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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We studied the effects of a nitric oxide synthase (NOS) inhibitor, N omega-nitro-L-arginine-methyl ester (L-
NAME
), on cardiac depression and bronchospasm provoked by systemic
anaphylaxis
in vivo in rabbits. Animals pretreated with L-
NAME
showed lower survival rates than control animals pretreated with normal saline. The survival rate in L-
NAME
-pretreated animals was increased by the administration of L-arginine after initiation of
anaphylaxis
. Cardiac output fell significantly in animals pretreated with L-
NAME
compared with controls, although venous return was increased. In animals pretreated with L-
NAME
, pulmonary resistance was significantly increased, and administration of arginine attenuated the bronchospasm. In conclusion, these results, along with the low survival rates in the L-
NAME
-treated animals, suggest that NO production may be beneficial to cardiac depression and bronchospasm in
anaphylaxis
in vivo.
...
PMID:Nitric oxide synthase inhibition is detrimental to cardiac function and promotes bronchospasm in anaphylaxis in rabbits. 749
We investigated whether a nitric oxide synthase (NOS) inhibitor improves cardiovascular depression associated with
anaphylaxis
. After induction of anaphylactic circulatory depression, one group received an NOS inhibitor (Group I, n = 6) and the other received saline solution (Group II, n = 5). Mean arterial pressure and right atrial pressure were significantly higher in Group I than in Group II. Hematocrit was significantly lower in Group I than in Group II. Cardiac output, stroke volume, mean pulmonary arterial pressure, the maximum rate of increase in left ventricular pressure, and the time constant of the fall in isovolumic left ventricular pressure did not differ between the groups. In conclusion, L-
NAME
attenuates hypotension, but does not improve cardiac depression in
anaphylaxis
in dogs. Our finding that NOS inhibitor did not improve cardiac function implies that the production of NO in
anaphylaxis
may have a protective effect with regard to cardiac performance.
...
PMID:An inhibitor of nitric oxide synthase, N omega-nitro-L-arginine-methyl ester, attenuates hypotension but does not improve cardiac depression in anaphylaxis in dogs. 765 70
In the present study, the vasomotor effects of the peptide leukotrienes (LTs) LTC4 and LTD4 on isolated canine venous capacitance vessels were evaluated. Both LTs evoked marked concentration-dependent relaxation of norepinephrine-contracted rings of mesenteric and splenic veins and inferior vena cava but had minimal activity in the femoral vein. Relaxation induced by either LT was abolished after physical removal of the vascular endothelium, whereas marked relaxation responses were evoked by glyceryl trinitrate in the same endothelium-denuded rings. The nitric oxide synthase antagonist NG-nitro-L-arginine methyl ester (L-
NAME
) completely abolished LT-induced mesenteric vein relaxation and unmasked a contractile effect of LTC4. Only partial attenuation of LT-induced relaxation of the inferior vena cava in the presence of L-
NAME
was observed. In the splenic vein, responses solely to LTC4 were very slightly reduced in the presence of L-
NAME
. Reduced hemoglobin (10(-6) and 10(-5) M) inhibited LTC4-evoked splenic vein relaxation and, in a concentration of 10(-5) M, inhibited LTD4-evoked relaxation of the splenic vein. On the other hand, methylene blue (10(-6) and 10(-5) M) attenuated splenic vein relaxation produced by both LTs but solely reduced LTC4-evoked inferior vena cava relaxation. Thus, the peptide LTs, the major components of the slow-reacting substance of
anaphylaxis
, exert a profound endothelium-dependent relaxant effect on venous capacitance vessels, which is only partially dependent on L-arginine and nitric oxide. A role for LT-evoked capacitance venodilation as a mechanism contributing to the reduced venous return and cardiac output associated with systemic
anaphylaxis
is postulated.
...
PMID:Leukotrienes C4 and D4 are potent endothelium-dependent relaxing agents in canine splanchnic venous capacitance vessels. 833 Mar 82
The role of nitric oxide (NO) was determined using a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-
NAME
; 20 mg/kg bolus and 0.05 mg/kg per min) in the renal sympathetic and hypotensive response to systemic
anaphylaxis
induced by Ascaris suum antigen (10 mg, i.v.) in naturally sensitized anesthetized dogs. Renal nerve activity (RNA) in animals pretreated with D-
NAME
, the biologically inactive enantiomer (n = 7), showed an initial increase (192 +/- 32%, (mean +/- SE) followed by a decrease (61 +/- 14%) after antigen. Pretreatment with L-
NAME
(n = 7) did not affect the initial sympathoexcitation but abolished the secondary sympathoinhibition (110 +/- 13%). However, the depressor response to antigen was not different between the L-
NAME
and D-
NAME
groups (-87 +/- 13 mmHg and -84 +/- 12 mmHg). In conclusion, NO is involved in the
anaphylaxis
-induced renal sympathoinhibitory response but not hypotension in anesthetized dogs.
...
