Thrombolysis, the only Optimally Rapid Reperfusion Treatment
Published on: 23rd June, 2017
OCLC Number/Unique Identifier: 7286427398
Thrombolysis with tissue plasminogen activator (tPA) has been plagued by inadequate efficacy and a high risk of intracranial hemorrhage (ICH), which led to its replacement by procedures like percutaneous coronary intervention (PCI) whenever possible. Since this requires hospitalization, it is time-consuming, and compromising salvage of brain tissue and myocardium. Thrombolysis is the only first-line treatment that can provide sufficiently timely treatment for optimal recovery of organ function. However, for this potential to be realized, its efficacy and safety must be significantly improved over the current method. By adopting the sequential, synergistic fibrinolytic paradigm of the endogenous system, already verified by a clinical trial, this becomes possible. The endogenous system’s function is evidenced by the fibrinolytic product D-dimer that is invariably present in blood, and which increases >20-fold in the presence of thromboembolism. This system uses tPA to initiate lysis, which is then completed by the other fibrin-specific activator prourokinase (proUK). Since tPA and proUK in combination are synergistic in fibrinolysis, it helps explain their efficacy at their low endogenous concentrations.
A new heart: portraying the physiologic anatomo-functional reconstruction in ischemic cardiomyopathy
Published on: 15th September, 2017
OCLC Number/Unique Identifier: 7286353710
Fiber-based model of the left ventricle is known since 1628 but the complex 3D structure of myocardial fibers has not taken into account in normalcy or in disease until the last decade. We here present the case of a 60-year-old female patient affected by ischemic cardiomyopathy and severe left ventricular dysfunction. Left ventricle was reconstructed according to a novel surgical technique aimed at rebuilding an elliptical ventricular chamber and redirecting myocardial bundles of fibers in a near-normal orientation, by means of an original suturing technique. Left ventricular torsion was restored, proving the reorientation of myocardial fibres’ bundles. The restored physiologic shape was maintained along the years, gradually improving global ejection fraction and diastolic indices, showing a positive remodeling induced by the optimised geometrical and functional parameters.
The unexpected and never proven before renewal of ventricular torsion is an adjunctive element of ventricular efficiency, mainly in ventricles that work at a critical mechanics. A new fiber-based reading of heart function could improve clinical and functional outcomes and address some unsolved issues in the surgical treatment of ischemic cardiomyopathy as well as in medical approaches to the diseased myocardium.
Endogenous sensitizer of beta-adrenergic receptors (ESBAR) and its analogs (review)
Published on: 29th October, 2018
OCLC Number/Unique Identifier: 7929276791
The results of the 20 years studies of the presence in blood serum and other body fluids of endogenous modulators of adrenergic and M-cholinergic impact as a component of humoral link of autonomic nervous system. The article is devoted to the endogenous sensitizer of beta-adrenergic receptor (ESBAR) - water-soluble low molecular weight substances, analogs of which are histidine, tryptophan, tyrosine, mildronat and preductal. It is shown, that separate dilutions of human serum and animal (as a source of ESBAR) and analogs of ESBAR ways to enhance the effectiveness of activation of beta-adrenoceptors (AR) of smooth muscle (uterus, coronary and renal arteries, trachea, stomach), myocardium, erythrocytes and platelets (respectively influenced of histidine and tryptophan). It is reported that content of ESBAR in human serum (according to the titers of its dilution) depends on the sex and the presence of somatic diseases, and at women are also on the stage of reproduction and obstetric complications It is discussed possible mechanisms of ESBAR action, its physiological role, including as a component of beta-adrenoceptor inhibitory mechanism for myometrium, as well as the prospect of the use of analogs of ESBAR, including for the prevention of preterm labor, and for the treatment of bronchial asthma, coronary heart disease, hypertension and heart failure.
Stem cells in heart failure some considerations
Published on: 25th January, 2018
OCLC Number/Unique Identifier: 7325111402
Stem cell treatments depend not only on the type of cell to be used but also on the different implantation techniques. Intravascular cell injections are known to rapidly separate from the vessels. On the other hand, it is also well known that direct injection into the myocardium provides better coupling within the heart muscle. That were the cases of Embriofetal stem cell (HFDSC) or Autologous stem cells (ABMSC) in our experience focused on direct approaches.
