Guidelines for experimental models of myocardial ischemia and infarction

Lindsey, Merry L.; Bolli, Roberto; Canty, John M.; Du, Xiao Jun; Frangogiannis, Nikolaos G.; Frantz, Stefan; Gourdie, Robert G.; Holmes, Jeffrey W.; Jones, Steven P.; Kloner, Robert A.; Lefer, David J.; Liao, Ronglih; Murphy, Elizabeth; Ping, Peipei; Przyklenk, Karin; Recchia, Fabio A.; Longacre, Lisa Schwartz; Ripplinger, Crystal M.; Eyk, Jennifer E. Van; Heusch, Gerd

doi:10.1152/ajpheart.00335.2017

Cited by 420 publications

(366 citation statements)

References 327 publications

(442 reference statements)

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“…; Lindsey et al. ). Lewis rats (females: 200–280 g, 14–20 weeks; males: 200–380 g, 10–16 weeks) were obtained from the local animal facility.…”

Section: Methodsmentioning

confidence: 97%

“…All protocols were approved by the Bioethical Committee of the district of D€ usseldorf, Germany (G1413/14, G1625/17, and G1655/18). The experimental protocols, measurements of coronary flow and left ventricular pressure (LVP), quantification of infarct size, and induction of IPC and RIPC were standard (Bøtker et al 2018;Lindsey et al 2018). Lewis rats (females: 200-280 g, 14-20 weeks; males: 200-380 g, 10-16 weeks) were obtained from the local animal facility.…”

Section: Methodsmentioning

confidence: 99%

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Sex is no determinant of cardioprotection by ischemic preconditioning in rats, but ischemic/reperfused tissue mass is for remote ischemic preconditioning

et al. 2019

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We determined the impact of sex on the magnitude of cardioprotection by local and remote ischemic preconditioning ( IPC and RIPC ) and of ischemic/reperfused peripheral tissue mass on protection by RIPC . Hearts of female and male Lewis rats were excised, perfused with buffer, and underwent either IPC by 3 × 5/5 min global zero‐flow ischemia/reperfusion ( GI /R) or time‐matched perfusion ( TP ) before 30/120 min GI /R. In a second approach, anesthetized female and male Lewis rats underwent RIPC , 3 × 5/5 min ischemia/reperfusion of one or both hindlimbs (1‐ RIPC or 2‐ RIPC ), or placebo. Thirty minutes after the RIPC /placebo protocol, hearts were excised and subjected to GI /R. In female and male hearts, infarct size was less with IPC than with TP before GI /R ( IPC + GI /R female : 12 ± 5%; IPC + GI /R male : 12 ± 7% vs. TP + GI /R female : 33 ± 5%; TP + GI /R male : 37 ± 7%, P < 0.001). With 2‐ RIPC , infarct size was less than with 1‐ RIPC in female and male rat hearts, respectively (2‐ RIPC + GI /R female : 15 ± 5% vs. 1‐ RIPC + GI /R female : 22 ± 7%, P = 0.026 and 2‐ RIPC + GI /R male : 16 ± 5% vs. 1‐ RIPC + GI /R male : 22 ± 8%, P = 0.016). Infarct size after the placebo protocol and GI /R was not different between female and male hearts (36 ± 8% vs. 34 ± 5%). Sex is no determinant of IPC ‐ and RIPC ‐induced cardioprotection in isolated Lewis rat hearts. RIPC ‐induced cardioprotection is greater with greater mass of ischemic/reperfused peripheral tissue.

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“…; Lindsey et al. ). Lewis rats (females: 200–280 g, 14–20 weeks; males: 200–380 g, 10–16 weeks) were obtained from the local animal facility.…”

Section: Methodsmentioning

confidence: 97%

Section: Methodsmentioning

confidence: 99%

Sex is no determinant of cardioprotection by ischemic preconditioning in rats, but ischemic/reperfused tissue mass is for remote ischemic preconditioning

et al. 2019

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“…Of 759 mice, 422 had echocardiography and plasma or gene RT-PCR data at days 0 ( n = 161; 70 F and 91 M), 1 ( n = 38; 15 F and 23 M), 3 ( n = 46; 18 F and 28 M), and 7 ( n = 95; 47 F and 48 M) post-MI. Both MI surgeries and echocardiography were performed according to established guidelines [49, 51]. …”

