scholarly journals Influence of Low Concentrations of Carbon Monoxide on Metabolism of Isolated Heart under Conditions of Ischemia-Reperfusion

2021 ◽  
Vol 6 (6) ◽  
pp. 230-238
Author(s):  
S. P. Beschasnyi ◽  
◽  
Ye. M. Lysenko
Keyword(s):  
Carbon Monoxide ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Volumetric Flow Rate ◽  
Myocardial Damage ◽  
Mouse Heart ◽  
Triphenyltetrazolium Chloride ◽  
Isolated Hearts ◽  
Low Concentrations ◽  
Vasoconstrictor Effect

The purpose of the study was to determine the effect of different concentrations of carbon monoxide on the metabolism of isolated mice hearts. Materials and methods. To elucidate the effect of low concentrations of carbon monoxide on the myocardium, we performed retrograde perfusion of isolated hearts of laboratory mice with Krebs-Henseleit solution, which was saturated with carbon monoxide for 5, 10, and 30 minutes. We then determined how different concentrations of carbon monoxide affected coronary volumetric flow rate, myocardial glucose and calcium uptake, creatinine release, and aspartate aminotransferase release. During perfusion, R-wave amplitude and R-R interval were measured using an electrocardiograph. To determine the effect of ischemia on the heart muscle during perfusion with solutions of different concentrations, we measured the area of the affected myocardium after staining with 2,3,5-triphenyltetrazolium chloride. Results and discussion. After these studies, it was found that different concentrations of carbon monoxide had a dose-dependent effect on the isolated mouse heart. However, the dependence of the effects does not follow the pattern «lowest concentration – lowest effect». At the same time, an increase in concentration did not mean an increase in adverse effects on the myocardium. Even on the contrary, the smallest concentration led to increased signs of ischemic myocardial damage. In particular, the use of the solution, through which carbon monoxide was passed for 5 minutes, caused vasoconstrictor effect during perfusion. At the end of reperfusion, vasoconstrictor effect was observed after using a solution through which carbon monoxide was passed for 10 minutes. Increased glucose uptake was observed in the group with 30-minute carbon monoxide permeation against the background of the minimal myocardial creatinine release. In this group there was also a decrease in Ca2+ loss at the beginning of reperfusion (immediately after ischemia). The above phenomenon explains the least degree of ischemic myocardial damage in the isolated mouse heart. The obtained data should be expanded. Since it is difficult to accurately determine the dose of carbon monoxide, then the use of donor compounds is promising. Such compounds include CORM-2 and CORM-3. Under physiological conditions, they decompose in a controlled manner, releasing a specific amount of carbon monoxide. Conclusion. The obtained results indicate that at different concentrations of carbon monoxide can differently influence different structures of cardiomyocyte: at one concentration it binds to calcium channels, other concentrations influence ion channels of plasma membrane, which can explain all these dependencies

scholarly journals The continuing evolution of the Langendorff and ejecting murine heart: new advances in cardiac phenotyping

2012 ◽  
Vol 303 (2) ◽  
pp. H156-H167 ◽  
Author(s):  
Ronglih Liao ◽  
Bruno K. Podesser ◽  
Chee Chew Lim
Keyword(s):  
Vascular Reactivity ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
In Vitro Assays ◽  
Mouse Heart ◽  
Heart Preparation ◽  
The Impact

The isolated retrograde-perfused Langendorff heart and the isolated ejecting heart have, over many decades, resulted in fundamental discoveries that form the underpinnings of our current understanding of the biology and physiology of the heart. These two experimental methodologies have proven invaluable in studying pharmacological effects on myocardial function, metabolism, and vascular reactivity and in the investigation of clinically relevant disease states such as ischemia-reperfusion injury, diabetes, obesity, and heart failure. With the advent of the genomics era, the isolated mouse heart preparation has gained prominence as an ex vivo research tool for investigators studying the impact of gene modification in the intact heart. This review summarizes the historical development of the isolated heart and provides a practical guide for the establishment of the Langendorff and ejecting heart preparations with a particular emphasis on the murine heart. In addition, current applications and novel methods of recording cardiovascular parameters in the isolated heart preparation will be discussed. With continued advances in methodological recordings, the isolated mouse heart preparation will remain physiologically relevant for the foreseeable future, serving as an integral bridge between in vitro assays and in vivo approaches.

scholarly journals Role of ischemic preconditioning in cardioprotective mechanisms of mCRP deposited myocardium in a rat model

