Fluorochemical emulsion APE-LM substantially improves cardiac preservation

1992 ◽  
Vol 263 (3) ◽  
pp. H730-H739 ◽  
Author(s):  
L. D. Segel ◽  
J. M. Minten ◽  
F. K. Schweighardt
Keyword(s):  
Cardiac Tissue ◽  
Contractile Function ◽  
Egg Yolk ◽  
Coronary Perfusion ◽  
Low Viscosity ◽  
Rat Hearts ◽  
Reperfusion Period ◽  
Salutary Effect ◽  
Emulsion Particle

We determined the efficacy of a novel fluorochemical emulsion for long-term hypothermic preservation of hearts. Rat hearts were preserved for 12 h at 12 degrees C with use of continuous low-pressure coronary perfusion with one of three oxygenated media (n = 6 hearts/groups): an "extracellular" crystalloid solution; APE-LM, a novel fluorochemical emulsion of perfluoroperhydrophenanthrene in egg yolk phospholipid; and FC-43, the Fluosol-43 (Oxypherol) fluorochemical emulsion of perfluorotributylamine in Pluronic F68. The emulsion media contained the same components as the crystalloid medium. All three media contained 0.5% albumin. An isolated working heart perfusion system was used to quantify the function of preserved hearts and controls (fresh hearts, n = 6). The APE-LM-preserved hearts were not significantly different from control hearts in contractile function, output, and energetics during a 4-h 37 degrees C reperfusion period. The control and APE-LM-preserved hearts had significantly better performance than crystalloid- and FC-43-preserved hearts. All preserved hearts gained fluid during preservation. The edema of APE-LM-preserved hearts, but not that of the other two preserved groups, was reversed during 37 degrees C reperfusion. These data provide the first evidence that a unique fluorochemical emulsion improves long-term preservation of cardiac tissue and produces significantly better recovery of cardiac function after preservation. This salutary effect was specifically associated with APE-LM emulsion and may result from its high O2 capacity, its biologically compatible emulsifier, and its superior physical properties, which include very small emulsion particle size (0.1–0.15 micron), low viscosity, and minimal toxicity.

Iron storage sites in the myocardium as revealed by cytohistochemistry

1988 ◽  
Vol 46 ◽  
pp. 394-395
Author(s):  
M. Ashraf ◽  
F. Thompson ◽  
S. Miki ◽  
P. Srivastava
Keyword(s):  
Cardiac Tissue ◽  
Coronary Perfusion ◽  
Intracellular Iron ◽  
Ether Anesthesia ◽  
Intense Staining ◽  
Iron Storage ◽  
Thin Sections ◽  
Rat Hearts ◽  
Cacodylate Buffer ◽  
Made In

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).

Downregulation of ventricular contractile function during early ischemia is flow but not pressure dependent

1998 ◽  
Vol 275 (5) ◽  
pp. H1520-H1523 ◽  
Author(s):  
Miao-Xiang He ◽  
H. Fred Downey
Keyword(s):  
Coronary Artery ◽  
Perfusion Pressure ◽  
Contractile Function ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Rat Hearts ◽  
Myocardial Contractile Force ◽  
Myocardial Contractile ◽  
Artery Obstruction

The mechanism responsible for the abrupt fall in myocardial contractile function following coronary artery obstruction is unknown. The “vascular collapse theory” hypothesizes that the fall in coronary perfusion pressure after coronary artery obstruction is responsible for contractile failure during early ischemia. To test the role of vascular collapse in downregulating myocardial contractile force at the onset of ischemia, coronary flow of isolated rat hearts was abruptly decreased by 50, 70, 85, and 100% of baseline, and subsequent changes in coronary perfusion pressure and ventricular function were recorded at 0.5-s intervals. At 1.5 s after flow reductions ranging from 50 to 100%, decreases in contractile function did not differ, although perfusion pressure varied significantly from 45 ± 1 to 20 ± 2 mmHg. When function fell to 50% of baseline, perfusion pressures ranged from 35 ± 0.5 to 2.5 ± 1 mmHg for flow reductions ranging from 50 to 100%. Identical contractile function at widely differing coronary perfusion pressures is incompatible with the vascular collapse theory.

