Physiology of the Heart Arnold M. Katz MD Publisher: LWW Release Date: ISBN : Author: Arnold M. Katz MD Download Here. Dr. Arnold Katz s internationally acclaimed classic, Physiology of the Heart, is now in its thoroughly revised Fifth Edition, incorporating the latest. Dr. Arnold Katz's across the world acclaimed vintage, Physiology of the Heart, is now in its completely revised 5th variation, incorporating the.
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This book is a record of the proceedings of the international symposium on Coronary Heart Surgery, A Rehabilitation Measure, held March 18, at the. Physiology of the heart by Arnold M. Katz Raven Press, New York () pages, $ ISBN 0––53–2. Arnold M. Katz. Raven Press, New York. Physiology of the heart. byKatz, Arnold M. Publication date For print- disabled users. Borrow this book to access EPUB and PDF files.
Open in a separate window Arnold M. Katz, MD Dr. Katz was born in Chicago in His father, Dr. Louis N. Katz, was a renowned cardiologist who had received a Lasker award and served as President of the American Heart Association and the American Physiological Society.
However, they are not sufficient to enable us to establish the optimal hemoglobin level to achieve the maximum benefit with the least possible complications. An interesting question is the fact that the decrease in hematocrit could be a marker for other factors that increase the mortality in patients with severe HF, for example, CRD.
Lower hemoglobin concentrations are associated with a poorer hemodynamic function, increases in serum urea nitrogen and creatinine, decreases in albumin, cholesterol and body mass index, a worse functional class, and a lower VO2 peak oxygen consumption. In patients with preserved ventricular function, the hyperdynamic state can play a role in ventricular hypertrophy, which, in turn, can promote a disproportion between the oxygen supply to the myocardium and the increased ventricular mass, a circumstance that is critical in the presence of significant coronary artery disease.
Studies carried out in animals show that an ischemic or hypertrophic heart is more vulnerable to slight decreases in hemoglobin than a normal heart, with a marked deterioration in the ischemia and the myocardial dysfunction. Under these conditions, the treatment with EPO is even more interesting because of its cytoprotective properties with respect to the myocardium.
In HF, anemia also influences hospital admissions, and a relationship between the hemoglobin levels and the number of admissions due to HF over the preceding year has been observed; in this respect, low hematocrit may be more of a risk factor for hospital admission than for mortality. The production and action of EPO are the critical points of erythropoiesis.
Erythropoietin is a glycoprotein that, in extrauterine life, is produced nearly exclusively in the peritubular fibroblasts of the renal cortex, without direct contact with the capillaries and tubular cells. Hypoxia can lead to a several hundred-fold increase in EPO. In the experimental setting, the increase in the intensity of hypoxia is accompanied by an exponential increase in the number of fibroblasts expressing the EPO gene.
Why in the kidneys? The possible physiological reasons and consequences of the localization of EPO production in the kidney is a question that has not been fully resolved. The simple fact that blood is made up of red cells and plasma provides a clue: what the organism regulates is the proportion of plasma that is constituted by circulating red cells hematocrit. The specific mechanisms of this coordination are relatively unknown, although we assume that there is an intrarenal connection between the pathways that monitor and regulate the fluid volume and those that control the erythroid cell volume.
This phenomenon may be of importance in HF, in which the accumulation of extracellular fluid and hemodilution can change the "perception" of the hematocrit on the part of the kidney. On the other hand, the kidney extracts only a small part of the oxygen delivered to it, a circumstance that makes it possible to detect slight changes in oxygenation. Moreover, the constancy of the ratio of the work performed oxygen consumption to the renal blood flow oxygen delivery makes it possible to separate the renal pO2 from the metabolic activity, meaning that the regulation of EPO synthesis can be reasonably, although not totally, independent of the reabsorptive activity.
Baseline hematopoietic stimulation originates in the physiological destruction of red blood cells, but its greatest intensity is observed in hemorrhage. Anemia of HF is usually mild, persistent and adaptive.
Thus, its effects would be analogous to minor hemorrhage with limited, but long-term, hemodynamic impact. The kidney has to restore volume depending on the amount of fluid lost and produce red cells to replace those lost, but nothing more.
Moreover, it has to be able to discern the proportion in which fluid is conserved and new red cells are produced. The joint regulation of these 2 mechanisms is more complex than that of each separately, and is 1 of the keys to research in a disease like HF. What makes up the chain of signals and mechanisms that increase endogenous erythropoietin?
The physiological sequence involved in the stimulation of EPO production is based on 2 transcription factors that can be activated by hypoxia, hypoxia-inducible factors 1, and 2 HIF-1 and HIF The great advance in recent years has been the discovery that transcriptionally active HIF-1 depends on a group of non-heme-iron-dependent prolyl hydroxylases that constitute the true oxygen-sensing mechanism. In contrast, HIF-2 appears to play a selective role in EPO expression, which is practically abolished in the knockouts for this gene.
Thus, references to its role are limited to supposition, firm, but still conjectural. Although the patient with HF can go through periods of systemic hypoxia, they are usually transient; brief hypoxia does not constitute a strong enough stimulus for sustained EPO induction. Hypoxia-inducible factor 1 is activated by means of phosphorylation under hypoxic conditions. It acts by transactivating more than 70 genes, at least 4 of which are highly relevant to the final effect of EPO: the transferrin gene, supplying iron to the erythroid cells; the vascular endothelial growth factor VEGF gene, a cofactor in the stimulation of these same cells and a determining element in angiogenesis and tissue perfusion; the tyrosine hydroxylase gene, involved in dopamine synthesis and respiratory regulation; and the nitric oxide synthase gene, which maintains normal arterial blood pressure under the potentially pressor effect of EPO.
