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Arterial Wave Reflections
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Myocardial oxygen requirements can be estimated from the area beneath the systolic part of the left ventricular pressure wave, as tension–time index (Sarnoff et al., 1958; Braunwald, 1969, 2009). The value may be reasonably approximated (ignoring isovolumic contraction and relaxation) by the area beneath the systolic part of the ascending aortic pressure wave (systolic pressure-time index) (O'Rourke, 1982a, 1982b). Myocardial oxygen supply is determined by the patency of coronary arteries and by the pressure gradient across the coronary bed during LV diastole. Since coronary vessels in the left ventricle are squeezed shut by contraction during systole, the walls of this chamber can only be perfused during diastole (Buckberg et al., 1972a, 1972b; Hoffman and Buckberg, 1978; Berne and Rubio, 1979). Left ventricular coronary perfusion pressure is that pressure maintained in the aorta throughout diastole; this can be estimated as the area beneath the diastolic part of the aortic pressure wave (diastolic pressure–time index) (see Figure 8.20) (when venous pressure is negligible). These areas are markedly influenced by systolic and diastolic time duration.
Interdependence Between Cardiac Function, Oxygen Demand, and Supply
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Joseph S. Janicki, Karl T. Weber, Ponnambalam Sundram
Coronary vasodilation represents the major compensatory response to an increase in O2 demand. We examined14 the degree to which coronary vascular resistance falls or, equivalently, the degree of coronary vasodilation during marked elevations in demand which were induced by increments in filling volume, heart rate, and contractile state. For a constant, normal coronary perfusion pressure of 80 mmHg, coronary flow increased and coronary vascular resistance decreased by an average amount of 45% (range 35 to 63%) from that measured for the nonworking state. This degree of vasodilation was achieved when average left ventricular end-diastolic pressure was 18 ± 1 mmHg, heart rate was 181 ±5 beats per minute, and the catecholamine, dobutamine, was being infused at 14 ± 2 μg/min. Beyond this level, additional increments in heart rate or dobutamine infusion rate were not accompanied by further coronary vasodilation and instead resulted in lactate production, a reduction in peak isovolumetric force, and the appearance of pulsus alternans. For a reduced perfusion pressure of 40 mmHg, lactate production occurred when end-diastolic pressure was 19 ± 1 mmHg, heart rate was 156 ±11 beats per minute, and dobutamine infusion rate was 5 ± 1 μg/min (Figure 4). The maximum decrease in coronary vascular resistance for the panischemic heart was only 13 ± 7%.
Cross Talk Between Heat Shock and Oxidative Stress Inducible Genes During Myocardial Adaptation to Ischemia
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Dipak K. Das, Nilanjana Maulik
Various methods are available to adapt the heart to ischemia. The one originally used consisted of subjecting the heart to repeated episodes of short durations of ischemia and reperfusion.17 This technique is very reproducible, and has been found to be valid for many animal models including dog, pig, rabbit, and rat.16–23 We will describe here the method used for the rat heart. Hearts can be excised from properly anesthetized rats, which are perfused for 10 min with nonrecirculating Krebs-Henseleit bicarbonate (KHB) buffer containing 3% bovine serum albumin. The KHB buffer consists of the following ion concentrations (in millimolars): 119.0 NaCl, 25.0 NaHCO3, 4.6 KCl, 1.2 KH2PO4, 1.2 MgSO4, 2.5 CaCl2, and 11.0 glucose. Coronary perfusion pressure and perfusate temperature are generally maintained at 100 cm H2O and 37°C, respectively. Hearts can be made globally ischemic by terminating the aortic flow for 5 min followed by 10 min of reperfusion (1 × PC). To induce repeated episodes of ischemia and reperfusion, this procedure may be repeated four times (4 × PC). Each preconditioning (1 × PC or 4 × PC) is followed by 60 min of reperfusion. Experiments are terminated at various points, viz., prior to preconditioning (baseline), after preconditioning, and after reperfusion. Heart biopsies are examined for the expression of oncogenes and stress-related genes, as well as antioxidative enzymes.
