Development Of Cardiovascular Failure Research Articles

CARDIORENAL SYNDROME: THE REVIEW OF CURRENT UNDERSTANDING

Introduction. The kidneys and heart rely on each other to function properly. For the kidneys to function, they require adequate blood flow, oxygen delivery and nutrients. If heart failure develops, cardiac output is reduced, which results in decreased renal blood flow, which can lead to reversible and sometimes irreversible kidney damage. For the heart to function, regulation of extracellular volume is required. If the extracellular volume is too low, the volume of blood is insufficient to maintain cardiac output, and if the extracellular volume is too large, fluid leaks out of the capillaries, resulting in edema.Purpose. To study the relationship of the dynamic balance of the “kidney-heart” system in health and disease.Material and methods. Review of modern and foreign literary sources; methods – description, analysis, abstracting.Results and its discussion. 5 forms of cardiorenal syndrome, peculiarities of classification, pathogenesis, clinical manifestations, dynamics of imbalance in the “kidney-heart” system, issues of correction of these disorders are analyzed. They include the treatment of kidney diseases and cardiovascular pathology, prevention of the development of cardiovascular failure in accordance with modern recommendations; diet; quitting smoking, alcohol, nephrotoxic substances; control of body weight, blood pressure, glycemia; the use of angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists or angiotensin receptor blockers, statins; decrease in intra-abdominal pressure and others.Findings. Approaches to the prevention and treatment of cardiorenal syndrome in patients with kidney and heart damage are important. It is necessary to develop and introduce new approaches to nephroprotection in patients with cardiorenal syndrome, which is possible with the joint work of a multidisciplinary team.

Activation of the PGI 2 /IP System Contributes to the Development of Circulatory Failure in a Rat Model of Endotoxic Shock

Prostacyclin levels are increased in septic patients and several animal models of septic shock, and selective inhibition of cyclooxygenase-2 improved cardiovascular dysfunction in rats treated with lipopolysaccharide (LPS). Here, we examine the specific role of prostacyclin and of the receptor for prostacyclin (IP) in the development of LPS-induced circulatory failure. Intravenous injection of LPS (10 mg/kg) into male Sprague-Dawley rats caused a strong increase in plasma prostacyclin levels, which was paralleled by a decrease in blood pressure and an increase in heart rate. Moreover, LPS injection increased the mRNA expression of the IP receptor in the heart, aorta, lung, liver, adrenal glands, and kidneys. Cotreatment with the IP antagonist CAY-10441 (1, 10, 30, and 100 mg/kg) dose-dependently moderated the LPS-induced changes in mean arterial blood pressure, heart rate, cardiac output, and systemic vascular resistance. The development of cardiovascular failure was ameliorated by CAY-10441 in spite of the typical LPS-induced increases in plasma levels of cytokines and NO. In vitro, cytokines dose- and time-dependently induced IP expression in rat vascular smooth muscle cells. Incubation of cells with the stable IP agonist iloprost in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-mehylxanthine resulted in higher cAMP levels in cytokine-treated cells compared with untreated cells. Taken together, our data demonstrate a prominent role of the prostacyclin/IP system in the development of LPS-induced cardiovascular failure.

MYOCARDIAL FUNCTION IN SEPTIC SHEEP

There is an ongoing discussion whether the heart is the primary target organ responsible for the development of cardiovascular failure during septic shock as well as its onset. We tried to study the reaction of the heart to sepsis in the early phase of 8 h, using a sublethal model of sepsis in six awake cross-bred Austrian mountain sheep. Sepsis was induced by infusion of a live Escherichia coli suspension at a dose of 5 x 10(7) colony-forming units per kg body weight over 8 h. Standard hemodynamic, hematologic and serum tumor necrosis factor (TNF) measurements were obtained. For evaluation of left ventricular performance we used the following methods, tested in five pilot experiments: 1) The shift of the end-systolic pressure-diameter relation. This was characterized by the calculated shift of the transverse external end-systolic diameter of the left ventricle at a "midrange" end-systolic pressure of 100 mmHg (end-systolic ventricular diameter deviation, ESVDD100). Calculations were performed using a second order regression function of the end-systolic pressure diameter points obtained by variation of afterload by a cuff occluder on the aorta; 2) The shift of the (dP/dt)max over end-diastolic diameter ratio compared to control values estimated by a graphical approach. Mean pulmonary pressure increased from 21 +/- 1 to 36 +/- 2 mmHg in the first hour after starting the E. coli infusion and remained elevated during the entire 8 h observation period. Serum TNF was found to peak 1 hour after start of E. coli infusion and was hardly detectable after 3 hours of bacteremia. Mean aortic pressure showed minor changes (maximum 105 +/- 3 mmHg, minimum 91 +/- 2 mmHg) and there were no statistically significant alterations of the cardiac index. ESVDD100 showed an "oscillatory" reaction in the first phase and a statistically significant decrease of contractility in the second phase (at 4 h). This was confirmed by the graphical method of the (dP/dt)max over end-diastolic diameter ratio. We may therefore conclude that there is no early depression of myocardial function or if so, it may be masked by adrenergic stimulation. In the later phase of the 8 h experiment there is a significantly decreased contractility of the heart. This may be compensated (e.g., "Starling" mechanism or heart rate increase) in this sublethal model.