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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The effect of acute consumption of a flavonol-rich cocoa drink on cerebral vasomotor reactivity in African Americans

Ku, ByungMo 08 October 2014 (has links)
African Americans (AA) are at great risk of cardiovascular diseases (CVD) which can lead to brain damage, dementia, and endothelial dysfunction. Decreased nitric oxide (NO) bioavailability contributes cardiovascular disease in AA population. Flavonols of the subclass known as flavonoids that have several beneficial effects on cerebral blood flow and cerebral vasomotor reactivity (CVMR). This study investigated the effects of the acute consumption of a flavanol-rich cocoa drink on CVMR. Ten non-smoking African American (6 males and 3 females) participants were randomly recruited. The subjects participated in two experimental sessions which were separated before and after the consumption of cocoa drink. For the pre-session, baseline CVMR was measured by the hypercapnia rebreathing (CVMR test) prior to the consumption of the cocoa drink and the again at 2h after consumption of one serving of the cocoa drink (45g of cocoa mixed with 8oz of cold water). Cerebral vascular conductance (CVC) was significantly increased in the post-study during hypercapnia rebreathing compared with the pre-study(post-study: 3.649 ± 1.833 CVC % of baseline/mmHg, pre-study: 2.483 ± 1.418 CVC % of baseline/mmHg vs. P < 0.05) Thus, CVMR was significantly increased in the post-study after the acute consumption of a flavonol-rich cocoa drink compared to the pre-study in AA. / text
2

RESPIRATORY CHEMOSENSITIVITY IN SYNCHRONIZED SWIMMERS AND SWIM-TRAINED WOMEN

Taylor, John Andrew, 1960- January 1987 (has links)
No description available.
3

Breathlessness and the pattern of breathing

Binks, Andrew Paul January 1998 (has links)
No description available.
4

Cardiac Responses to Carbon Dioxide in Developing Zebrafish (Danio rerio)

Miller, Scott 29 May 2013 (has links)
The ontogeny of carbon dioxide (CO2) sensing in zebrafish (Danio rerio) has not been studied. In this thesis, CO2-mediated increases in heart rate were used to gauge the capacity of zebrafish larvae to sense CO2. CO2 is thought to be sensed through neuroepithelial cells (NECs), which are homologous to mammalian carotid body glomus cells. Owing to its role in facilitating intracellular acidification during exposure to hypercapnia, it was hypothesized that carbonic anhydrase (CA) is involved in CO2 sensing, and that inhibition of CA would blunt the downstream responses. The cardiac response to hypercapnia (0.75% CO2) was reduced in fish exposed to acetazolamide, a CA inhibitor, and in fish experiencing CA knockdown. Based on pharmacological evidence using β-adrenergic receptor (ß-AR) antagonists, and confirmed by β1AR gene knockdown, the efferent limb of the reflex tachycardia accompanying hypercapnia is probably mediated by sympathetic adrenergic neurons interacting with cardiac β1 receptors.
5

Cardiac Responses to Carbon Dioxide in Developing Zebrafish (Danio rerio)

Miller, Scott January 2013 (has links)
The ontogeny of carbon dioxide (CO2) sensing in zebrafish (Danio rerio) has not been studied. In this thesis, CO2-mediated increases in heart rate were used to gauge the capacity of zebrafish larvae to sense CO2. CO2 is thought to be sensed through neuroepithelial cells (NECs), which are homologous to mammalian carotid body glomus cells. Owing to its role in facilitating intracellular acidification during exposure to hypercapnia, it was hypothesized that carbonic anhydrase (CA) is involved in CO2 sensing, and that inhibition of CA would blunt the downstream responses. The cardiac response to hypercapnia (0.75% CO2) was reduced in fish exposed to acetazolamide, a CA inhibitor, and in fish experiencing CA knockdown. Based on pharmacological evidence using β-adrenergic receptor (ß-AR) antagonists, and confirmed by β1AR gene knockdown, the efferent limb of the reflex tachycardia accompanying hypercapnia is probably mediated by sympathetic adrenergic neurons interacting with cardiac β1 receptors.
6

Role of Intracellular Ca2+ and pH in CO2/pH Chemosensitivity in Neuroepithelial Cells of the Zebrafish (Danio rerio) Gill Filament

