Endogenous nitric oxide and allergic bronchial hyperresponsiveness in guinea pigs

1997 ◽  
Vol 273 (3) ◽  
pp. L656-L662 ◽  
Author(s):  
S. Mehta ◽  
J. M. Drazen ◽  
C. M. Lilly
Keyword(s):  
Nitric Oxide ◽  
Guinea Pigs ◽  
Bronchial Hyperresponsiveness ◽  
No Synthase ◽  
Similar Degree ◽  
Endogenous Nitric Oxide ◽  
Expired Gas ◽  
Airway Tone ◽  
Bronchodilator Activity

To address the role of endogenous pulmonary nitric oxide (NO) in the modulation of airway tone, we investigated changes in expired NO levels, measured by chemiluminescence, and the effect of inhibition of NO synthase on inflammation-associated bronchial hyperresponsiveness in guinea pigs. Mixed expired gas NO levels were similar at baseline in antigen-exposed and unexposed animals and increased transiently to a similar degree during histamine-induced bronchoconstriction in both groups of animals [155 +/- 12% (15 +/- 1 to 23 +/- 4 ppb, P < 0.01) and 162 +/- 19% (16 +/- 2 to 25 +/- 3 ppb, P < 0.01) of baseline, respectively, after administration of 30 nmol/kg histamine]. Although inhibition of NO synthase with intravenous NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) enhanced bronchial responsiveness to histamine by 30 +/- 8% in unexposed animals (P < 0.05), L-NAME did not enhance histamine responsiveness in antigen-exposed animals exhibiting bronchial hyperresponsiveness 24 h after antigen exposure. Thus bronchial hyperresponsiveness induced by repeated pulmonary antigen exposure may be associated with a transient defect in NO-related homeostatic bronchodilator activity.

Endogenous nitric oxide modulates responses of tissue and airway resistance to vagal stimulation in piglets

2002 ◽  
Vol 93 (2) ◽  
pp. 450-456 ◽  
Author(s):  
Mohammad Y. Khassawneh ◽  
Ismail A. Dreshaj ◽  
Shijian Liu ◽  
Chung-Ho Chang ◽  
Musa A. Haxhiu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Airway Resistance ◽  
Vagal Stimulation ◽  
No Synthase ◽  
Excitatory Response ◽  
Tissue Resistance ◽  
Before And After ◽  
Endogenous Nitric Oxide ◽  
Cholinergic Effects

The role of endogenous nitric oxide (NO) in modulating the excitatory response of distal airways to vagal stimulation is unknown. In decerebrate, ventilated, open-chest piglets aged 3–10 days, lung resistance (Rl) was partitioned into tissue resistance (Rti) and airway resistance (Raw) by using alveolar capsules. Changes in Rl, Rti, and Raw were evaluated during vagal stimulation at increasing frequency before and after NO synthase blockade with N ω-nitro-l-arginine methyl ester (l-NAME). Vagal stimulation increased Rl by elevating both Rti and Raw. NO synthase blockade significantly increased baseline Rti, but not Raw, and significantly augmented the effects of vagal stimulation on both Rti and Raw. Vagal stimulation also resulted in a significant increase in cGMP levels in lung tissue before, but not after, l-NAME infusion. In seven additional piglets after Rl was elevated by histamine infusion in the presence of cholinergic blockade with atropine, vagal stimulation failed to elicit any change in Rl, Rti, or Raw. Therefore, endogenous NO not only plays a role in modulating baseline Rti, but it opposes the excitatory cholinergic effects on both the tissue and airway components of Rl. We speculate that activation of the NO/cGMP pathway during cholinergic stimulation plays an important role in modulating peripheral as well as central contractile elements in the developing lung.

scholarly journals Role of endogenous nitric oxide in allergen-induced airway responses in guinea-pigs

1998 ◽  
Vol 124 (6) ◽  
pp. 1019-1028 ◽  
Author(s):  
Hiroaki Iijima ◽  
Yoshiyuki Uchida ◽  
Takeo Endo ◽  
Anbo Xiang ◽  
Manabu Shirato ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guinea Pigs ◽  
Endogenous Nitric Oxide ◽  
Airway Responses

Endogenous pulmonary nitric oxide in the regulation of airway microvascular leak

1998 ◽  
Vol 275 (5) ◽  
pp. L961-L968 ◽  
Author(s):  
Sanjay Mehta ◽  
Jacques Boudreau ◽  
Craig M. Lilly ◽  
Jeffrey M. Drazen
Keyword(s):  
Nitric Oxide ◽  
Guinea Pigs ◽  
No Synthase ◽  
Blue Dye ◽  
Type Ii ◽  
Airway Function ◽  
Dependent Activity ◽  
Endogenous Nitric Oxide ◽  
Nos Inhibitor ◽  
And Control

