
No Release ◽  
Inducible Nitric Oxide

Role of nitric oxide in gut ischemia-reperfusion-induced hepatic microvascular dysfunction

1997 ◽  
Vol 273 (5) ◽  
pp. G1007-G1013 ◽  
Author(s):  
Yoshinori Horie ◽  
Robert Wolf ◽  
D. Neil Granger
Keyword(s):  
Nitric Oxide ◽  
Important Determinant ◽  
Leukocyte Adhesion ◽  
Ischemia Reperfusion ◽  
Protective Action ◽  
Microvascular Dysfunction ◽  
Artery Occlusion ◽  
No Donor ◽  
Synthase Inhibitor

The overall objective of this study was to assess the contribution of an altered bioavailability of nitric oxide (NO) to the leukocyte adhesion and hypoxic stress elicited in the liver by gut ischemia-reperfusion (I/R). The accumulation of leukocytes, number of nonperfused sinusoids (NPS), and NADH autofluorescence were monitored (by intravital microscopy) in mouse liver after 15 min of superior mesenteric artery occlusion and 60 min of reperfusion. Leukostasis, NPS, and NADH autofluorescence (indicating hypoxia) were all increased in the liver at 60 min after gut I/R. The NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA) exaggerated the liver leukostasis elicited by gut I/R, responses that were prevented by coadministration of l-arginine. The NO donor diethylenetriamine-NO (DETA-NO) andl-arginine were both effective in attenuating the gut I/R-induced leukostasis and increased NADH autofluorescence, whereas neither DETA nord-arginine exerted a protective action. These findings indicate that NO is an important determinant of the liver leukostasis, impaired sinusoidal perfusion, and tissue hypoxia elicited by gut I/R.

Nitric oxide attenuates leukocyte-endothelial interaction via P-selectin in splanchnic ischemia-reperfusion

1994 ◽  
Vol 267 (4) ◽  
pp. G562-G568 ◽  
Author(s):  
T. W. Gauthier ◽  
K. L. Davenpeck ◽  
A. M. Lefer
Keyword(s):  
Nitric Oxide ◽  
Ischemia Reperfusion ◽  
Nitrogen Concentration ◽  
Amino Nitrogen ◽  
Immunohistochemical Localization ◽  
Positive Staining ◽  
Lower Plasma ◽  
No Donor ◽  
Endothelial Adhesion Molecule ◽  
Splanchnic Artery

We studied the effects of exogenous nitric oxide (NO) on leukocyte-endothelial interaction after 60 min of splanchnic artery ischemia and 120 min of reperfusion (SAO/R) in pentobarbital sodium-anesthetized rats via intravital microscopy. Treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 20 micrograms/kg bolus followed by infusion at 20 micrograms.kg-1.h-1), beginning 10 min before reperfusion, resulted in significantly decreased leukocyte-endothelial interaction. This was manifested by a significant decrease in leukocyte rolling and adherence in the postcapillary venules. Tissue protection was demonstrated by a significantly lower plasma free amino-nitrogen concentration in the SNAP-treated SAO/R rats compared with those receiving NO-depleted SNAP (P < 0.05). Immunohistochemical localization of P-selectin showed significantly decreased P-selectin expression on the venular endothelium after SAO/R in rats given SNAP 10 min before reperfusion (23.0 +/- 3.2% vs. 54.9 +/- 12.1% positive staining, respectively, P < 0.01). From these data, we conclude that the effects of exogenous NO on leukocyte-endothelial interaction after ischemia-reperfusion appear to be at least partially mediated through the endothelial adhesion molecule P-selectin.

Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?

1995 ◽  
Vol 268 (2) ◽  
pp. G207-G214 ◽  
Author(s):  
A. Rodriguez-Membrilla ◽  
V. Martinez ◽  
M. Jimenez ◽  
E. Gonalons ◽  
P. Vergara
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Motor Pattern ◽  
No Synthase ◽  
Phase Iii ◽  
Motor Patterns ◽  
No Donor ◽  
Postprandial State ◽  
Synthase Inhibitor

The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.

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