Effect of 3-morpholinosydnonimine (SIN-1) and NG-nitro-l-arginine (NNA) on isolated perfused anaphylactic guinea-pig hearts

Thelen, Katrin I.; Dembińska-Kieć, A.; Pallapies, Dirk; Simmet, Th.; Peskar, Bernhard A.

doi:10.1007/bf00175475

Cited by 14 publications

(6 citation statements)

References 28 publications

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“…Indeed, inhibition of NO synthesis aggravates anaphylactic constriction of regional vasculature, such as coronary artery (27) and pulmonary circulation (23). We herein showed that NO inhibition pronounced hepatic anaphylactic venoconstriction.…”

Section: Discussionmentioning

confidence: 48%

“…With respect to the effects of NO on anaphylaxis, NO contributes to acute hypotension of anaphylaxis (20). NO also modulates anaphylaxisinduced changes in regional hemodynamics of coronary circulation (27) and pulmonary circulation (23) by serving as an endogenously released vasodilator. However, it has not been known whether NO modulates the change in hepatic hemodynamics during anaphylaxis.…”

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confidence: 99%

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NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

Ruan¹,

Shibamoto²,

Shimo³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Ruan, Zonghai, Toshishige Shibamoto, Tomohiro Shimo, Hideaki Tsuchida, Tomonobu Koizumi, and Matomo Nishio. NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver. Am J Physiol Regul Integr Comp Physiol 286: R94-R100, 2004. First published October 2, 2003 10.1152/ ajpregu.00648.2002The pathophysiology of the hepatic vascular response to anaphylaxis in guinea pig is not known. We studied effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused livers derived from guinea pigs sensitized with ovalbumin. We also determined whether nitric oxide (NO) or carbon monoxide (CO) modulates the hepatic anaphylaxis. The livers were perfused portally and recirculatingly at constant flow with diluted blood. With the use of the double-occlusion technique to estimate the hepatic sinusoidal pressure (P do), portal venous resistance (Rpv) and hepatic venous resistance (Rhv) were calculated. An antigen injection caused venoconstriction characterized by an increase in R pv greater than Rhv and was accompanied by a large liver weight gain. Pretreatment with the NO synthase inhibitor N G -nitro-L-arginine methyl ester, but not the heme oxygenase inhibitor zinc protoporphyrin IX, potentiated the antigen-induced venoconstriction by increasing both R pv and Rhv (2.2-and 1.2-fold increase, respectively). In conclusion, anaphylaxis causes both pre-and postsinusoidal constriction in isolated guinea pig livers. However, the increases in postsinusoidal resistance and Pdo cause hepatic congestion. Endogenously produced NO, but not CO, modulates these responses. hepatic circulation; antigen; double occlusion pressure; hepatic vascular resistance ANAPHYLAXIS IS AN immediate, type-1 hypersensitivity reaction that occurs after exposure of sensitized organisms and tissues to sensitizing antigen. The most common life-threatening feature of acute anaphylaxis is cardiovascular collapse and shock, although there are other life-threatening effects, including bronchospasm, angioedema, and pulmonary edema (24). Cardiovascular manifestation includes a rapid and precipitous decrease in systemic arterial pressure with a concomitant decrease in cardiac output (5). Anaphylactic hypotension is primarily caused by alterations in the systemic circulation that influence blood flow to the heart because left ventricular function is relatively well preserved during anaphylactic shock (5). Peripheral circulatory collapse is ascribed to hypovolemia, which results from a plasma volume loss. The latter could be the result of vasodilation with the peripheral pooling in largecapacity splanchnic venous beds and increased vascular permeability with a shift of intravascular fluid to the extravascular space.In canine experimental models of anaphylactic shock, congestion of livers and the upstream splanchnic organs is important in the pathogenesis of circulatory collapse. Actually, eviscerated dogs did not develop anaphylactic shock (17). Enjeti et al. (5) reported that the severity of th...

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Section: Discussionmentioning

confidence: 48%

mentioning

confidence: 99%

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

Ruan¹,

Shibamoto²,

Shimo³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The produced nitric oxide activates cGMP, which subsequently causes vasodilatation in smooth muscle cells [15] and possibly decreases contractility in myocytes [14]. In vitro studies have shown that NO functionally antagonizes the effects of the vasoconstrictors released during anaphylaxis [16] as well as that NO production might reduce some pathophysiological changes associated with anaphylaxis, except for vasodilatation [17].…”