Endogenous nitric oxide (NO) is an important modulator of airway function, but its role in the regulation of airway microvascular leak (AMVL) remains unclear. Thus we assessed the effects of NO synthase (NOS) inhibition on expired NO (ENO) levels and on AMVL measured by the Evans blue dye technique in guinea pigs. In control unsensitized animals, systemic N G-nitro-l-arginine methyl ester (l-NAME) reduced ENO by 70 ± 8% ( P < 0.01) and reduced AMVL by 92 ± 1 and 44 ± 17% ( P < 0.05 for both) in the extrapulmonary and intrapulmonary airways, respectively. In animals sensitized and challenged with intratracheal antigen, markedly increased levels of AMVL and ENO were similarly attenuated byl-NAME. In contrast, aminoguanidine, a relatively selective type II NOS inhibitor, reduced ENO in both antigen-sensitized and control unsensitized animals by 39 ± 3% ( P < 0.01) but had no effect on AMVL. These data indicate that endogenous pulmonary NO contributes to both basal and antigen-stimulated levels of AMVL in guinea pigs and that this NO-dependent activity does not appear to be derived from type II NOS.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

Role of endogenous nitric oxide (NO) and NO synthases in healing of indomethacin-induced intestinal ulcers in rats

Life Sciences ◽  
2007 ◽  
Vol 80 (4) ◽  
pp. 329-336 ◽  
Author(s):  
Koji Takeuchi ◽  
Ryo Hatazawa ◽  
Mayu Tanigami ◽  
Akiko Tanaka ◽  
Ryoko Ohno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endogenous Nitric Oxide ◽  
Intestinal Ulcers

Nitric oxide: a new role in intensive care

2020 ◽  
Vol 22 (1) ◽  
pp. 72-79
Author(s):  
Alexandra Lee ◽  
◽  
Warwick Butt ◽  
◽  
◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potential Role ◽  
Nitric Oxide Donors ◽  
Ischaemia Reperfusion Injury ◽  
Surface Receptors ◽  
The Past ◽  
Ischaemia Reperfusion ◽  
Human Experiments ◽  
Endogenous Nitric Oxide

Inhaled nitric oxide has been used for 30 years to improve oxygenation and decrease pulmonary vascular resistance. In the past 15 years, there has been increased understanding of the role of endogenous nitric oxide on cell surface receptors, mitochondria, and intracellular processes involving calcium and superoxide radicals. This has led to several animal and human experiments revealing a potential role for administered nitric oxide or nitric oxide donors in patients with systemic inflammatory response syndrome or ischaemia–reperfusion injury, and in patients for whom exposure of blood to artificial surfaces has occurred.

Nitric oxide modulates epicardial coronary basal vasomotor tone in awake dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1250-H1254 ◽  
Author(s):  
A. Chu ◽  
D. E. Chambers ◽  
C. C. Lin ◽  
W. D. Kuehl ◽  
F. R. Cobb
Keyword(s):  
Nitric Oxide ◽  
Coronary Flow ◽  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Vasomotor Tone ◽  
Coronary Vasomotor Tone ◽  
Endogenous Nitric Oxide

This study evaluates the role of endogenous nitric oxide in the modulation of basal coronary vasomotor tone by studying the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation from L-arginine, on resting epicardial coronary diameter and coronary flow. L-NMMA (5 mg/kg) was infused in seven awake dogs chronically instrumented with coronary dimension crystals for measurement of epicardial coronary diameter, and Doppler flow probes for quantitation of phasic coronary flow (vasomotion of distal regulatory resistance coronary vessels). Epicardial coronary diameter decreased 5.5% from 3.47 +/- 0.17 to 3.28 +/- 0.15 mm (mean +/- SE). The diameter change was gradual, reaching a maximum at 13 +/- 2 min after infusion, and persistent, lasting greater than 90 min. Phasic coronary flow did not change. Mean aortic pressure significantly increased from 99 +/- 3 to 111 +/- 3 mmHg and heart rate decreased from 56 +/- 4 to 46 +/- 3 beats/min. Left ventricular end-diastolic pressure and contractility were not significantly altered. L-Arginine (66 mg/kg) but not D-arginine reversed all hemodynamic parameters. These data support an important role of nitric oxide in modulating basal epicardial coronary vasomotor tone and systemic vascular resistance.

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