PMID:Participation of nitric oxide in the sympathetic response to anaphylactic hypotension in anesthetized dogs. 883 48
The inhibitory effects of endogenous nitric oxide could explain the decreased mesenteric mast cell degranulation after
anaphylaxis
in genetically hypertensive rats (SHR). SHR and normotensive rats (NT) were sensitized to ovalbumin and challenged 14 days later. Degranulation of mast cells was assessed in duodenum, mesentery and skin by increased microvascular permeability using extravasation of Evans blue dye (20mg/kg, i.v.), and in the mesentery also by light microscopy after staining with toluidine blue. Pretreatment with an inhibitor of nitric oxide synthesis, L-
NAME
(30 mg/kg, i.v.) did not change dye extravasation after immunological challenge or after compound 48/80 in mesentery of either SHR or NT. PCA was also defective in SHR. Pretreatment with L-
NAME
did not affect either the defective PCA in SHR or the normal PCA reaction in NT. Our results show that inhibition by endogenous nitric oxide is not the cause of the defective mast cell degranulation in the SHR nor did it modulate degranulation of mesenteric or skin mast cells in NT.
...
PMID:Endogenous nitric oxide does not modulate mesenteric mast cell degranulation in rats. 1278 88
1. The role of shear stress in nitric oxide (NO)-mediated attenuation of anaphylactic venoconstriction was studied using an isolated ovalbumin-sensitized guinea pig liver. 2. Guinea pigs were actively sensitized by a subcutaneous injection of 1 mg ovalbumin. Two weeks after sensitization, the livers were perfused with diluted blood under constant flow or constant perfusion pressure. The constant flow could result in increased shear stress during constriction, while the constant perfusion pressure could prevent changes in shear stress. Using the double occlusion technique to estimate the hepatic sinusoidal pressure, pre- and postsinusoidal constriction was evaluated. Hepatic
anaphylaxis
was induced by an injection of ovalbumin (4 microg) into the perfusate, the volume of which was 40 mL. 3. Under either constant flow or pressure,
anaphylaxis
caused venoconstriction of predominantly presinusoids over postsinusoids, although anaphylactic venoconstriction under constant pressure was significantly greater than that under constant flow. When shear stress was held constant by maintaining constant perfusion pressure, a NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-
NAME
, 100 micromol/L), potentiated similarly both pre- and postsinusoidal constriction induced by
anaphylaxis
. This suggests that hepatic
anaphylaxis
shear stress-independently generates NO, resulting in dilatation of both pre- and postsinusoidal vessels in a similar magnitude. In contrast, when shear stress was allowed to rise under constant flow, anaphylactic presinusoidal constriction was preferentially potentiated by L-
NAME
. 4. Hepatic
anaphylaxis
can increase NO production in a shear stress-independent manner and dilates similarly both pre- and postsinusoids, while NO produced in a shear stress-dependent manner attenuates predominantly venoconstriction of the presinusoids where shear stress is preferentially increased.
...
PMID:Anaphylactic hepatic venoconstriction is attenuated by nitric oxide released via shear stress-dependent and -independent mechanisms in Guinea pig. 1581 Sep 93
Effects of hematocrit (Hct) on N-nitro-L-arginine methyl ester (L-
NAME
)-induced modulation of anaphylactic venoconstriction were determined in isolated perfused rat livers. The rats were sensitized with ovalbumin (1 mg), and the livers were excised 2 weeks later and perfused portally and recirculatingly under constant flow at Hct of 0%, 5%, 16%, and 22%. The hepatic sinusoidal pressure was estimated via the double occlusion pressure (Pdo), and the presinusoidal resistance (Rpre) and the postsinusoidal resistance (Rhv) were calculated. The antigen of ovalbumin 0.1 mg was injected into the reservoir at 10 minutes after pretreatment with L-
NAME
(100 microM) or D-
NAME
(100 microM). Perfusate viscosity, a determinant of vascular resistance and shear stress, was increased in parallel with Hct. In the D-
NAME
groups, antigen caused predominant presinusoidal constriction. The magnitude of venoconstriction was significantly smaller at Hct 0% than at Hct 5% to 22%, whereas no significant differences were found among Hct 5% to 22%. L-
NAME
potentiated the antigen-induced increase in Rpre, but not in Rpost at Hct 5% to 22% as compared with D-
NAME
. But the augmentative effects of L-
NAME
were similar in magnitude among Hct 5% to 22%. These findings suggest that hepatic
anaphylaxis
increases production of nitric oxide, which consequently attenuates anaphylactic presinusoidal constriction in rat livers, and that these effects are independent of perfusate Hct or viscosity in blood-perfused rat livers.
...