Section: Introductionmentioning

confidence: 99%

Methylene Blue Modulates Transendothelial Migration of Peripheral Blood Cells

et al. 2013

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Vasoplegia is a severe complication after cardiac surgery. Within the last years the administration of nitric oxide synthase inhibitor methylene blue (MB) became a new therapeutic strategy. Our aim was to investigate the role of MB on transendothelial migration of circulating blood cells, the potential role of cyclic cGMP, eNOS and iNOS in this process, and the influence of MB on endothelial cell apoptosis. Human vascular endothelial cells (HuMEC-1) were treated for 30 minutes or 2 hours with different concentrations of MB. Inflammation was mimicked by LPS stimulation prior and after MB. Transmigration of PBMCs and T-Lymphocytes through the treated endothelial cells was investigated. The influence of MB upon the different subsets of PBMCs (Granulocytes, T- and B-Lymphocytes, and Monocytes) was assessed after transmigration by means of flow-cytometry. The effect of MB on cell apoptosis was evaluated using Annexin-V and Propidium Iodide stainings. Analyses of the expression of cyclic cGMP, eNOS and iNOS were performed by means of RT-PCR and Western Blot. Results were analyzed using unpaired Students T-test. Analysis of endothelial cell apoptosis by MB indicated a dose-dependent increase of apoptotic cells. We observed time- and dose-dependent effects of MB on transendothelial migration of PBMCs. The prophylactic administration of MB led to an increase of transendothelial migration of PBMCs but not Jurkat cells. Furthermore, HuMEC-1 secretion of cGMP correlated with iNOS expression after MB administration but not with eNOS expression. Expression of these molecules was reduced after MB administration at protein level. This study clearly reveals that endothelial response to MB is dose- and especially time-dependent. MB shows different effects on circulating blood cell-subtypes, and modifies the release patterns of eNOS, iNOS, and cGMP. The transendothelial migration is modulated after treatment with MB. Furthermore, MB provokes apoptosis of endothelial cells in a dose/time-dependent manner.

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“…Compared to SNP, SIN-1 appeared to be less potent and effective in raising cutaneous blood flow, which is in line with its relatively low relaxant activity in other vascular beds (Thelen et al, 1992). Further, albeit inconclusive, evidence for NO being the active entity came from the ability of methylene blue to attenuate the vasodilator response to SNP.…”

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confidence: 92%

Mediation by prostaglandins of the nitric oxide‐induced neurogenic vasodilatation in rat skin

Holzer

Jocič

Peskar

1995

British J Pharmacology

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1 Intraplantar administration of the nitric oxide (NO) donor, sodium nitroprusside (SNP), induces hyperaemia in the rat paw skin, which is in part due to release of calcitonin gene-related peptide (CGRP) from afferent nerve fibres. The present study examined whether prostaglandins or other inflammatory mediators participate in the neurogenic vasodilatation caused by SNP. Blood flow in the plantar hindpaw skin of urethane-anaesthetized rats was measured by laser Doppler flowmetry. 2 The hyperaemic responses to intraplantar administration of the NO donors SNP (150 pmol) and 3-morpholino-sydnonimine (SIN-1, 15 nmol) were attenuated by 45% and 61%, respectively, after injection of the CGRP antagonist, CGRP837 (50 nmol kg', i.v.) which did not significantly change baseline blood flow. 3 The NO synthase inhibitor N0-nitro-L-arginine methyl ester (L-NAME, 15 mg kg-', i.v.), the bradykinin antagonist Hoe-140 (100 nmol kg-1, i.v.) and the histamine antagonists, pyrilamine (2 mg kg-, i.v.) plus cimetidine (10 mg kg-', i.p.) were without effect on baseline blood flow and the vasodilatation caused by SNP.4 The cyclo-oxygenase inhibitors, indomethacin (10 mg kg-', i.p.) and flurbiprofen (5 mg kg-I, i.p.) depressed the SNP-induced hyperaemia by 65% and 42%, respectively, without altering baseline blood flow. The ability of CGRP837 to inhibit the vasodilator response to SNP was lost in indomethacintreated rats. 5 Intraplantar administration of prostaglandin E2 (PGE2, 15 pmol) evoked cutaneous vasodilatation which was attenuated by 66% after administration of CGRP837 but remained unaltered by indomethacin or L-NAME. 6 These data indicate that the neurogenic hyperaemia which in rat skin is induced by intraplantar administration of NO donors involves the formation of prostaglandins which in turn cause release of the vasodilator peptide, CGRP, from perivascular afferent nerve fibres.

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Effect of 3-morpholinosydnonimine (SIN-1) and NG-nitro-l-arginine (NNA) on isolated perfused anaphylactic guinea-pig hearts

Cited by 14 publications

References 28 publications

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver

Methylene Blue Modulates Transendothelial Migration of Peripheral Blood Cells

Mediation by prostaglandins of the nitric oxide‐induced neurogenic vasodilatation in rat skin

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