Influence of Histidine on the contractility and adrenaline inotropic effect in the experiments with myocardium of right ventricular of Non pregnant and Pregnant Rats
Published on: 19th November, 2018
OCLC Number/Unique Identifier: 7929237612
It was investigated contractility and adrenoreactivity of intact myocardium strips of right ventricular in experiment with 60 rats. They were assessed by the force of induce contraction and its changes under the influence of adrenaline (10-9 or 10-5 g / ml). Found that these indicators do not depend on the phases of the estrous cycle and the presence of pregnancy. Histidine (10-10-10-4 g / ml) did not increase the response to adrenalin (10-9 g / ml), but increased the force of the contractions in rats in progesterone dominance (trend) and pregnancy (statistically significant). Against the background of propranolol (10-8 g / mL) or atenolol (10-8, 10-6 g / mL), adrenaline (10-5 g / mL) instead of increasing the force of contraction reduced it (probably due to activation of beta3-, alpha1 - and alpha1 a2- adrenergic receptors), and histidine (10-4 g / mL) prevented this reduction, but does not restore full ability of adrenaline to exert a positive inotropic effect. On the background of nicergoline (10-8 g / mL or nicergoline and propranolol (10-8 g / mL), adrenaline (10-5 g / mL) did not alter the force of contraction, and histidine (10-4 g/mL) restore ability of adrenaline to exert a positive inotropic effect but only in the experiments with nicergoline. Concluded that histidine increases the efficiency of the activation of all three (beta1-, beta2- and beta3-) populations of myocardial beta-adrenoceptoprs, including at lower by adrenergic blockers. Therefore, histidine proposed as an antagonist of beta-adrenergic blockers and as resensitizator of these receptors.
Core Tip: In the experiments with strips of the right ventricle of 40 nonpregnant and 20 pregnant rats histidine (10-10-10-4 g /mL) did not increase the response to adrenaline (10-9 g / ml), but increased the force of contractions in pregnant rats. On the background of propranolol (10-8 g / mL) or atenolol (10-8, 10-6 g / mL), adrenaline (10-5g/mL) showed a negative inotropic effect, and histidine (10-4 g / mL) prevented it, but does not restore the ability of adrenaline to show positive inotropic effect,. i.e histidine exhibits the properties of the antagonist of beta-blockers and of resensitizator of beta-adrenoceptors
The complex interplay in the regulation of cardiac pathophysiologic functionalities by protein kinases and phosphatases
Published on: 26th August, 2021
OCLC Number/Unique Identifier: 9225959643
Protein phosphorylation regulates several dimensions of cell fate and is substantially dysregulated in pathophysiological instances as evident spatiotemporally via intracellular localizations or compartmentalizations with discrete control by specific kinases and phosphatases. Cardiovascular disease manifests as an intricately complex entity presenting as a derangement of the cardiovascular system. Cardiac or heart failure connotes the pathophysiological state in which deficient cardiac output compromises the body burden and requirements. Protein kinases regulate several pathophysiological processes and are emerging targets for drug lead or discovery. The protein kinases are family members of the serine/threonine phosphatases. Protein kinases covalently modify proteins by attaching phosphate groups from ATP to residues of serine, threonine and/or tyrosine. Protein kinases and phosphatases are pivotal in the regulatory mechanisms in the reversible phosphorylation of diverse effectors whereby discrete signaling molecules regulate cardiac excitation and contraction. Protein phosphorylation is critical for the sustenance of cardiac functionalities. The two major contributory ingredients to progressive myocardium derangement are dysregulation of Ca2+ processes and contemporaneous elevated concentrations of reactive oxygen species, ROS. Certain cardiac abnormalities include cardiac myopathy or hypertrophy due to response in untoward haemodynamic demand with concomitant progressive heart failure. The homeostasis or equilibrium between protein kinases and phosphatases influence cardiac morphology and excitability during pathological and physiological processes of the cardiovascular system. Inasmuch as protein kinases regulate numerous dimensions of normal cellular functions, the pathophysiological dysfunctionality of protein kinase signaling pathways undergirds the molecular aspects of several cardiovascular diseases or disorders as related in this study. These have presented protein kinases as essential and potential targets for drug discovery and heart disease therapy.
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