Inducible nitric oxide synthase activation after ischemia/reperfusion contributes to myocardial dysfunction and extent of infarct size in rabbits: evidence for a late phase of nitric oxide-mediated reperfusion injury

Wildhirt, Stephen M.; Weismueller, Susanne; Schulze, C.; Conrad, Nicole; Kornberg, Arno; Reichart, Bruno

doi:10.1016/s0008-6363(99)00080-2

Cited by 92 publications

(83 citation statements)

References 51 publications

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“…Inflammatory marker levels, such as CRP, IL-1 and IL-6, increase after PTCA (Kloner et al 1991;Balligand et al 1994;Azar et al 1997;Matsumara et al 1998;Wildhirt et al 1999).…”

Section: Discussionmentioning

confidence: 99%

“…An increase in NO synthesis and inducible nitric oxide synthase (iNOS) activity decreases myocardial blood flow and tissue oxygenation, causing ischemia in the myocytes (Balligand et al 1994;Wildhirt et al 1999;Sumeray et al 2000). In experimental ischemia models, inhibition of NOS was shown to prevent tissue damage (Camussi et al 1991;Seo et al 1995;Halliwil et al 2000;Szwed et al 2001aSzwed et al , 2001b.…”

Section: Discussionmentioning

confidence: 99%

“…When given before cardiologic interventions, TMZ has been found to improve ventricular function without altering hemodynamics, limit infarct area, and reduce both platelet aggregation and leukocyte migration to the area (Fabiani et al 1992;Steg et al 2001). Preliminary clinical studies tend to confirm a direct benefit of a metabolic approach with TMZ in left ventricular dysfunction (Wildhirt et al 1999;Zhao et al 2000;Belardinelli and Purcaro 2001). A significant improvement in ejection fraction was also found with TMZ, compared with placebo, in a group of patients undergoing PTCA (Brottier et al 1990;Birand et al 1998).…”

Section: Discussionmentioning

confidence: 99%

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Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Kuralay

Altekin

Yazlar

et al. 2006

Tohoku J. Exp. Med.

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Percutaneous transluminal coronary angioplasty (PTCA) has been recognized as a reliable treatment procedure for acute reversible ischemia and reperfusion. Ischemic reperfusion cycle in PTCA leads to the systemic inflammation and extensive tissue injury by the production of reactive oxygen species including nitric oxide (NO) radicals. In patients with coronary artery disease, undergoing PTCA, the effects of trimetazidine (TMZ), a piperazine-derivative anti-anginal drug, were studied on several indirect markers of systemic inflammatory response: tumor necrosis factor-α (TNF-α ), C-reactive protein (CRP) and NO products (nitrite and nitrate). Patients (n = 11 each group) were untreated or pre-treated with TMZ (20 mg per orally three times a day), begun three days prior to PTCA, and marker levels were measured before the start of TMZ therapy (baseline), just before PTCA (0 hr), and 4, 24, and 48 hrs after PTCA. The baseline levels of markers were not significantly different between the untreated and pre-treated patients. In contrast, all parameters were lower in the TMZtreated group than those in the matched control group in the pre-and post-angioplasty periods. Interestingly, in the TMZ group, CRP and nitrite levels were significantly lower than in the control group at each time point of the pre-and post-angioplasty periods, but the TNF-α levels were significantly decreased only in the post-angioplasty period. Preprocedural treatment with oral TMZ for three days significantly suppressed the elevation of inflammatory markers before and shortly after PTCA. We suggest the usefulness of TMZ in preventing inflammatory cardiovascular events after PTCA.trimetazidine; percutaneous transluminal coronary angioplasty; C-reactive protein; nitric oxide; tumor necrosis factor-α .