Ghrelin induces vasoconstriction in the rat coronary vasculature without altering cardiac peptide secretion

2004 ◽  
Vol 287 (4) ◽  
pp. H1522-H1529 ◽  
Author(s):  
Chris J. Pemberton ◽  
Heikki Tokola ◽  
Zsolt Bagi ◽  
Akos Koller ◽  
Juhani Pöntinen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Natriuretic Peptide ◽  
Cardiac Tissue ◽  
Contractile Function ◽  
Isolated Heart ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Neonatal Cardiomyocytes ◽  
Peptide Secretion ◽  
Coronary Arterioles

We administered ghrelin, a novel growth hormone-releasing hormone, to isolated perfused rat hearts, coronary arterioles, and cultured neonatal cardiomyocytes to determine its effects on coronary vascular tone, contractility, and natriuretic peptide secretion and gene expression. We also determined cardiac levels of ghrelin and whether the heart is a source of the circulating peptide. Ghrelin dose dependently increased coronary perfusion pressure (44 ± 9%, P < 0.01), constricted isolated coronary arterioles (12 ± 2%, P < 0.05), and significantly enhanced the pressure-induced myogenic tone of arterioles. These effects were blocked by diltiazem, an L-type Ca2+ channel blocker, and bisindolylmaleimide (Bis), a protein kinase C (PKC) inhibitor. Interestingly, coinfusion of ghrelin with diltiazem completely restored myocardial contractile function that was decreased 30 ± 3% ( P < 0.01) by diltiazem alone. In contrast, combination of ghrelin with diltiazem or Bis did not significantly alter atrial natriuretic peptide (ANP) secretion, which was decreased 40% ( P < 0.01) and 50% ( P < 0.05) by these agents alone, respectively. Administration of ghrelin to cultured cardiomyocytes had no effect on ANP or B-type natriuretic peptide secretion or gene expression. Detectable amounts of low-molecular-weight ghrelin were present in cardiac tissue extracts but not in isolated heart perfusate. Thus we provide the first evidence that ghrelin has a coronary vasoconstrictor action that is dependent on Ca2+ and PKC. Furthermore, the data obtained from diltiazem infusion suggest that ghrelin has a role in regulation of contractility when L-type Ca2+ channels are blocked. Finally, the observation that immunoreactive ghrelin is found in cardiac tissue suggests the presence of a local cardiac ghrelin system.

scholarly journals 3D ultrasound coronarography: first proof of concept study on isolated beating rat hearts

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
O Demeulenaere ◽  
P Mateo ◽  
P Sandoval ◽  
O Villemain ◽  
M Tanter ◽  
...  
Keyword(s):  
Contrast Agents ◽  
Flow Velocity ◽  
Coronary Flow ◽  
3D Ultrasound ◽  
Frame Rate ◽  
Doppler Imaging ◽  
Coronary Perfusion ◽  
Blood Flows ◽  
Flow Reserve ◽  
Rat Hearts

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Bettencourt Foundation Background/Introduction We demonstrated recently that Ultrafast ultrasound Doppler imaging can image the intramyocardial coronary circulation in beating hearts of large animals and patients [1]. Yet, ultrasound spatial resolution remains limited by wave physics and coronaries smaller than ∼100 µm could not be imaged. Ultrasound Localization Microscopy (ULM) [2] was recently introduced to tackle this issue and exploit the micrometric localization of microbubble contrast agents at ultrafast frame rate in order to image blood flows in micrometer vessels. Purpose The objective of this work was to demonstrate that 3D ultrafast ultrasound with contrast agents can provide the full 3D mapping of the coronary microcirculation with quantitative flow velocity on a beating rat heart. Methods Acquisitions were performed on ex vivo rat hearts (n = 5) with retrograde perfusion (Langendorff model). A flow of a Krebs–Henseleit solution mixed with a diluted microbubbles solution (0.22%) was perfused at controlled pressure into the coronary arteries (between 5 and 15 mL/min). We used a 32 × 32 elements, 8-MHz matrix-array ultrasound transducer connected to a 1024-channel programmable ultrasound scanner. An ultrafast Doppler imaging sequence consisting of 9 plane waves was transmitted at a PRF of 20 kHz during 270 ms and repeated 40 times. After beamforming and SVD clutter filtering, the microbubbles were localized and tracked in 3D. Flow velocity were mapped at baseline and after infusion of Adenosine (10e-5 µMol) at constant coronary perfusion pressure (120 mm Hg). Eventually, the hearts were fixed using formaldehyde perfusion and imaged by µCT after injection of radio opaque agent. Results We successfully imaged the coronary blood flows of entire rat hearts. It revealed the entire vasculature from large main coronaries arteries (cross section up to 1 mm) to small arterioles (smaller than 40 µm). Coronary flow velocities ranged from [1 – 50] cm/s depending on the arteries diameter. Velocity estimates were validated in vitro in tubes of Ø0.58mm and were in good agreement with theoretical values of a Poiseuille’s flow (relative ratio of 10% for maximum velocities). After Adenosine infusion, perfusion flow rates increased 102% ± 50% (p &lt; 0.05) on average. Eventually, anatomy revealed by 3D ultrasound coronarography was in accordance with the anatomy revealed by the µCT. Conclusion(s) We demonstrated the feasibility of 3D ultrasound coronarography on isolated beating rat hearts. This technique has the potential to become a novel imaging tool to investigate the coronary micro-circulation and quantify non-invasively the Coronary Flow Reserve (CFR). Abstract Figure. Ultrasound coronarography