In the renal medulla, the pO2 is permanently under 10 mm Hg, whereas in the cortex, it is more variable, with a mean close to the threshold for HIF stimulation 30 mm Hg.
Changes in these concentrations are determinant in induction of the EPO gene. A higher Ang II level results in greater sodium reabsorption and, thus, an increased adenosine triphosphate and oxygen consumption, secondary to the increased tubular reabsorptive function.
In healthy subjects, the EPO concentrations are correlated with the proximal tubular sodium reabsorption rate. In contrast, acetazolamide, which acts on the proximal tubule, significantly decreases EPO production in response to normobaric hypoxia and functional anemia. To date, studies addressing this assumption have not been performed in humans. One relevant question is whether the changes observed in Ang II are due to a direct stimulation of the peritubular fibroblasts that synthesize EPO or to hemodynamic effects induced by Ang II.
In addition, there are elements that coregulate gene expression, the importance of which is still not fully known, but that might explain the differences in EPO mRNA synthesis observed under conditions equivalent to hypoxia.
These 2 factors can be increased in the presence of inflammation, and thus, constitute plausible explanations for the decrease in EPO synthesis in inflammatory conditions.
With respect to the stimulation of EPO gene expression, it should be mentioned that there is an inverse relationship between GATA and nitric oxide, a circumstance that indicates a role of the decrease in the latter in the reduced EPO production.
There are EPO receptors EPO-R in the erythroblasts, but they are also found in the placenta, heart, retina, brain, and endothelial cells.
While the intracellular transduction of EPO is known to take place, there are considerable gaps in our knowledge with respect to how this hormone regulates the survival, proliferation and differentiation of erythroid progenitor cells. In this respect, it has recently been demonstrated that EPO is a potent trophic and apoptotic factor, with protective effects in brain and retinal cells, in the renal epithelium and, as mentioned above, in myocardial cells, as well.
In the absence of bleeding, this suggests peripheral resistance to the action of endogenous EPO. In contrast, concentric hypertrophy in DHF facilitates ejection but impairs filling and can cause heart muscle to deteriorate.
Differences in the molecular signals that initiate dilatation and concentric hypertrophy can explain why many drugs that improve prognosis in SHF have little if any benefit in DHF. Ejection fraction , Heart failure , Cardiac architecture , Sarcomere addition , Hypertrophic signalling It is the pervading law of all things organic and inorganic, of all things physical and metaphysical, of all things human and all things superhuman, of all true manifestations of the head, of the heart, of the soul… that form ever follows function.
This is the law. Sullivan, Konstam, These haemodynamic abnormalities activate neurohumoral responses that, while providing some compensation for the impaired cardiac performance, can cause additional damage by increasing energy expenditure in failing hearts, which are already energy-starved, 4 and by stimulating proliferative signalling pathways that have maladaptive effects on cardiac myocytes.
Two clinical measurements have long been used to define the interplay between the heart and circulation. The second, based on clinical data obtained at the bedside since the nineteenth century, characterizes cardiac architecture by distinguishing between left ventricular dilatation and concentric hypertrophy.
The accuracy of these distinctions, initially validated at autopsy, is now greatly improved by modern imaging techniques. Heart failure occurs when a ventricle with a normal or high EDV is unable to eject a normal stroke volume SV , or when a ventricle with a normal or low EDV cannot accept a normal venous return.
However, EF has the disadvantage of being a chimeric index because the major determinants of SV, the numerator, are physiological variables that include preload, afterload, inotropy, lusitropy, heart rate, and the synchrony of left ventricle LV ejection; whereas EDV, the denominator, is determined largely by architectural variables that include LV wall thickness and the size and shape of its cavity.
Ventricular architecture Louis H. Sullivan, often viewed as the creator of the skyscraper, altered the design of large buildings from a heavy stack of horizontal layers that rested on thick walls to a much lighter vertical structure supported by a steel frame. The resulting increase in the ability to adapt the form of a building to its intended function led to Sullivan's recognition as one of the founders of modern architecture. In muscle, as in buildings, architecture is normally matched to function, in this case by biological processes that control the size, shape and composition of cardiac 6 and skeletal 7 myocytes.
The first, now generally called concentric hypertrophy, was initially viewed as a compensatory response to overload, whereas dilatation, the other type of cardiac enlargement, was quickly recognized to be progressive and to have a poor prognosis. Early estimates of the relationship between end-diastolic volume and stroke volume In the early s, two groups noted that because Starling's Law of the Heart predicts that increasing venous return normally increases both EDV and SV, the relationship between these variables could provide an index of cardiac performance that is independent of the patient's size and body position.
In Starr et al. They also observed that this ratio was increased significantly in six patients who had been in congestive heart failure but were clinically compensated at the time of the study. The following year Lysholm et al.
Anfinsen at the National Institutes of Health in Bethesda. In Katz became the first Philip J. In he moved to the University of Connecticut School of Medicine to become the first chief of cardiology. Since his retirement in he has been acting as visiting professor of Medicine and Physiology at Dartmouth Medical School.
Katz Prize in his honour. Katz passed away at his home in Norwich, Vermont on January 25, He is survived by his wife of 56 years, Phyllis B. Katz, and their 4 children and 8 grandchildren. Publications incomplete list [ edit ] Physiology of the Heart  Heart Failure: Pathophysiology, Molecular Biology, Clinical Management  Effects of acetate and other short-chain fatty acids on yeast metabolism  Regulation of myocardial contractility an odyssey  Regulation of coronary flow.
Influence of tropomyosin upon the reactions of actomyosin at low ionic strength. Circulation Research. J Mol Cell Cardiol. J Biol Chem.