Abdallah, Sara 04 February 2013 (has links)
Neuroepithelial cells (NECs) of the zebrafish gill filament have been previously identified as bimodal O2 and CO2/H+ sensors that depolarize in response to chemostimuli via inhibition of background K+ channels. To further elucidate the signaling pathway underlying CO2/H+ chemoreception in the NECs we employed microspectrofluorometric techniques to examine the effects of hypercapnia on [Ca2+]i and pHi. NECs increased their [Ca2+]i in response to acidic hypercapnia (5% CO2, pH 6.6) and isocapnic acidosis (normocapnia, pH 6.6), but not to isohydric hypercapnia (5% CO2, pH 7.8). The acid- induced increase in [Ca2+]i persisted in the absence of extracellular Ca2+, and Ca2+ channel blockers (Cd2+, Ni2+ and nifedipine). NECs exhibited a rapid and reversible drop in pHi in response to acidic hypercapnia and isohydric hypercapnia. Isocapnic acidosis also induced intracellular acidification within NECs, but it was less severe than the drop in pHi elicited by acidic hypercapnia and isohydric hypercapnia. The rate and magnitude of intracellular acidification was reduced by the CA-inhibitor, acetazolamide, without effect on the acid-induced increase in [Ca2+]i. Acetate was used to investigate the relationship between pHi and [Ca2+]i. Acetate induced intracellular acidification without augmentation of [Ca2+]i. The results of this thesis demonstrate that (1) extracellular acidification, but not CO2, is critical to the hypercapnia-induced increase in [Ca2+]i (2) the increase in [Ca2+]i is independent of the drop in pHi (3) the increase in [Ca2+]i is not mediated by the influx of Ca2+ across the plasma membrane.
7

Role of Intracellular Ca2+ and pH in CO2/pH Chemosensitivity in Neuroepithelial Cells of the Zebrafish (Danio rerio) Gill Filament

Abdallah, Sara 04 February 2013 (has links)
Neuroepithelial cells (NECs) of the zebrafish gill filament have been previously identified as bimodal O2 and CO2/H+ sensors that depolarize in response to chemostimuli via inhibition of background K+ channels. To further elucidate the signaling pathway underlying CO2/H+ chemoreception in the NECs we employed microspectrofluorometric techniques to examine the effects of hypercapnia on [Ca2+]i and pHi. NECs increased their [Ca2+]i in response to acidic hypercapnia (5% CO2, pH 6.6) and isocapnic acidosis (normocapnia, pH 6.6), but not to isohydric hypercapnia (5% CO2, pH 7.8). The acid- induced increase in [Ca2+]i persisted in the absence of extracellular Ca2+, and Ca2+ channel blockers (Cd2+, Ni2+ and nifedipine). NECs exhibited a rapid and reversible drop in pHi in response to acidic hypercapnia and isohydric hypercapnia. Isocapnic acidosis also induced intracellular acidification within NECs, but it was less severe than the drop in pHi elicited by acidic hypercapnia and isohydric hypercapnia. The rate and magnitude of intracellular acidification was reduced by the CA-inhibitor, acetazolamide, without effect on the acid-induced increase in [Ca2+]i. Acetate was used to investigate the relationship between pHi and [Ca2+]i. Acetate induced intracellular acidification without augmentation of [Ca2+]i. The results of this thesis demonstrate that (1) extracellular acidification, but not CO2, is critical to the hypercapnia-induced increase in [Ca2+]i (2) the increase in [Ca2+]i is independent of the drop in pHi (3) the increase in [Ca2+]i is not mediated by the influx of Ca2+ across the plasma membrane.
8

Mechanisms of excitation in arterial chemoreceptors

McCloskey, D. I. January 1966 (has links)
No description available.
9

Human responses to simulated high altitude

Croft, Quentin January 2010 (has links)
No description available.
10

Role of Intracellular Ca2+ and pH in CO2/pH Chemosensitivity in Neuroepithelial Cells of the Zebrafish (Danio rerio) Gill Filament

Abdallah, Sara January 2013 (has links)
Neuroepithelial cells (NECs) of the zebrafish gill filament have been previously identified as bimodal O2 and CO2/H+ sensors that depolarize in response to chemostimuli via inhibition of background K+ channels. To further elucidate the signaling pathway underlying CO2/H+ chemoreception in the NECs we employed microspectrofluorometric techniques to examine the effects of hypercapnia on [Ca2+]i and pHi. NECs increased their [Ca2+]i in response to acidic hypercapnia (5% CO2, pH 6.6) and isocapnic acidosis (normocapnia, pH 6.6), but not to isohydric hypercapnia (5% CO2, pH 7.8). The acid- induced increase in [Ca2+]i persisted in the absence of extracellular Ca2+, and Ca2+ channel blockers (Cd2+, Ni2+ and nifedipine). NECs exhibited a rapid and reversible drop in pHi in response to acidic hypercapnia and isohydric hypercapnia. Isocapnic acidosis also induced intracellular acidification within NECs, but it was less severe than the drop in pHi elicited by acidic hypercapnia and isohydric hypercapnia. The rate and magnitude of intracellular acidification was reduced by the CA-inhibitor, acetazolamide, without effect on the acid-induced increase in [Ca2+]i. Acetate was used to investigate the relationship between pHi and [Ca2+]i. Acetate induced intracellular acidification without augmentation of [Ca2+]i. The results of this thesis demonstrate that (1) extracellular acidification, but not CO2, is critical to the hypercapnia-induced increase in [Ca2+]i (2) the increase in [Ca2+]i is independent of the drop in pHi (3) the increase in [Ca2+]i is not mediated by the influx of Ca2+ across the plasma membrane.

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