scholarly journals Cardiac MRI and Myocardial Injury in COVID-19: Diagnosis, Risk Stratification and Prognosis

Diagnostics ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 130
Author(s):  
Saagar K. Sanghvi ◽  
Logan S. Schwarzman ◽  
Noreen T. Nazir
Keyword(s):  
Risk Stratification ◽  
Myocardial Injury ◽  
Cardiac Tissue ◽  
Contractile Function ◽  
Imaging Modality ◽  
Acute Myocarditis ◽  
Myocardial Inflammation ◽  
Critical Data ◽  
Non Invasive ◽  
Risk Of Exposure

Myocardial injury is a common complication of the COVID-19 illness and is associated with a worsened prognosis. Systemic hyperinflammation seen in the advanced stage of COVID-19 likely contributes to myocardial injury. Cardiac magnetic resonance imaging (CMR) is the preferred imaging modality for non-invasive evaluation in acute myocarditis, enabling risk stratification and prognostication. Modified scanning protocols in the pandemic setting reduce risk of exposure while providing critical data regarding cardiac tissue inflammation and fibrosis, chamber remodeling, and contractile function. The growing use of CMR in clinical practice to assess myocardial injury will improve understanding of the acute and chronic sequelae of myocardial inflammation from various pathological etiologies.

scholarly journals Endothelial dysfunction in obstructive sleep apnea patients

2021 ◽  
Author(s):  
Michał Harańczyk ◽  
Małgorzata Konieczyńska ◽  
Wojciech Płazak
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Endothelial Dysfunction ◽  
Right Ventricular ◽  
Contractile Function ◽  
Sleep Apnea Syndrome ◽  
Apnea Hypopnea Index ◽  
Endothelin 1 ◽  
Obstructive Sleep

Abstract Purpose Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for cardiovascular diseases. The aim of the study was to assess the influence of OSAS on endothelial dysfunction and thrombosis biomarkers and to evaluate the effect of treatment with continuous positive airway pressure (CPAP) on biomarker levels. Methods NT-proBNP, sICAM-1, endothelin-1, von Willebrand factor, D-dimers, and thrombin-antithrombin complex (TAT) were measured in 50 patients diagnosed with moderate-to-severe OSAS. All patients underwent transthoracic echocardiography, and 38 months after the inclusion, 16 CPAP users and 22 non-CPAP users were reassessed. Results Sleep-related indices of apnea-hypopnea index (AHI) and mean SpO2 were associated with higher sICAM-1 levels (AHI < 30: 7.3 ± 4.7 vs. AHI ≥ 30: 19.5 ± 19.4 mg/ml, p = 0.04; SpO2 ≥ 90%: 11.9 ± 9.3 vs. SpO2 < 90%: 23.6 ± 25.8, p = 0.04). sICAM-1 levels were significantly higher in obese patients, particularly with BMI ≥ 40. Plasma levels of TAT were significantly correlated with the increased right ventricular size (right ventricular diameter ≤ 37 mm: 0.86 ± 0.70 vs. > 37 mm: 1.96 ± 1.20 ng/ml, p = 0.04). Endothelin-1 levels were higher in patients with decreased right ventricular function (right ventricle TDI-derived S′ ≥ 12 cm/s: 11.5 ± 10.9 vs. < 12 cm/s: 26.0 ± 13.2 pg/ml, p = 0.04). An increase in NT-proBNP was related to impaired parameters of the right ventricular contractile function. There were no correlations between long-term CPAP therapy and the levels of biomarkers. Conclusion Severe OSAS influences endothelial damage as manifested by an increase in sICAM-1 levels. Changes in right ventricular structure and function, observed mainly in patients with higher TAT and endothelin-1 levels, are also manifested by an increase in NT-proBNP levels. Long-term CPAP treatment does not seem to influence biomarkers in patients with moderate-to-severe OSAS, which may help to explain the lack of influence of CPAP on cardiovascular risk reduction.

