The mechanisms controlling erythropoiesis have posed a fascinating problem for almost a century. In dealing with this problem, experimentors in this field have faced dual difficulties. As well as elucidating what are now believed to be the true mechanism of control, they were concomitantly required to dispel earlier, deeply rooted misconceptions. It has long been known that the red blood cell mass is designed almost exclusively for the purpose of transporting oxygen. Its functional capacity, then, must primarily be determined by the concentration of haemoglobin it maintains in the circulating blood.

The work described in this thesis has had as its aim the development of quantitative techniques for the study of the moments at which neurons in the mammalian cerebral cortex produce action potentials both in the presence and absence of externally applied stimulation. In support of the usefulness of these techniques as tools in biological research exploratory experiments are to be described in which a quantitative estimate was made of the influence exerted by a stimulus upon neurons in locations classically considered to be remote from the sphere of influence of the stimulus. In the course of these experiments several analytical techniques have been applied to the action potentials continually generated by neurons in the unstimulated brain.

Studies concerned, in whole or in part, with the manifold aspects of histamine release began with the first, albeit unrecognized, report of the phenomenon by Schmidt-Mulheim (1880), in which "peptone-shock" in the dog was described. No attempt is made, herein, to provide a comprehensive survey of the literature that has since accumulated. The review of the earlier literature is restricted to those papers which have been most helpful to the author in gaining an understanding of previously established facts; in this, invaluable assistance has been provided by the existing reviews, especially those of Feldberg (1941), Dragstedt (1941), Dale (1950) and Code (1952). [...]

Thesis (Ph. D.)--University of Toronto, 2008. / Includes bibliographical references.

Thesis (Ph. D.)--New York University, School of Education, 1967. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves [106]-120).

Thesis (M.D.)--University of Pennsylvania--1806. / Microform version available in the Readex Early American Imprints series.

Thesis (Ph. D.)--New York University, Graduate School of Arts and Science, 2005. / Typescript. Includes bibliographical references (leaves 312-349). Also available in electronic format on the World Wide Web. Access restricted to users affiliated with the licensed institutions.

Thesis (Ph. D.)--New York University, Graduate School of Arts and Science, 2005 / Typescript. Includes bibliographical references (leaves 183-214). Also available in electronic format on the World Wide Web. Access restricted to users affiliated with the licensed institutions.

Ph.D--University of Strasbourg, 1702.

<p> The objective of this dissertation was to systematically investigate the hemodynamic response to exercise in heart failure with reduced ejection fraction (HFrEF) and healthy individuals of a similar age, with an emphasis on how the sympathetic nervous system (SNS) may contribute to the dysregulation of the cardiovascular system in this cohort. The first study aimed to determine how varying levels of metaboreceptor activation alters the mean arterial pressure (MAP) response as well as the degree in which cardiac output (CO) and systemic vascular conductance (SVC) contribute to the metaboreflex-induced increase in MAP. We observed similar increases in MAP induced by metaboreceptor activation in both groups; however, this response was driven primarily by increases in CO in the control group and reductions in SVC in the HFrEF group. These data suggest a preserved role of the metaboreflex-induced increase in MAP in HFrEF, but suggest that this response is governed by the peripheral circulation in this cohort, a maladaptation that may exacerbate systolic dysfunction through an increase in afterload. The second study of this dissertation was focused on investigating the peripheral vasodilatory and hyperemic response to exercise in isolation of central hemodynamic limitations in both the upper and lower limbs. This study documented an impaired hyperemic response to both static-intermittent handgrip exercise as well as dynamic single-leg knee-extensor exercise in HFrEF patients - impairments primarily attributed to vasodilatory dysfunction, as the increase in MAP induced by these exercise modalities was preserved compared to healthy individuals. Together, these findings have identified a significant attenuation of the exercise-induced hyperemic response during both upper and lower limb exercise, implicating maladaptions in the peripheral hemodynamic response to exercise as a potential contributor limiting exercise capacity in this patient group. The third study sought to address the contribution of the alpha-adrenergic receptor pathway in the regulation of blood flow to exercising skeletal muscle in HFrEF patients. At rest, alpha-1-adrenergic receptor vasoconstriction induced by local intra-arterial infusion of phenylephrine (PE) was reduced in HFrEF compared to control subjects. During exercise, the vasoconstrictor responsiveness to PE was significantly attenuated in the control group and preserved in HFrEF patients compared to rest. Additionally, nonspecific alpha-adrenergic receptor antagonism induced by local intra-arterial infusion of phentolamine increased blood flow to a greater degree in HFrEF compared to the control subjects, both at rest and during exercise. Together, these findings demonstrate a marked contribution of alpha-adrenergic receptor restraint of leg blood flow in HFrEF patients during exercise. Collectively, these three studies have provided new insight into the role the SNS and peripheral hemodynamics play in the maladaptive cardiovascular response to exercise displayed in patients with HFrEF, further implicating the peripheral expression of SNS activity as a primary contributor to impaired exercise capacity in this patient group. </p>