2020 ◽  
Author(s):  
Eun Na Kim ◽  
Jae-Sung Choi ◽  
Chong Jai Kim ◽  
So Ra Kim ◽  
Ki-Bong Kim ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Mrna Expression ◽  
Ischemic Preconditioning ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Study Groups ◽  
Area At Risk ◽  
Triphenyltetrazolium Chloride

AbstractThe deposition of monomeric C-reactive protein (mCRP) in the myocardium aggravates ischemia-reperfusion injury (IRI) and myocardial infarction. Ischemic preconditioning (IPC) is known to protect the myocardium against IRI. We evaluated the effects of IPC on mCRP-deposited myocardium due to IRI in a rat model. Myocardial IRI was produced by ligation of the coronary artery. Direct IPC was applied before IRI using multiple short direct occlusions of the coronary artery. CRP was infused intravenously after IRI. The study groups included the following: sham (n=3), IRI only (n=5), IRI+CRP (n=9), and IPC+IRI+CRP (n=6) groups. The infarct area and area at risk were assessed using Evans blue and 2,3,5-triphenyltetrazolium chloride (2,3,5-TTC) staining. Additionally, mCRP immunostaining and interleukin (IL)-6 mRNA reverse transcriptase-polymerase chain reaction (RT-PCR) were performed. In the IRI+CRP group, the infarcted area, mCRP deposition, and IL-6 mRNA expression were higher than those in the IRI only group. However, in the IPC+IRI+CRP group, the infarction (20% vs. 34% p=0.085) and mCRP myocardial deposition (21% vs. 44%, p=0.026) were lower and IL-6 mRNA expression was higher than those in the IRI+CRP group (fold change, 407 vs. 326, p=0.808), although this was not statistically significant. IPC has cardioprotective effects against myocardial damage caused by mCRP deposition. This protective effect is related to the increase in IL-6 mRNA expression.

Carbon monoxide increases inducible NOS expression that mediates CO-induced myocardial damage during ischemia-reperfusion

2015 ◽  
Vol 308 (7) ◽  
pp. H759-H767 ◽  
Author(s):  
Grégory Meyer ◽  
Lucas André ◽  
Adrien Kleindienst ◽  
François Singh ◽  
Stéphane Tanguy ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Myocardial Damage ◽  
Environmental Pollutant ◽  
No Synthase ◽  
No Production ◽  
Cellular Mechanisms ◽  
Mortality And Morbidity ◽  
Before And After

We investigated the role of inducible nitric oxide (NO) synthase (iNOS) on ischemic myocardial damage in rats exposed to daily low nontoxic levels of carbon monoxide (CO). CO is a ubiquitous environmental pollutant that impacts on mortality and morbidity from cardiovascular diseases. We have previously shown that CO exposure aggravates myocardial ischemia-reperfusion (I/R) injury partly because of increased oxidative stress. Nevertheless, cellular mechanisms underlying cardiac CO toxicity remain hypothetical. Wistar rats were exposed to simulated urban CO pollution for 4 wk. First, the effects of CO exposure on NO production and NO synthase (NOS) expression were evaluated. Myocardial I/R was performed on isolated perfused hearts in the presence or absence of S-methyl-isothiourea (1 μM), a NOS inhibitor highly specific for iNOS. Finally, Ca2+ handling was evaluated in isolated myocytes before and after an anoxia-reoxygenation performed with or without S-methyl-isothiourea or N-acetylcystein (20 μM), a nonspecific antioxidant. Our main results revealed that 1) CO exposure altered the pattern of NOS expression, which is characterized by increased neuronal NOS and iNOS expression; 2) cardiac NO production increased in CO rats because of its overexpression of iNOS; and 3) the use of a specific inhibitor of iNOS reduced myocardial hypersensitivity to I/R (infarct size, 29 vs. 51% of risk zone) in CO rat hearts. These last results are explained by the deleterious effects of NO and reactive oxygen species overproduction by iNOS on diastolic Ca2+ overload and myofilaments Ca2+ sensitivity. In conclusion, this study highlights the involvement of iNOS overexpression in the pathogenesis of simulated urban CO air pollution exposure.

