scholarly journals Cardiac functions of Osteichthyes.

Dobutsu seiri ◽  
1989 ◽  
Vol 6 (3) ◽  
pp. 154-161 ◽  
Author(s):  
Kenji NANBA ◽  
Kazumasa UEMATSU
Keyword(s):  
Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 563
Author(s):  
Magali Seguret ◽  
Eva Vermersch ◽  
Charlène Jouve ◽  
Jean-Sébastien Hulot

Cardiac tissue engineering aims at creating contractile structures that can optimally reproduce the features of human cardiac tissue. These constructs are becoming valuable tools to model some of the cardiac functions, to set preclinical platforms for drug testing, or to alternatively be used as therapies for cardiac repair approaches. Most of the recent developments in cardiac tissue engineering have been made possible by important advances regarding the efficient generation of cardiac cells from pluripotent stem cells and the use of novel biomaterials and microfabrication methods. Different combinations of cells, biomaterials, scaffolds, and geometries are however possible, which results in different types of structures with gradual complexities and abilities to mimic the native cardiac tissue. Here, we intend to cover key aspects of tissue engineering applied to cardiology and the consequent development of cardiac organoids. This review presents various facets of the construction of human cardiac 3D constructs, from the choice of the components to their patterning, the final geometry of generated tissues, and the subsequent readouts and applications to model and treat cardiac diseases.


2013 ◽  
Vol 62 (18) ◽  
pp. C46-C47
Author(s):  
Adem Adar ◽  
Abdulkadir Kırış ◽  
Yılmaz Bülbül ◽  
Hüseyin Bektaş ◽  
Sercan Okutucu ◽  
...  

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
H A Awad ◽  
M Z Mahmoud ◽  
M S Aboelwafa ◽  
A M Shabana ◽  
B M Shehata ◽  
...  

Abstract We report the use of Levosimendan, calcium sensitizer, inodilator in a neonate with post-operative refractory cardiogenic shock. Currently, no data are available on the use of levosimendan in newborns outside the cardiosurgical setting. A 38-week neonate -with isolated exomphalos major-presented post-operatively with pulmonary hypertension, refractory cardiogenic shock (inspite of receiving, a bolus of 10ml/kg, Dopamine and Dobutamine 15µg/kg/min, Adrenaline up to 1mg/Kg/min, Noradrenaline 0.5mg/Kg/min, Terlipressin 20µg/Kg/hour, Milrinone 25µg/Kg/min) and arrhythmia (supraventricular tachycardia). Levosimendan was introduced as an intravenous infusion with an initial rate of 0.1 up to 0.2µg/Kg/min in addition to Noradrenaline 1µg/Kg/min, Dopamine 15µg/Kg/min and Furosemide infusion 0.1mg/Kg/hour. The patient improved evidenced by normalization of vital signs and restoration of perfusion with better cardiac functions by echocardiography. Conclusion: Levosimendan has positive inotropic, lusitropic and vasodilating effects for the treatment of heart failure yet further studies in neonates are still required.


2014 ◽  
Vol 7 (2) ◽  
pp. 111-115 ◽  
Author(s):  
Juliana Ivanova ◽  
Yordanka Gluhcheva ◽  
Sonja Arpadjan ◽  
Mariana Mitewa

ABSTRACT Cadmium (Cd) is a well-known nephrotoxic agent. Cd-induced renal dysfunction has been considered as one of the causes leading to the development of hypertension. The correlation between Cd concentration in blood and urine and cardiovascular diseases has been discussed in many epidemiological studies. A therapy with chelating agents is utilized for the treatment of toxic metal intoxication. Herein we present novel information indicating that monensin (applied as tetraethylammonium salt) is a promising chelating agent for the treatment of Cd-induced renal and cardiac dysfunction. The study was performed using the ICR mouse model. Adult ICR male mice were divided into three groups with six animals in each group: control (received distilled water and food ad libitum for 28 days); Cd-intoxicated (treated orally with 20 mg/kg b.w. Cd(II) acetate from day 1 to day 14 of the experimental protocol), and monensin treated group (intoxicated with Cd(II) acetate as described for the Cd-intoxicated group followed by oral treatment with 16 mg/kg b.w. tetraethylammonium salt of monensic acid for 2 weeks). Cd intoxication of the animals resulted in an increase of the organ weight/body weight indexes. Cd elevated significantly creatinine and glucose level in serum. Monensin treatment improved the organ weight/body weight ratios. The therapy of the Cd-intoxicated animals with monensin ameliorated the creatinine and glucose level in serum and decreased the concentration of the toxic metal ions in the heart and kidneys by 54 % and 64 %, respectively


2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Venkata N Garikipati ◽  
Prasanna Krishnamurthy ◽  
Suresh K Verma ◽  
Alexandra R Mackie ◽  
Erin E Vaughan ◽  
...  

