Thesis (M.S.)--University of Wisconsin--Madison, 1966. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis--Wisconsin. / Includes bibliographical references (leaves 94-98).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1982. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 267-288).

Thesis (M.S.)--University of Wisconsin--Madison, 1969. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

No description available.

No description available.

The purpose of this study was to describe the cardiovascular changes that occur when fish swim, and to determine some of the mechanisms by which these changes are regulated. Two levels of exercise were used: moderate and severe. Moderate exercise was induced by conditioning the fish to swim against a moderate water velocity (1.7 ft/sec) in a respirometer tube. The effects of severe exercise were studied by forcing the fish to swim by chasing it. Changes in blood pressures in the ventral aorta, dorsal aorta, and sub-intestinal vein as well as changes in heart rate and breathing rate during swimming activity in rainbow trout were measured. Blood pressures both afferent and efferent to the gills increased during moderate swimming and then returned to pre-exercise levels within 30 min. Dorsal aortic blood pressure tended to increase during severe exercise, and tended to decrease lower than pre-exercise levels after severe exercise. The increases in blood pressure during swimming may be due in part to the interaction of circulating catecholamines with ∝-adrenergic receptors and to an increase in cardiac output. Venous blood pressure was characterized by periodic increases during moderate swimming. The pressure changes were not in phase with body movements. Heart rate increased about 15% during both moderate and severe exercise and then gradually returned to normal. The increase in heart rate was aneural in origin. Breathing rate increased about 30% during moderate exercise and about 60% during severe exercise. It took about 10 minutes to return to pre-exercise levels after moderate exercise, and about 60 min after severe exercise. Changes in partial pressure of oxygen and carbon dioxide in blood and water, afferent and efferent to the gills of rainbow trout, were determined before, during and after moderate swimming activity. Neither blood nor water PO₂ afferent or efferent to the gills changed markedly during or after exercise. Arterial blood was always greater than 95% saturated with oxygen. Venous blood was 38% saturated with oxygen, falling to a minimum of 29% during exercise. Arterial blood PCO₂ was 2.3 mm Hg. Venous blood PCO₂ increased from 5.7 mm Hg to 8.0 mm Hg during exercise and remained elevated throughout the recovery period. Cardiac output, stroke volume, ventilation volume, and the volume of water pumped par breath all increased by a factor of between 4 and 5 during moderate exercise. All tended to remain elevated from 10 to 30 minutes after exercise and then, gradually decreased to pre-exercise levels. From the above data it was possible to analyse the effects of exercise on the gas exchange, process. The analysis included calculating effectiveness (the ratio of actual gas transfer to the maximum rate of gas transfer possible expressed as a percentage) and the transfer factor (the actual rate of gas transfer ÷mean partial pressure gradient between the blood and the water). The transfer factor for oxygen increased almost 5 fold during exercise indicating that there was an increase in effective exchange area, a decrease in diffusion distance, an increase in diffusion coefficient, or a combination of these factors. The relative volume of blood in various tissues before and after severe swimming activity was estimated by injecting a small amount of radioiodinated serum albumin into the vascular compartment. There were no major changes in the distribution of blood in trout, after 5 or 15 minutes severe exercise. In both resting and exercised fish the ratio of blood, volume in the red muscle to that in white muscle was about 3. In summary, the compensatory changes which occur when rainbow trout swim, are primarily those which increase the flow of blood and water across the respiratory interface in order to maintain the arterial blood saturated with oxygen. The increase in blood flow also enables the fish to deliver more oxygen to its tissues. / Science, Faculty of / Zoology, Department of / Graduate

The sympathetic nervous system is important in maintaining cardiovascular homeostasis. Elevated cardiovascular-related sympathetic activity can lead to neurogenic hypertension and a host of other serious cardiac-related abnormalities. The paraventricular nucleus (PVN) of the hypothalamus plays an important role in sympathetic cardiovascular regulation. Neurons from the PVN project to the rostral ventrolateral medulla (RVLM), which is the main brain stem sympathetic cardiovascular control center. While RVLM-projecting PVN neurons have been well characterized, the topographical organization within the PVN subnuclei is still not fully known. This neuroanatomical study aimed to map the topographical distribution of RVLM-projecting PVN neurons. Four different carboxylate FluoSphereTM retrograde tracers (blue, 365/415; green, 505/515; red, 565/580; and far-red, 660/680) were injected at different rostro-caudal coordinates within the RVLM. The vast majority of RVLM-projecting PVN neurons were ipsilateral and located in the medial parvocellular subnucleus. Whereas most neurons were ipsilateral, there is a small fraction of neurons that crossed the midline. RVLM-projecting neurons were also identified within the dorsal, ventral, and posterior parvocellular subnuclei of the PVN with no labeling found in the anterior parvocellular or magnocellular subnuclei. Additionally, we observed different efficiencies of the retrograde tracers with blue (365/415) being the least efficient and red (565/580) being the best. These neuroanatomical data will serve as important preliminary data for future research investigating the functional and histochemical properties of these PVN neurons.

No description available.

The sympathetic nervous system is crucial for controlling multiple cardiac functions and its overactivity is associated with many cardiovascular diseases (CVD). Chronic intermittent hypoxia (CIH) is a current model for sleep apnea, which constitutes a major risk factor for CVD through sympathetic overactivity. However, a comprehensive neuroanatomical map of the sympathetic innervation of the heart is unavailable which impedes our understanding of the remodeling of this map in pathological conditions. First, we used a combination of state-of-the-art techniques, including flat-mount tissue processing, immunohistochemistry for tyrosine hydroxylase (TH, a sympathetic marker), confocal microscopy and Neurolucida 360 software to trace, digitize, and quantitatively map the topographical sympathetic innervation in the whole heart of mice. Then we integrated our tracing data onto a 3D heart scaffold. Second, we determined the remodeling of sympathetic innervation in CIH, by exposing mice to either room air or CIH for 8-10 weeks. We found that (1) 4–5 extrinsic TH-IR nerve bundles entered the right atrium from the superior vena cava and the left atrium from the left precaval vein. Although these bundles projected to different areas of the atria, their projection fields partially overlapped. (2) TH-IR axon and terminal density varied considerably between different sites of the heart with the greatest density of innervation near the sinoatrial node region (P < 0.05, n = 6). (3) TH-IR axons also innervated blood vessels and adipocytes. (4) In ventricles: TH-IR axons formed dense terminal networks in the epicardium, myocardium, and vasculature. (5) TH-IR axons were traced and integrated into 3D heart scaffolds. (6) CIH significantly increased TH-IR innervation and complexity in the heart. Collectively, this work provided detailed mapping of catecholaminergic axons and terminal structures in the whole heart at single-cell/axon/varicosity scale in normal and CIH conditions. This work may provide a foundation for the functional study of sympathetic control of the heart and valuable neuromodulation strategies to treat CVD.