One-day Hypothermic Preservation of Isolated Hearts with Halothane Improves Cardiac Function Better than Low Calcium

1995 ◽  
Vol 83 (5) ◽  
pp. 1065-1077 ◽  
Author(s):  
David F. Stowe ◽  
Helmut Habazettl ◽  
Bernhard M. Graf ◽  
John P. Kampine ◽  
Zeljko J. Bosnjak
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Negative Inotropic Effect ◽  
Protective Effects ◽  
Isolated Hearts ◽  
Hypothermic Preservation ◽  
Normothermic Perfusion ◽  
Heart Study ◽  
Better Than

Abstract Background Halothane exerts a potent negative inotropic effect on the heart and mimics many of the cardiac effects of lowered extracellular CaCl2. Reduced slow inward Calcium2+ current and sarcoplasmic reticular effects on intracellular Calcium2+ are likely involved. The authors reported previously that halothane protects against hypoxic and ischemia reperfusion injury in isolated hearts. The aim of this isolated heart study was to compare protective effects of halothane and low CaCl sub 2 (0.5 mM) administered during 1 day of hypothermic perfusion on return of normothermic perfusion.

Hydrogen sulfide contributes to cardioprotection during ischemia–reperfusion injury by opening KATP channels

2007 ◽  
Vol 85 (12) ◽  
pp. 1248-1253 ◽  
Author(s):  
Zhifei Zhang ◽  
Haixia Huang ◽  
Ping Liu ◽  
Chaoshu Tang ◽  
Jun Wang
Keyword(s):  
Cardiac Myocytes ◽  
Ischemia Reperfusion Injury ◽  
Heart Function ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Katp Channels ◽  
Open Probability ◽  
Isolated Hearts ◽  
Heart Perfusion ◽  
Myocardial Ischemia Reperfusion

The present study was undertaken to investigate the protective effect of H2S against myocardial ischemia–reperfusion (I/R) injury and its possible mechanism by using isolated heart perfusion and patch clamp recordings. Rat isolated hearts were Langendorff-perfused and subjected to a 30-minute ischemia insult followed by a 30-minute reperfusion. The heart function was assessed by measuring the LVDP, ±dP/dtmax, and the arrhythmia score. The results showed that the treatment of hearts with a H2S donor (40 μmol/L NaHS) during reperfusion resulted in significant improvement in heart function compared with the I/R group (LVDP recovered to 85.0% ± 6.4% vs. 35.0% ± 6.1%, +dP/dtmax recovered to 80.9% ± 4.2% vs. 43.0% ± 6.4%, and –dP/dtmax recovered to 87.4% ± 7.3% vs. 53.8% ± 4.9%; p < 0.01). The arrhythmia scores also improved in the NaHS group compared with the I/R group (1.5 ± 0.2 vs. 4.0 ± 0.4, respectively; p < 0.001). The cardioprotective effect of NaHS during reperfusion could be blocked by an ATP-sensitive potassium channel (KATP) blocker (10 μmol/L glibenclamide). In single cardiac myocytes, NaHS increased the open probability of KATP channels from 0.07 ± 0.03 to 0.15 ± 0.08 after application of 40 μmol/L NaHS and from 0.07 ± 0.03 to 0.36 ± 0.15 after application of 100 μmol/L NaHS. These findings provide the first evidence that H2S increases the open probability of KATP in cardiac myocytes, which may be responsible for cardioprotection against I/R injury during reperfusion.

Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent

2002 ◽  
Vol 282 (2) ◽  
pp. H547-H555 ◽  
Author(s):  
Johanna T. A. Meij ◽  
Farah Sheikh ◽  
Sarah K. Jimenez ◽  
Peter W. Nickerson ◽  
Elissavet Kardami ◽  
...  
Keyword(s):  
T Cell ◽  
Myocardial Injury ◽  
Cardiac Myocyte ◽  
Cardiac Tissue ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Fgf Receptor ◽  
T Cell Infiltration

Fibroblast growth factor-2 (FGF-2) is cardioprotective when added exogenously, stimulates cardiac myocyte proliferation, and is a mediator of tissue repair after injury. Furthermore, transgenic (TG) mice overexpressing FGF-2 in cardiac muscle demonstrate increased resistance to injury in an isolated heart model of ischemia-reperfusion. We investigated how increasing the endogenous FGF-2 levels in the heart affects the extent of myocardial damage induced by isoproterenol in vivo. Histopathological evaluation of hearts after intraperitoneal injection of isoproterenol yielded significantly higher scores for myocardial damage in FGF-2 TG lines compared with non-TG mice. After 1 day, FGF-2 TG mouse hearts displayed more cellular infiltration correlating with increased tissue damage. Immunostaining of non-TG and FGF-2 TG mouse hearts showed the presence of leukocytes in the infiltrate, including T cells expressing FGF receptor-1. Treatment of mice with T cell suppressors cyclosporin A and anti-CD3ε significantly decreased the level of myocardial injury observed after isoproterenol and equalized the histopathology scores in FGF-2 TG and non-TG hearts. These data demonstrate a direct T cell involvement in the response to isoproterenol-induced injury in vivo. Moreover, the findings indicate that the exacerbation of myocardial damage in FGF-2 TG mice was dependent on T cell infiltration, implicating FGF-2 in the inflammatory response seen in cardiac tissue after injury in vivo.