Doppler ultrasonography of the ophthalmic artery in perimenopausal and postmenopausal women: a new approach
Published in Climacteric, 2020
A. L. P. Saramago, A. L. D. Diniz
A stiffer artery propagates a pulse wave faster than a more compliant vessel, leading to earlier return of the reflected wave, with increased systolic pressure and reduced diastolic pressure39. Increased systolic pressure causes greater stress on the vessel wall, which, over time, can accelerate the stiffening and remodeling process. A decrease in diastolic pressure may reduce coronary perfusion pressure, reducing coronary blood flow reserve, which may increase the risk of cardiac events40. Also, increased arterial stiffness results in failure to suppress pulse oscillations downstream of the central arteries. Decreased pulse suppression potentially increases the risk from microvascular damage to highly perfused organs such as the brain and kidneys41. Arterial stiffness indices provide a non-invasive assessment of vasculature, and may provide relevant information about individuals’ future risk of morbidity and mortality. Although arterial stiffness is mainly attributed to changes in the intrinsic structure of vessels, several lifestyle factors may transiently increase or decrease arterial stiffness, such as caffeine consumption42, smoking43, and aerobic exercise44. Chronic exposure to these factors, however, may lead to more permanent changes in arterial stiffness.
Cardioprotective effects of Galium verum L. extract against myocardial ischemia-reperfusion injury
Published in Archives of Physiology and Biochemistry, 2020
Jovana Bradic, Nevena Jeremic, Anica Petkovic, Jovana Jeremic, Vladimir Zivkovic, Ivan Srejovic, Jasmina Sretenovic, Stevan Matic, Vladimir Jakovljevic, Marina Tomovic
A day after accomplishing 28-day drinking protocol after a short-term ketamine/xylazine-induced narcosis, rats were sacrificed by decapitation. The chest was then opened via midline thoracotomy. The hearts were immediately removed and immersed in cold saline and were then attached on a cannula of the Langendorff perfusion apparatus to provide retrograde perfusion under constant coronary perfusion pressure CPP = 70 cmH2O. Krebs–Henseleit buffer was used for retrograde perfusion (in mmol/l: NaCl 118, KCl 4.7, CaCl2.2H2O 2.5, MgSO4.7H2O 1.7, NaHCO3 25, KH2PO4 1.2, glucose 11, and pyruvate 2). The buffer was balanced with 95% O2 and 5% CO2, with a pH of 7.4 and a temperature of 37 °C. After placing the sensor in the left ventricle, the following parameters of myocardial function have been continuously measured: maximum rate of pressure development in the left ventricle (dp/dt max), minimum rate of pressure development in the left ventricle (dp/dt min), systolic left ventricular pressure (SLVP), diastolic left ventricular pressure (DLVP), and heart rate (HR). Coronary flow (CF) was measured flowmetrically.
Participation of voltage-gated sodium and calcium channels in the acute cardiac effects of toluene
Published in Toxicology Mechanisms and Methods, 2018
M. Carreón-Garcidueñas, D. Godínez-Hernández, N. Alvarado-Gómez, L. F. Ortega-Varela, C. Cervantes-Durán, M. Y. Gauthereau-Torres
On the other hand, our results provide evidence that during adrenergic stimulation, cardiac function (left ventricular developed pressure) may increase as a result of two factors: (a) direct β1-adrenergic stimulation of the myocardium and (b) increased coronary perfusion pressure produced in response to high blood pressure as a consequence of vasoconstriction. We found in literature a report that describe a positive inotropic effect produced by an increase in coronary perfusion pressure (Lange et al. 2004). The results of this study indicate that the mechanisms responsible for this positive inotropic effect could be an increase in flow over the necessary demands the stretching of cardiac fibers as a result of distended vessels, and/or a direct effect of the pressure that increases intracellular calcium (Lange et al. 2004). Therefore, the increase in myocardial contraction can be observed not only by the direct adrenergic action in the myocardium, but also by the increase in coronary perfusion pressure and the resulting flow of a higher blood pressure that, according to our findings, begins with coronary vasoconstriction, that is significantly higher in the hearts of animals exposed to toluene.