Section: Materials and Methods (Detailed Methods In Supplemental Matementioning

confidence: 99%

LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling

et al. 2018

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Sex differences in heart failure development following myocardial infarction (MI) are not fully understood. We hypothesized that differential MI signaling could explain variations in outcomes. Analysis of the mouse heart attack research tool 1.0 (422 mice; young = 5.4 ± 0.1; old = 23.3 ± 0.1 months of age) was used to dissect MI signaling pathways, which was validated in a new cohort of mice (4.8 ± 0.2 months of age); and substantiated in humans. Plasma collected at visit 2 from the MI subset of the Jackson Heart Study (JHS; a community-based study consisting of middle aged and older adults of African ancestry) underwent glycoproteomics grouped by outcome: (1) heart failure hospitalization after visit 2 (n = 3 men/12 women) and (2) without hospitalization through 2012 (n = 24 men/21 women). Compared to young male mice, the infarct region of young females had fewer, but more efficient tissue clearing neutrophils with reduced pro-inflammatory gene expression. Apolipoprotein (Apo) F, which acts upstream of the liver X receptors/retinoid X receptor (LXR/RXR) pathway, was elevated in the day 7 infarcts of old mice compared to young controls and was increased in both men and women with heart failure. In vitro, Apo F stimulated CD36 and peroxisome proliferator-activated receptor (PPAR)γ activation in male neutrophils to turn off NF-κB activation and stimulate LXR/RXR signaling to initiate resolution. Female neutrophils were desensitized to Apo F and instead relied on thrombospondin-1 stimulation of CD36 to upregulate AMP-activated protein kinase, resulting in an overall better wound healing strategy. With age, female mice were desensitized to LXR/RXR signaling, resulting in enhanced interleukin-6 activation, a finding replicated in the JHS community cohort. This is the first report to uncover sex differences in post-MI neutrophil signaling that yielded better outcomes in young females and worse outcomes with age.Electronic supplementary materialThe online version of this article (10.1007/s00395-018-0699-5) contains supplementary material, which is available to authorized users.

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“…All surgeries were performed between 10 am and 2 pm to avoid circadian rhythm-associated irregularities according to recently published guidelines for experimental models of myocardial ischemia and infarction. 14 What Are the Clinical Implications?…”

Section: Murine Model Of Myocardial Ischemia Reperfusionmentioning

confidence: 99%

Platelet Serotonin Aggravates Myocardial Ischemia/Reperfusion Injury via Neutrophil Degranulation

et al. 2019

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BACKGROUND: Platelets store large amounts of serotonin that they release during thrombus formation or acute inflammation. This facilitates hemostasis and modulates the inflammatory response. METHODS:Infarct size, heart function, and inflammatory cell composition were analyzed in mouse models of myocardial reperfusion injury with genetic and pharmacological depletion of platelet serotonin. These studies were complemented by in vitro serotonin stimulation assays of platelets and leukocytes in mice and men, and by measuring plasma serotonin levels and leukocyte activation in patients with acute coronary syndrome. RESULTS:Platelet-derived serotonin induced neutrophil degranulation with release of myeloperoxidase and hydrogen peroxide (H 2 O 2 ) and increased expression of membrane-bound leukocyte adhesion molecule CD11b, leading to enhanced inflammation in the infarct area and reduced myocardial salvage. In patients hospitalized with acute coronary syndrome, plasmatic serotonin levels correlated with CD11b expression on neutrophils and myeloperoxidase plasma levels. Longterm serotonin reuptake inhibition-reported to protect patients with depression from cardiovascular events-resulted in the depletion of platelet serotonin stores in mice. These mice displayed a reduction in neutrophil degranulation and preserved cardiac function. In line, patients with depression using serotonin reuptake inhibition, presented with suppressed levels of CD11b surface expression on neutrophils and lower myeloperoxidase levels in blood. CONCLUSIONS:Taken together, we identify serotonin as a potent therapeutic target in neutrophil-dependent thromboinflammation during myocardial reperfusion injury.

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Guidelines for experimental models of myocardial ischemia and infarction

Cited by 420 publications

References 327 publications

Sex is no determinant of cardioprotection by ischemic preconditioning in rats, but ischemic/reperfused tissue mass is for remote ischemic preconditioning

Sex is no determinant of cardioprotection by ischemic preconditioning in rats, but ischemic/reperfused tissue mass is for remote ischemic preconditioning

LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling

Platelet Serotonin Aggravates Myocardial Ischemia/Reperfusion Injury via Neutrophil Degranulation

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