PMID:Effects of Hct on L-NAME-induced potentiation of anaphylactic presinusoidal constriction in perfused rat livers. 1689 11
1. The effects of the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-
NAME
) on
anaphylaxis
-induced venoconstriction were examined in rat isolated livers perfused with blood-free solutions in order to clarify the role of NO in anaphylactic venoconstriction. 2. Rats were sensitized with ovalbumin (1 mg) and, 2 weeks later, livers were excised and perfused portally in a recirculating manner at a constant flow with Krebs'-Henseleit solution. The antigen (ovalbumin; 0.1 mg) was injected into the reservoir 10 min after pretreatment with L-
NAME
(100 micromol/L) or D-
NAME
(100 micromol/L) and changes in portal vein pressure (Ppv), hepatic vein pressure (Phv) and perfusate flow were monitored. In addition, concentrations of the stable metabolites of NO ( and ) were determined in the perfusate using an HPLC-Griess system. 3. The antigen caused hepatic venoconstriction, as evidenced by an increase in Ppv from a mean (SEM) baseline value of 7.7 +/- 0.1 cmH2O to a peak of 21.4 +/- 1.1 cmH2O at 3 min in D-
NAME
-pretreated livers. Pretreatment with L-
NAME
augmented anaphylactic venoconstriction, as reflected by a higher Ppv (27.4 +/- 0.8 cmH2O) after antigen than observed following D-
NAME
pretreatment. The addition of L-arginine, a precursor for the synthesis of NO, reversed the augmentation of anaphylactic venoconstricion by L-
NAME
. This suggests that hepatic
anaphylaxis
increased the production of NO, which consequently attenuated anaphylactic venoconstriction. However, perfusate NOx levels did not increase significantly after antigen in livers pretreated with either L-
NAME
or D-
NAME
. 4. In conclusion, L-
NAME
potentiates rat anaphylactic hepatic venoconstriction, suggesting that NO contributes to the attenuation of the venoconstriction. However, this functional evidence was not accompanied by corresponding changes in perfusate NOx concentrations.
...
PMID:N(G)-nitro-L-arginine methyl ester potentiates anaphylactic venoconstriction in rat perfused livers. 1704 17
Platelet-activating factor (PAF), one of vasoconstrictive lipid mediators, is involved in systemic
anaphylaxis
. On the other hand, nitric oxide (NO) is known to attenuate anaphylactic venoconstriction of the pre-sinusoids in isolated guinea pig and rat livers. However, it is not known whether NO attenuates PAF-induced hepatic venoconstriction. We therefore determined the effects of L-
NAME
, a NO synthase inhibitor, on PAF-induced venoconstriction in blood- and constant flow-perfused isolated livers of mice, rats and guinea pigs. The sinusoidal pressure was measured by the double occlusion pressure (Pdo), and was used to determine the pre- (Rpre) and post-sinusoidal (Rpost) resistances. PAF (0.01-1 microM) concentration-dependently caused predominant pre-sinusoidal constriction in all livers of three species studied. The guinea pig livers were the most sensitive to PAF, while the mouse livers were the weakest in responsiveness. L-
NAME
pretreatment selectively increased the basal Rpre in all of three species. L-
NAME
also significantly augmented the PAF-induced increases in Rpre, but not in Rpost, in rat and guinea pig livers. This augmentation was stronger in rat livers than in guinea pig livers at the high concentration of 0.1 microM PAF. However, L-
NAME
did not augment PAF-induced venoconstriction in mouse livers. In conclusion, in rat and guinea pig livers, NO may be released selectively from the pre-sinusoids in response to PAF, and then attenuate the PAF-induced pre-sinusoidal constriction. In mouse liver, PAF-induced venoconstriction is weak and not modulated by NO.
...
PMID:L-NAME augments PAF-induced venoconstriction in isolated perfused livers of rat and guinea pig, but not mouse. 1739 49
Allergy to components of the diet is followed by gut inflammation which in children, sometimes progress to mucosal lesions and
anaphylaxis
. In newborns suffering of cow's milk allergy, bloody stools, rectal bleeding and ulcerations are found. The rat systemic
anaphylaxis
is a suitable model to study the intestinal lesions associated to allergy. In the present study we used this model to investigate some mechanisms involved. We found that 15 min after antigen challenge of sensitized rats, hemorrhagic lesions develop in the small intestine. The lesions were more severe in jejunum and ileum compared to duodenum. Pretreatment of the rats with a platelet-activating factor-receptor antagonist (WEB-2170) reduced the lesions whereas inhibition of endogenous nitric oxide by l-
NAME
, greatly increased the hemorrhagic lesions and mortality. Both, lesions and mortality were reversed by l-arginine. The hemorrhagic lesions were also significantly reduced by the mast cell stabilizers, disodium cromoglycate and ketotifen as well as by neutrophils depletion (with anti-PMN antibodies) or inhibition of selectin binding (by treatment with fucoidan). Thus, the intestinal hemorrhagic lesions in this model are dependent on platelet-activating factor, mast cell granule-derived mediators and neutrophils. Endogenous nitric oxide and supplementation with l-arginine has a protective role, reducing the lesions and preventing mortality. These results contributed to elucidate mechanisms involved in intestinal lesions which could be of relevance to human small bowel injury associated to allergy.
...
PMID:Small bowel injury associated to allergy is triggered by platelet-activating factor, mast cells, neutrophils and protected by nitric oxide. 1818 53
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