scholarly journals Innovative Biotechnology for Generation of Cardiac Tissue

2021 ◽  
Vol 11 (12) ◽  
pp. 5603
Author(s):  
Greta Ionela Barbulescu ◽  
Florina Maria Bojin ◽  
Valentin Laurentiu Ordodi ◽  
Iacob Daniel Goje ◽  
Taddeus Paul Buica ◽  
...  
Keyword(s):  
Stem Cells ◽  
Electric Field ◽  
Cardiac Tissue ◽  
Sodium Dodecyl ◽  
Human Mesenchymal Stem Cells ◽  
Coronary Perfusion ◽  
Decellularized Extracellular Matrix ◽  
Life Saving ◽  
Cellular Debris ◽  
End Stage

Heart transplantation remains the only curative treatment for end-stage heart failure. This life-saving option continues to be limited by the low number of organ donors, graft rejection and adverse effects of immunosuppressants. Engineering bioartificial hearts from acellular native-derived scaffolds and stem cells has gained attention because of its potential to overcome these limitations. In this study, rat hearts (n = 20) were decellularized by means of coronary perfusion with 1% sodium dodecyl sulfate (SDS) in a modified Langendorff device. The electrical field behavior of the SDS molecule was studied and it was assumed that when applying an alternating current, the exposure time of the tissue to the detergent might decrease. To repopulate the decellularized extracellular matrix (ECM), human mesenchymal stem cells (hMSCs) were used, induced to differentiate into cardiomyocytes (CMs) with 5-azacytidine (5-aza). The results showed no cellular debris and an intact ECM following decellularization. Decellularization in the presence of an electric field proved to be faster, decreasing the potential risk of ECM damage due to the detergent. After cell seeding and culturing of eight scaffolds with hMSCs, the recellularization process was analyzed using optic microscopy (OM), which showed cells suggestive for CMs. This study presents a novel and efficient decellularization protocol using an electric field and suggests that hMSCs can be useful in the generation of a bioartificial heart.

scholarly journals Artificial Cardiac Muscle with or without the Use of Scaffolds

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Yifei Li ◽  
Donghui Zhang
Keyword(s):  
Tissue Engineering ◽  
Cardiovascular Diseases ◽  
Cardiac Tissue ◽  
Contractile Function ◽  
Rapid Development ◽  
Treatment Options ◽  
Cardiac Tissue Engineering ◽  
Hydrogel Scaffold ◽  
Fibrous Matrix ◽  
Advantages And Disadvantages

During the past several decades, major advances and improvements now promote better treatment options for cardiovascular diseases. However, these diseases still remain the single leading cause of death worldwide. The rapid development of cardiac tissue engineering has provided the opportunity to potentially restore the contractile function and retain the pumping feature of injured hearts. This conception of cardiac tissue engineering can enable researchers to produce autologous and functional biomaterials which represents a promising technique to benefit patients with cardiovascular diseases. Such an approach will ultimately reshape existing heart transplantation protocols. Notable efforts are accelerating the development of cardiac tissue engineering, particularly to create larger tissue with enhanced functionality. Decellularized scaffolds, polymer synthetics fibrous matrix, and natural materials are used to build robust cardiac tissue scaffolds to imitate the morphological and physiological patterns of natural tissue. This ultimately helps cells to implant properly to obtain endogenous biological capacity. However, newer designs such as the hydrogel scaffold-free matrix can increase the applicability of artificial tissue to engineering strategies. In this review, we summarize all the methods to produce artificial cardiac tissue using scaffold and scaffold-free technology, their advantages and disadvantages, and their relevance to clinical practice.

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