1991
DOI: 10.1159/000235376
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Effect of Nitric Oxide Generators on Ischemia-Reperfusion Injury and Histamine Release in Isolated Perfused Guinea Pig Heart

Abstract: In an ischemia-reperfusion model obtained in isolated perfused guinea pig heart by means of a double ligature of the left anterior descending coronary artery, the reperfusion of the ischemic myocardium leads to a release of lactate dehydrogenase and histamine, related to a decrease in the microdensitometry of cardiac mast cells and to a tissue calcium overload. The perfusion of the heart with L-arginine and with nitric oxide donors significantly reduces the release of histamine, the loss of mast cell metachrom… Show more

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Cited by 16 publications
(17 citation statements)
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“…It has been implicated in a number of physiological processes, including vasodilatation, smooth muscle relaxation and inhibition of platelet aggregation-adhesion. It also inhibits the neutrophil infiltration, release of histamine, degranulation of mast cells and accumulation of intracellular calcium [15][16][17]. The inhibition of mast cell degranulation, ischemia formation and platelet adhesion/ aggregation leads to a decrease in adhesion formation [4,[18][19][20][21].…”
Section: Discussionmentioning
confidence: 99%
“…It has been implicated in a number of physiological processes, including vasodilatation, smooth muscle relaxation and inhibition of platelet aggregation-adhesion. It also inhibits the neutrophil infiltration, release of histamine, degranulation of mast cells and accumulation of intracellular calcium [15][16][17]. The inhibition of mast cell degranulation, ischemia formation and platelet adhesion/ aggregation leads to a decrease in adhesion formation [4,[18][19][20][21].…”
Section: Discussionmentioning
confidence: 99%
“…NO modulates platelet adhesion and aggregation, leukocyte adhesion, endothelin generation and plasminogen activator enzymatic function [4,5,7,22]. It was suggested that neutrophil adherence is prevented by NO since it was shown that the use of NOS inhibitors (N·-t-BOC-ˆ-nitro-L-arginine) increased neutrophil adherence in cat mesentery [5,23].…”
Section: Discussionmentioning
confidence: 99%
“…The use of NO donors may be a reasonable therapeutic approach to reducing mast cell-dependent inflammation. It has been reported that NO have a beneficial role in the prevention of postischemic tissue injury in various organs including intestine, heart, lung and kidney [7][8][9][10]26]. The inhibition of mast cell degranulation, ischemia formation and platelet adhesion/aggregation leads to a decrease in adhesion formation [16,17,27,28].…”
Section: Discussionmentioning
confidence: 99%
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“…Several reports suggest that mast cell stabilizers such as disodium cromoglycate and lodoxamide tromethamine diminish acute I/R damage in both rat and rabbit hearts (19,27,37) possibly via inhibition of TNF-␣ release (11), whereas other investigators found that antigen-evoked "mast cell depletion" or lodoxamide tromethamine has no effect on I/R or hypoxia/reoxygenation injury in the rat heart (8, 36). The possible role of mast cell-derived histamine in acute ischemia as well as ischemic preconditioning has been discussed; however, several investigators have concluded that mast cell-derived histamine is not involved (3,22,37).In addition to their possible role in preconditioning and acute ischemic injury, mast cells have been proposed to play a role in postinfarction myocardial remodeling. Mast cell accumulation was observed in areas of collagen deposition in a canine model of I/R (9), in the subepicardium of infarcted and non-infarcted regions in rats (7), and in human hearts displaying ischemic as well as idiopathic cardiomyopathy (29).…”
mentioning
confidence: 99%