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“…Inflammatory marker levels, such as CRP, IL-1 and IL-6, increase after PTCA (Kloner et al 1991;Balligand et al 1994;Azar et al 1997;Matsumara et al 1998;Wildhirt et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Kuralay

Altekin

Yazlar

et al. 2006

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…Oxidative stress also induces nitric oxide synthase (iNOS) expression, which aggravates tubular injury by supplying additional NO for ONOO 2 formation in the presence of excess ROS. 26,27 mRNA expression for renal iNOS was increased in WT mice but significantly attenuated in CD47 2/2 mice ( Figure 8C). BM to engraft WT mice has been documented previously, 29 putatively from augmented recipient phagocytosis of donor BM cells in vivo.…”

Section: Cd47mentioning

confidence: 96%

Activation of Parenchymal CD47 Promotes Renal Ischemia-Reperfusion Injury

Rogers

Thomson

Isenberg

2012

Journal of the American Society of Nephrology

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Ischemia-reperfusion injury (IRI) contributes to decreased allograft function and allograft rejection in transplanted kidneys. Thrombospondin-1 is a stress protein typically secreted in response to hypoxia and the ligand activator for the ubiquitously expressed receptor CD47. The function of activated CD47 in IRI remains completely unknown. Here, we found that both CD47 and its ligand thrombospondin-1 were upregulated after renal IRI in mice. CD47-knockout mice were protected against renal dysfunction and tubular damage, suggesting that the development of IRI requires intact CD47 signaling. Chimeric CD47-knockout mice engrafted with wild-type hematopoietic cells had significantly lower serum creatinine and less tubular damage than wild-type controls after IRI, suggesting that CD47 signaling in parenchymal cells predominantly mediates renal damage. Treatment with a CD47-blocking antibody protected mice from renal dysfunction and tubular damage compared with an isotype control. Taken together, these data imply that CD47 on parenchymal cells promotes injury after renal ischemia and reperfusion. Therefore, CD47 blockade may have therapeutic potential to prevent or suppress ischemia-reperfusion-mediated damage.

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“…9,10 In addition, in a recent clinical trial, infliximab-which is used to manage diseases such as rheumatoid arthritis and Crohn's disease and dermatologic, chronic ocular and neurological diseases-was indicated as an alternative conservative therapy. [11][12][13] However, no study has investigated the effects of infliximab on I/R damage in rat kidneys. Therefore, this study was undertaken to examine whether infliximab shows a protective effect in experimental rat models with I/Rinduced renal damage.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Infliximab on Ischemia/Reperfusion-Induced Damage in Rat Kidney

et al. 2012

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Objective: To investigate the protective effect of infliximab on ischemia-reperfusion (I/R) injury of the rat kidney. Methods: Twenty-eight male Wistar albino rats were divided into four groups: sham-operated, I/R, I/R with infliximab administered before ischemia [I/R þ infliximab (bi)], and I/R with infliximab administered before reperfusion [I/R þ infliximab (br)]. After a right nephrectomy to produce damage, the left renal vessels were occluded for 60 min, followed by 24-h reperfusion in rats. Changes in the rat kidney were observed by measuring the tissue levels of malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), and superoxide dismutase (SOD) and by evaluating hematoxylin-eosin (H&E)-stained and periodic acid-Schiff (PAS) sections. Results: The MDA and MPO levels in the I/R group were significantly higher than in the other groups (p < 0.05), and the SOD and GSH levels in the I/R þ infliximab (bi) and I/R þ infliximab (br) groups were significantly higher than in the I/R group (p < 0.05). However, histological examination revealed that the I/R þ infliximab (bi) group and the I/R þ infliximab (br) group had significantly fewer tubular changes and interstitial inflammatory cell infiltration than the I/R group. Conclusion: These results show that infliximab may protect against I/R injury in the rat I/R model.

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Inducible nitric oxide synthase activation after ischemia/reperfusion contributes to myocardial dysfunction and extent of infarct size in rabbits: evidence for a late phase of nitric oxide-mediated reperfusion injury

Cited by 92 publications

References 51 publications

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Activation of Parenchymal CD47 Promotes Renal Ischemia-Reperfusion Injury

Protective Effect of Infliximab on Ischemia/Reperfusion-Induced Damage in Rat Kidney

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