scholarly journals Ad5-spike COVID-19 vaccine does not aggravate heart damage after ischemic injury

2021 ◽  
Author(s):  
Shanshan Gu ◽  
Zhongyan Chen ◽  
Xiangfu Meng ◽  
Ge Liu ◽  
He Xu ◽  
...  
Keyword(s):  
At Risk ◽  
Recombinant Adenovirus ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Adenovirus Type ◽  
Spike Protein ◽  
Systematic Evaluation ◽  
Mouse Heart ◽  
Heart Damage

Abstract Hopes for a COVID-19 vaccine are now a reality. The spike protein of SARS-CoV-2, which majorly binds to the host receptor ACE2 for cell entry, is used by most of the COVID-19 vaccine candidates as a choice of antigen. ACE2 is highly expressed in the heart and is known to be protective in multiple organs. Interaction of spike with ACE2 has been reported to reduce ACE2 expression and affect ACE2-mediated signal transduction in the heart. However, whether a spike-encoding vaccine will aggravate myocardial damage after a heart attack via affecting ACE2 remains unclear. Therefore, for patients with or at risk of heart diseases, questions arise around the safety of the spike-based vaccines. Here, we demonstrate that ACE2 is up-regulated and protective in the injured mouse heart after myocardial ischemia/reperfusion (I/R). Infecting human cardiomyocyte, smooth muscle cells, endothelial cells, and cardiac fibroblasts with a recombinant adenovirus type-5 vectored COVID-19 vaccine expressing the spike protein (AdSpike) does not affect cell survival and cardiomyocyte function, whether the cells are subjected to hypoxia-reoxygenation injury or not. This observation is further confirmed in human engineered heart tissues. Furthermore, AdSpike vaccination does not aggravate heart damage in wild-type or humanized ACE2 mice after I/R injury, even at a dose that is ten-fold higher as used in human. This study represents the first systematic evaluation of the safety of a leading COVID-19 vaccine under a disease context and may provide important information to ensure maximal protection from COVID-19 in patients with or at risk of heart diseases.

Study of nickel-molybdenum catalysts for methanation of carbon monoxide

1980 ◽  
Vol 45 (3) ◽  
pp. 783-790 ◽  
Author(s):  
Petr Taras ◽  
Milan Pospíšil
Keyword(s):  
Carbon Monoxide ◽  
Catalytic Activity ◽  
Mixed Oxides ◽  
Minor Component ◽  
Fast Neutrons ◽  
Scanning Calorimetry ◽  
Low Concentrations ◽  
Γ Rays ◽  
Molybdenum Catalysts ◽  
Kinetics Of

Catalytic activity of nickel-molybdenum catalysts for methanation of carbon monoxide and hydrogen was studied by means of differential scanning calorimetry. The activity of NiMoOx systems exceeds that of carrier-free nickel if x < 2, and is conditioned by the oxidation degree of molybdenum, changing in dependence on the composition in the region Mo-MoO2. The activity of the catalysts is adversely affected by irradiation by fast neutrons, dose 28.1 Gy, or by γ rays using doses in the region 0.8-52 kGy. The system is most susceptible to irradiation in the region of low concentrations of the minor component (about 1 mol.%). The dependence of changes in catalytic activity of γ-irradiated samples on the dose exhibits a maximum in the range of 2-5 kGy. The changes in catalytic activity are stimulated by the change of reactivity of the starting mixed oxides, leading to different kinetics of their reduction and modification of their adsorption properties. The irradiation of the catalysts results in lowered concentration of the active centres for the methanation reaction.

scholarly journals Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Qt Interval ◽  
Troponin I ◽  
Morphological Changes ◽  
Carbon Monoxide Poisoning ◽  
Myocardial Damage ◽  
Qt Dispersion ◽  
Ecg Changes ◽  
Corrected Qt Interval ◽  
Logistic Analysis

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

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