Acute ethanol exposure increases the susceptibility of the donor hearts to ischemia/reperfusion injury after transplantation in rats

Li, S; Korkmaz, Sevil; Loganathan, Sivakkanan; Weymann, Alexander; Radovits, Tamás; Barnucz, Enikő; Hirschberg, Kristóf; Hegedűs, Péter; Zhou, Yandong; Li, Tao; Páli, S; Veres, G.; Kretzler, Matthias; Szabó, G

doi:10.1055/s-0032-1332604

Cited by 11 publications

(16 citation statements)

References 7 publications

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“…Sinus node dysfunction is a common complication in the early post‐HTx setting, sometimes requiring permanent pacemaker placement, and has been linked to ischemia‐reperfusion injury . Some studies suggest alcohol increases donor heart susceptibility to this type of injury . Additionally, direct alcoholic toxicity to the intracardiac conduction system may mediate a negative chronotropic effect .…”

Section: Discussionmentioning

confidence: 99%

The effect of donor alcohol abuse on outcomes following heart transplantation

Newman

Liebo

Lowes

et al. 2019

Clinical Transplantation

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Background: Current guidelines recommend against the use of hearts from donors that abuse alcohol. We explored the effect of donor alcohol abuse (AA) on cardiac allograft function and outcomes in heart transplant (HTx) recipients. Methods:Overall, 370 HTx recipients were divided into two groups: (a) the alcoholic donor group (AD, n = 58) and (b) the non-alcoholic donor group (NAD, n = 312). Results:Recipients in the AD group had a slower heart rate (86 ± 13 vs 93 ± 13, P = 0.004) and an increased incidence of early atrial fibrillation (AF) (30% vs 11%, P = 0.003). Echocardiographic left ventricular mass was higher among alcoholic donors (171.7 ± 66.7 vs 151.6 ± 54.7, P = 0.02). This difference remained present 1 year following HTx (185 ± 43 vs 166 ± 42, P = 0.007). E/E′ was higher in the AD group (9.5 ± 3.9 vs 8.4 ± 2.9, P = 0.04) and a larger number of AD recipients had a ventilatory equivalent for VCO 2 > 34 (50% vs 31%, P = 0.04) on cardiopulmonary exercise test. There was no significant difference in rejection, cardiac allograft vasculopathy (CAV), or survival between the groups. Conclusions:Our data suggest that donor AA does not impact rejection, CAV, or intermediate-term survival, but may cause increased incidence of post-HTx AF and impaired cardiac allograft diastolic function. K E Y W O R D Satrial fibrillation, diastolic dysfunction, donor characteristics, heart transplantation

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Section: Discussionmentioning

confidence: 99%

The effect of donor alcohol abuse on outcomes following heart transplantation

Newman

Liebo

Lowes

et al. 2019

Clinical Transplantation

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“…Terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling staining. We performed terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining to detect DNA-strand breaks as previously described (20). Sections were deparaffinized with xylene and passed through decreasing concentrations of ethanol and then washed with phosphate buffered saline (PBS, ϫ1) for 3 ϫ 5 min.…”

Section: Methodsmentioning

confidence: 99%

Left ventricular pressure-volume measurements and myocardial gene expression profile in type 2 diabetic Goto-Kakizaki rats

Korkmaz‐Icöz

Lehner

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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The Goto-Kakizaki (GK) rat, a non-obese model of type 2 diabetes mellitus (T2DM), was generated by the selective inbreeding of glucose-intolerant Wistar rats. This is a convenient model for studying diabetes-induced cardiomyopathy independently from the effects of the metabolic syndrome. We investigated the myocardial functional and structural changes and underlying molecular pathomechanisms of short-term and mild T2DM. The presence of DM was confirmed by an impaired oral glucose tolerance in the GK rats compared with the age-matched nondiabetic Wistar rats. Data from cardiac catheterization showed that in GK rats, although the systolic indexes were not altered, the diastolic stiffness was increased compared with nondiabetics (end-diastolic-pressure-volume-relationship: 0.12 ± 0.04 vs. 0.05 ± 0.01 mmHg/μl, P < 0.05). Additionally, DM was associated with left-ventricular hypertrophy and histological evidence of increased myocardial fibrosis. The plasma pro-B-type natriuretic peptide, the cardiac troponin-T, glucose, and the urinary glucose concentrations were significantly higher in GK rats. Among the 125 genes surveyed using PCR arrays, DM significantly altered the expression of five genes [upregulation of natriuretic peptide precursor-A and connective tissue growth factor, downregulation of c-reactive protein, interleukin-1β, and tumor necrosis factor (TNF)-α mRNA-level]. Of the altered genes, which were evaluated by Western blot, only TNF-α protein expression was significantly decreased. The ECG recordings revealed no significant differences. In conclusion, while systolic dysfunction, myocardial inflammation, and abnormal electrical conduction remain absent, short-term and mild T2DM induce the alteration of cardiac TNF-α at both the mRNA and protein levels. Further assessments are required to reveal if TNF-α plays a role in the early stage of diabetic cardiomyopathy development.

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“…A total of 24 rats successfully underwent the experimental surgery. Successful establishment of the AMI model was confirmed by regional cyanosis of the myocardial surface, which was represented by ST-segment elevation (SPR-838; Millar Instruments, Houston, TX, USA) and analyzed using analysis software (PVAN 2.9; Millar Instruments) (20).…”

Section: Methodsmentioning

confidence: 99%

Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways

Chen

Wang

2015

Molecular Medicine Reports

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Paeoniflorin (PF) is the main active component of the commonly used Traditional Chinese Medicine peony, Paeonia Suffruticosa. PF has diverse biological functions and exhibits anti‑oxidative, anti‑inflammatory and anti‑apoptotic activity. Inducible nitric oxide synthase (iNOS) is a catalyzing enzyme that is involved in the synthesis of nitric oxide (NO). NO has an important regulatory role in the cardiovascular, immune and nervous systems. PF has previously been demonstrated to inhibit the gene expression of iNOS. The present study aimed to identify a potentially novel cytoprotective function of PF, and to elucidate its effects against myocardial ischemic damage in a rat model of acute myocardial infarction (AMI). PF was able to significantly decrease the myocardial infarct size as well as the activities of creatine kinase (CK), the MB isoenzyme of CK, lactate dehydrogenase and cardiac troponin T. In addition, in the PF‑treated groups, the expression levels of tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and nuclear factor‑κB were markedly inhibited. Furthermore, treatment with PF inhibited the activities and protein expression levels of iNOS. Decreased caspase‑3 and caspase‑9 activities were also observed in the AMI rat model treated with various doses of PF. The results of the present study indicated that the cardioprotective effects of PF may be associated with the inhibition of inflammation and iNOS signaling pathways.

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Acute ethanol exposure increases the susceptibility of the donor hearts to ischemia/reperfusion injury after transplantation in rats

Cited by 11 publications

References 7 publications

The effect of donor alcohol abuse on outcomes following heart transplantation

The effect of donor alcohol abuse on outcomes following heart transplantation

Left ventricular pressure-volume measurements and myocardial gene expression profile in type 2 diabetic Goto-Kakizaki rats

Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways

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