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This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

This thesis examined the impact of oxygen (O2) availability on prefrontal cortex and muscle tissue oxygenation during repeated-sprint exercise (RSE) in men and women. Men and women matched for initial-sprint mechanical work performed during ten, 10-s sprints (30s of rest) in normoxia (21% FIO2) and acute hypoxia (13% FIO2). Mechanical work and arterial O2-saturation (SPO2) were obtained for every sprint. Oxy- and deoxygenated haemoglobin concentrations (O2Hb, HHb) were obtained via near-infrared spectroscopy. Hypoxia elicited lower SPO2 and work (14.8% & 7.4%, P < 0.05), larger (45.1%, P < 0.05) and earlier reductions in cortical oxygenation, and no differences between sexes. Cortical de-oxygenation and work decrement were strongly correlated (R2=0.85, P < 0.05). Muscle de-oxygenation was greater in men than women (67.3%, P < 0.05). These results show that O2 availability influences cortical oxygenation and performance equally in men and women, and suggest a more efficient muscle O2 uptake in women.

Chiu, Wui Man., Thesis (M.Phil.)--Chinese University of Hong Kong, 2008., Includes bibliographical references (leaves 107-128)., s in English and Chinese., p.i, 中文摘要 --- p.iv, Acknowledgements --- p.vi, Publications --- p.viii, Table of Contents --- p.ix, List of Tables --- p.xiv, List of Figures --- p.xv, List of Abbreviations --- p.xviii, Chapter Chapter 1 --- Introduction --- p.1, Chapter 1.1 --- Hypoxic-ischemic encephalopathy in human infants --- p.1, Chapter 1.1.1 --- Incidence --- p.1, Chapter 1.1.2 --- Biphasic development of HI brain damage --- p.2, Chapter 1.1.2.1 --- Initiating mechanism: energy failure in immature brain --- p.3, Chapter 1.1.2.2 --- Biochemical cascades --- p.4, Chapter 1.1.2.2.1 --- Excitatory amino acid receptor activation by glutamate --- p.4, Chapter 1.1.2.2.2 --- Intracellular calcium accumulation --- p.4, Chapter 1.1.2.2.3 --- Formation of free radicals --- p.5, Chapter 1.1.2.2.3.1 --- Reactive oxygen species (ROS) --- p.5, Chapter 1.1.2.2.3.2 --- Nitric oxide (NO) --- p.6, Chapter 1.1.2.3 --- Release of inflammatory mediators --- p.6, Chapter 1.1.2.4 --- Mitochondrial dysfunction --- p.7, Chapter 1.1.2.5 --- Final path to death: necrosis or apoptosis --- p.8, Chapter 1.1.2.6 --- Ways to change: neuronal survival and proliferation signaling --- p.8, Chapter 1.1.3 --- Interventions for neonatal hypoxia-ischemia --- p.9, Chapter 1.2 --- Animal models mimicking hypoxia-ischemia brain injury --- p.12, Chapter 1.2.1 --- Comparisons of animal models of hypoxia-ischemia --- p.12, Chapter 1.2.2 --- Development of neonatal rat model with hypoxic-ischemic damage --- p.14, Chapter 1.3 --- Neural stem/progenitor cells --- p.15, Chapter 1.3.1 --- Effect of hypoxic-ischemia on neural stem/progenitor cells --- p.17, Chapter 1.4 --- Thrombopoietin --- p.18, Chapter Chapter 2 --- Objectives --- p.23, Chapter Chapter 3 --- Materials and Methodology --- p.24, Chapter 3.1 --- Establishment of neonatal rat model of HI brain damage and effects of TPO on neural protection --- p.24, Chapter 3.1.1 --- Animal protocols --- p.24, Chapter 3.1.2 --- Induction of HI brain damage in neonatal rats --- p.24, Chapter 3.1.3 --- Treatment with TPO --- p.25, Chapter 3.1.4 --- Sacrifice of rats --- p.25, Chapter 3.1.5 --- Read-out measurements --- p.26, Chapter 3.1.5.1 --- Brain weight --- p.26, Chapter 3.1.5.2 --- Gross injury assessment of the right hemisphere --- p.26, Chapter 3.1.5.3 --- Histology --- p.27, Chapter 3.1.5.4 --- Blood cell count --- p.27, Chapter 3.1.5.6 --- Functional assessments --- p.28, Chapter 3.1.5.6.1 --- Grip traction test --- p.28, Chapter 3.1.5.6.2 --- Elevated body swing test --- p.28, Chapter 3.1.5.7 --- