Ischaemia-induced Osborn waves.
Ontology highlight
ABSTRACT:
SUBMITTER: Cha KC
PROVIDER: S-EPMC9036072 | biostudies-literature | 2022 Apr
REPOSITORIES: biostudies-literature
Publications
Ischaemia-induced Osborn waves.
Cha Kyoung-Chul KC Ahn Sung Gyun SG Hwang Sung Oh SO
European heart journal. Case reports 20220405 4
Similar Datasets
Project description:Heart rates during ischaemia and reperfusion are possible determinants of reperfusion arrhythmias. We used ivabradine, a selective If current inhibitor, to assess the effects of heart rate reduction (HRR) during ischaemia-reperfusion on reperfusion ventricular arrhythmias and assessed potential anti-arrhythmic mechanisms by optical mapping. Five groups of rat hearts were subjected to regional ischaemia by left anterior descending artery occlusion for 8min followed by 10min of reperfusion: (1) Control n=10; (2) 1?M of ivabradine perfusion n=10; (3) 1?M of ivabradine+5Hz atrial pacing throughout ischaemia-reperfusion n=5; (4) 1?M of ivabradine+5Hz pacing only at reperfusion; (5) 100?M of ivabradine was used as a 1ml bolus upon reperfusion. For optical mapping, 10 hearts (ivabradine n=5; 5Hz pacing n=5) were subjected to global ischaemia whilst transmembrane voltage transients were recorded. Epicardial activation was mapped, and the rate of development of ischaemia-induced electrophysiological changes was assessed. HRR observed in the ivabradine group during both ischaemia (195±11bpm vs. control 272±14bpm, p<0.05) and at reperfusion (168±13bpm vs. 276±14bpm, p<0.05) was associated with reduced reperfusion ventricular fibrillation (VF) incidence (20% vs. 90%, p<0.05). Pacing throughout ischaemia-reperfusion abolished the protective effects of ivabradine (100% VF), whereas pacing at reperfusion only partially attenuated this effect (40% VF). Ivabradine, given as a bolus at reperfusion, did not significantly affect VF incidence (80% VF). Optical mapping experiments showed a delay to ischaemia-induced conduction slowing (time to 50% conduction slowing: 10.2±1.3min vs. 5.1±0.7min, p<0.05) and to loss of electrical excitability in ivabradine-perfused hearts (27.7±4.3min vs. 14.5±0.6min, p<0.05). Ivabradine administered throughout ischaemia and reperfusion reduced reperfusion VF incidence through HRR. Heart rate during ischaemia is a major determinant of reperfusion arrhythmias. Heart rate at reperfusion alone was not a determinant of reperfusion VF, as neither a bolus of ivabradine nor pacing immediately prior to reperfusion significantly altered reperfusion VF incidence. This anti-arrhythmic effect of heart rate reduction during ischaemia may reflect slower development of ischaemia-induced electrophysiological changes.
| S-EPMC3654199 | biostudies-literature
Project description:Background and purposeCytochrome c when released from mitochondria into cytosol triggers assembly of the apoptosome resulting in caspase activation. Recent evidence suggests that reduced cytochrome c is unable to activate the caspase cascade. In this study, we investigated whether a chemical reductant of cytochrome c, N,N,N',N'-tetramethylphenylene-1,4-diamine (TMPD), which we have previously shown to block cytochrome c-induced caspase activation, could prevent ischaemia-induced apoptosis in the rat perfused heart.Experimental approachThe Langendorff-perfused rat hearts were pretreated with TMPD and subjected to stop-flow ischaemia or ischaemia/reperfusion. The activation of caspases (measured as DEVD-p-nitroanilide-cleaving activity), nuclear apoptosis of cardiomyocytes (measured by dUTP nick end labelling assay), mitochondrial and cytosolic levels of cytochrome c (measured spectrophotometrically and by elisa), and reperfusion-induced necrosis (measured as the activity of creatine kinase released into perfusate) were assessed.Key resultsWe found that perfusion of the hearts with TMPD strongly inhibited ischaemia- or ischaemia/reperfusion-induced activation of caspases and partially prevented nuclear apoptosis in cardiomyocytes. TMPD did not prevent ischaemia- or ischaemia/reperfusion-induced release of cytochrome c from mitochondria into cytosol. TMPD also inhibited ischaemia/reperfusion-induced necrosis.Conclusions and implicationsThese results suggest that TMPD or related molecules might be used to protect the heart against damage induced by ischaemia/reperfusion. The mechanism of this protective effect of TMPD probably involves electron reduction of cytochrome c (without decreasing its release) which then inhibits the activation of caspases.
| S-EPMC3051385 | biostudies-literature
Project description:We present measurements of laser-induced shockwave pressure rise time in liquids on a sub-nanosecond scale, using custom-designed single-mode fiber optic hydrophone. The measurements are aimed at the study of the shockwave generation process, helping to improve the effectiveness of various applications and decrease possible accidental damage from shockwaves. The developed method allows measurement of the fast shockwave rise time as close as 10 µm from an 8 µm sized laser-induced plasma shockwave source, significantly improving the spatial and temporal resolution of the pressure measurement over other types of hydrophones. The spatial and temporal limitations of the presented hydrophone measurements are investigated theoretically, with actual experimental results agreeing well with the predictions. To demonstrate the capabilities of the fast sensor, we were able to show that the shockwave rise time is linked to liquid viscosity exhibiting logarithmic dependency in the low viscosity regime (from 0.4 cSt to 50 cSt). Additionally, the shockwave rise time dependency on propagation distance close to the source in water was investigated, with shock wave rise times measured down to only 150 ps. It was found that at short propagation distances in water halving the shock wave peak pressure results in the rise time increase by approximately factor of 1.6. These results extend the understanding of shockwave behavior in low viscosity liquids.
| S-EPMC9974415 | biostudies-literature
Project description:RNF4, a poly-SUMO-specific E3 ubiquitin ligase, is associated with protein degradation, DNA damage repair and tumour progression. However, the effect of RNF4 in cardiomyocytes remains to be explored. Here, we identified the alteration of RNF4 from ischaemic hearts and oxidative stress-induced apoptotic cardiomyocytes. Upon myocardial infarction (MI) or H2 O2 /ATO treatment, RNF4 increased rapidly and then decreased gradually. PML SUMOylation and PML nuclear body (PML-NB) formation first enhanced and then degraded upon oxidative stress. Reactive oxygen species (ROS) inhibitor was able to attenuate the elevation of RNF4 expression and PML SUMOylation. PML overexpression and RNF4 knockdown by small interfering RNA (siRNA) enhanced PML SUMOylation, promoted p53 recruitment and activation and exacerbated H2 O2 /ATO-induced cardiomyocyte apoptosis which could be partially reversed by knockdown of p53. In vivo, knockdown of endogenous RNF4 via in vivo adeno-associated virus infection deteriorated post-MI structure remodelling including more extensive interstitial fibrosis and severely fractured and disordered structure. Furthermore, knockdown of RNF4 worsened ischaemia-induced cardiac dysfunction of MI models. Our results reveal a novel myocardial apoptosis regulation model that is composed of RNF4, PML and p53. The modulation of these proteins may provide a new approach to tackling cardiac ischaemia.
| S-EPMC7520334 | biostudies-literature
Project description:Electric corona discharge in a multi-phase system results in complex electro-hydrodynamic phenomena. We observed unconventional shock wave propagation on an oil thin film sprayed over a polymer-coated conductor. A hair-thin single shock wave arose when the high voltage bias of an overhung steel needle was abruptly removed. However, such solitary waves possess neither interference nor reflection properties commonly known for ordinary waves, and also differ from the solitons in a canal or an optical fiber. We also observed time-retarded movement for dispersed oil droplets at various distances from the epicenter which have no physical contact, as if a wave propagating on a continuous medium. Such a causality phenomenon for noncontact droplets to move resembling wave propagation could not be possibly described by the conventional surface wave equation. Our systematic studies reveal a mechanism involving oil surface charges driven by reminiscent electric fields in the air when the needle bias is suddenly removed.
| S-EPMC6292859 | biostudies-literature
Project description:Diverse bioinspired antifouling strategies have demonstrated effective fouling-resistant properties with good biocompatibility, sustainability, and long-term activity. However, previous studies on bioinspired antifouling materials have mainly focused on material aspects or static architectures of nature without serious consideration of kinetic topographies or dynamic motion. Here, we propose a magnetically responsive multilayered composite that can generate coordinated, undulatory topographical waves with controlled length and time scales as a new class of dynamic antifouling materials. The undulatory surface waves of the dynamic composite induce local and global vortices near the material surface and thereby sweep away foulants from the surface, fundamentally inhibiting their initial attachment. As a result, the dynamic composite material with undulating topographical waves provides an effective means for efficient suppression of biofilm formation without surface modification with chemical moieties or nanoscale architectures.
| S-EPMC6884415 | biostudies-literature
Project description:We present here a combined theoretical and experimental investigation on effective excitation of microcantilever by using photoacoustic waves. The photoacoustic waves arose from a vibrating Al foil induced by an intensity-modulated laser. We demonstrate that, superior to photothermal excitation, this new configuration avoids direct heating of the microcantilever, thus minimizing undesired thermal effects on the vibration of microcantilever, while still keeps the advantage of being a remote, non-contact excitation method. We also measured the vibration amplitude of the microcantilever as a function of distance between the microcantilever and the Al foil and found that the amplitudes decay gradually according to the inverse distance law. This method is universal and can be adopted in bio-microelectromechanical systems (BioMEMs) for the detection of small signals where detrimental thermal effects must be avoided.
| S-EPMC4728694 | biostudies-other
Project description:AimsAnti-platelet agents, such as dipyridamole, have several clinical benefits for peripheral artery disease with the speculation of angiogenic potential that could preserve ischaemic tissue viability, yet the effect of dipyridamole on ischaemic arteriogenesis or angiogenesis is unknown. Here we test the hypothesis that dipyridamole therapy augments arteriolar vessel development and function during chronic ischaemia.Methods and resultsMice were treated with 200 mg/kg dipyridamole twice daily to achieve therapeutic plasma levels (0.8-1.2 microg/mL). Chronic hindlimb ischaemia was induced by permanent femoral artery ligation followed by measurement of tissue perfusion using laser Doppler blood flow along with quantification of vascular density, cell proliferation, and activation of nitric oxide (NO) metabolism. Dipyridamole treatment quickly restored ischaemic hindlimb blood flow, increased vascular density and cell proliferation, and enhanced collateral artery perfusion compared with control treatments. The beneficial effects of dipyridamole on blood flow and vascular density were dependent on NO production as dipyridamole did not augment ischaemic tissue reperfusion, vascular density, or endothelial cell proliferation in endothelial NO synthase (eNOS)-deficient mice. Blood and tissue nitrite levels were significantly higher in dipyridamole-treated mice compared with controls and eNOS(-/-) mice, verifying increased NO production that was regulated in a PKA-dependent manner.ConclusionDipyridamole augments nitrite/NO production, leading to enhanced arteriogenesis activity and blood perfusion in ischaemic limbs. Together, these data suggest that dipyridamole can augment ischaemic vessel function and restore blood flow, which may be beneficial in peripheral artery disease.
| S-EPMC2819839 | biostudies-literature
Project description:Acute myocardial ischaemia and reperfusion (I-R) are major causes of ventricular arrhythmias in patients with a history of coronary artery disease. Ursodeoxycholic acid (UDCA) has previously been shown to be antiarrhythmic in fetal hearts. This study was performed to investigate if UDCA protects against ischaemia-induced and reperfusion-induced arrhythmias in the adult myocardium, and compares the effect of acute (perfusion only) versus prolonged (2 weeks pre-treatment plus perfusion) UDCA administration. Langendorff-perfused adult Sprague-Dawley rat hearts were subjected to acute regional ischaemia by ligation of the left anterior descending artery (10 min), followed by reperfusion (2 min), and arrhythmia incidence quantified. Prolonged UDCA administration reduced the incidence of acute ischaemia-induced arrhythmias (p = 0.028), with a reduction in number of ventricular ectopic beats during the ischaemic phase compared with acute treatment (10 ± 3 vs 58 ± 15, p = 0.036). No antiarrhythmic effect was observed in the acute UDCA administration group. Neither acute nor prolonged UDCA treatment altered the incidence of reperfusion arrhythmias. The antiarrhythmic effect of UDCA may be partially mediated by an increase in cardiac wavelength, due to the attenuation of conduction velocity slowing (p = 0.03), and the preservation of Connexin43 phosphorylation during acute ischaemia (p = 0.0027). The potential antiarrhythmic effects of prolonged UDCA administration merit further investigation.
| S-EPMC7499428 | biostudies-literature
Project description:HIF-2 represents a tissue-specific isoform of the hypoxia-inducible factors (HIFs) which regulate oxygen homeostasis in the cell. In acute oxygen deficiency, HIF transcription factors ensure the timely restoration of adequate oxygen supply. Particularly in medical conditions such as stroke, which have a high mortality risk due to ischaemic brain damage, rapid recovery of oxygen supply is of extraordinary importance. Nevertheless, the endogenous mechanisms are often not sufficient to respond to severe hypoxic stress with restoring oxygenation and fail to protect the tissue. Herein, we analysed murine neurospheres without functioning HIF-2α and found that special importance in the differentiation of neurons can be attributed to HIF-2 in the brain. Other processes, such as cell migration and signal transduction of different signalling pathways, appear to be mediated to some extent via HIF-2 and illustrate the function of HIF-2 in brain remodelling. Without hypoxic stress, HIF-2 in the brain presumably focuses on the fine-tuning of the neural network. However, a therapeutically increase of HIF-2 has the potential to regenerate or replace destroyed brain tissue and help minimize the consequences of an ischaemic stroke.
| S-EPMC8302505 | biostudies-literature