We hypothesized that IL-10 regulates miR-375 signaling in EPCs to enhance their survival and function in ischemic myocardium after MI. miR-375 knock down EPC were transplanted intramyocardially after induction of MI. Mice receiving EPC treated with miR-375 inhibitor showed increased number of GFP+EPCs retention that was associated with reduced EPC apoptosis in the myocardium. The engraftment of EPC into the vascular structures and the associated capillary density was significantly higher in miR-375-treated mice. The above findings further correlated with reduced infarct size, fibrosis and enhanced LV function (echocardiography) in miR-375 knock down EPC group as compared to scrambled EPC. Our in vitro studies revealed that the knockdown of miR-375 enhanced EPC proliferation, migration; tube formation ability and inhibited cell apoptosis, while the up-regulation of miR-375 with the mimic had the opposite effects. In addition, we found that miR-375 negatively regulates the expression of 3-phosphoinositide-dependent protein kinase 1 (PDK1) by directly targeting the 3'UTR of the PDK1 transcript. Interestingly, EPC isolated from IL-10-deficient mice has elevated basal levels of miR-375 and exhibited poor proliferation and tube formation ability where as miR-375 knock down in EPC isolated from IL-10 deficient mice attenuated these effects. Furthermore, transplantation of miR-375 knock down IL-10 deficient EPC after MI resulted in attenuated cardiac functions compared to scramble IL-10 deficient EPCs. Taken together, our studies suggest that IL-10 regulated miR-375 enhances EPC survival and function, associated with efficient myocardial repair via activation of PDK-1/AKT signaling cascades.


2018 ◽  
Vol 4 (11) ◽  
pp. eaat9365 ◽  
Author(s):  
Junnan Tang ◽  
Jinqiang Wang ◽  
Ke Huang ◽  
Yanqi Ye ◽  
Teng Su ◽  
...  

We engineered a microneedle patch integrated with cardiac stromal cells (MN-CSCs) for therapeutic heart regeneration after acute myocardial infarction (MI). To perform cell-based heart regeneration, cells are currently delivered to the heart via direct muscle injection, intravascular infusion, or transplantation of epicardial patches. The first two approaches suffer from poor cell retention, while epicardial patches integrate slowly with host myocardium. Here, we used polymeric MNs to create “channels” between host myocardium and therapeutic CSCs. These channels allow regenerative factors secreted by CSCs to be released into the injured myocardium to promote heart repair. In the rat MI model study, the application of the MN-CSC patch effectively augmented cardiac functions and enhanced angiomyogenesis. In the porcine MI model study, MN-CSC patch application was nontoxic and resulted in cardiac function protection. The MN system represents an innovative approach delivering therapeutic cells for heart regeneration.


2018 ◽  
Vol 36 (11) ◽  
pp. 1205-1210
Author(s):  
Didem Arman ◽  
Secil Ercin ◽  
Sevilay Topcuoğlu ◽  
Ayşem Kaya ◽  
Taner Yavuz ◽  
...  

Objective The present study aimed to assess the global oxidant and antioxidant status in infants born to preeclamptic mothers and their correlation with cardiac functions. Study Design We compared 40 infants born to preeclamptic mothers with 40 premature infants born to normotensive mothers. We assessed the relationship between echocardiographic measurements and total antioxidant capacity (TAC) and total oxidant status (TOS) values. Results In the study group, TAC, TOS, and oxidative stress index (OSI) levels were significantly higher in the cord blood (p = 0.03, 0.04, and 0.039, respectively) than in the control group. We did not observe any correlation between echocardiographic measurements and TAC, TOS, and OSI levels in infants born to preeclamptic mothers. Conclusion Compared with the control group, despite higher TAC levels in infants born to preeclamptic mothers, concurrent elevated OSI levels reveal that the oxidant–antioxidant balance is disturbed in favor of oxidants. Furthermore, the findings of this study suggest that echocardiographic parameters are unaffected by the oxidant status.


2000 ◽  
Vol 278 (1) ◽  
pp. H106-H116 ◽  
Author(s):  
Rafael Rubio ◽  
Guillermo Ceballos

Coronary flow regulates cardiac functions, and it has been suggested that endothelial membrane glycosylated proteins are the primary shear stress mechanosensors. Our hypothesis was that if these proteins are the sensors for flow, then intracoronary perfusion of lectins or specific antibodies should differentially depress coronary flow-enhanced responses of different parenchymal cell types such as auricular-ventricular (A-V) nodal cells (dromotropic effect), contractile myocytes (inotropic effect), and junctional Purkinje-muscle cells (spontaneous ventricular rhythm). The coronary flow stimulatory effects on A-V delay and spontaneous ventricular rhythm were selectively depressed by six of eight lectins. None of the lectins depressed the coronary flow inotropic effect. Antibodies against endothelial surface proteins, αvβ5-integrin and sialyl-Lewisb glycan, depressed the dromotropic but not the inotropic effects of coronary flow, whereas the vascular cell adhesion molecule 1 antibody had no effect on the dromotropic, but enhanced the inotropic, effect. The fact that lectins and antibodies differentially depressed regional coronary flow effects suggests that there is a chemical distinctiveness in their intravascular endothelial cell surfaces. However, nonselective cross-linking of endothelial glycocalyx proteins with 2,000-kDa dextran-aldehyde or vitronectin indistinctively depressed the dromotropic and inotropic effects of coronary flow. These results indicate that coronary flow-induced stress acts on specific structures located in the capillary intravascular membrane glycocalyx.


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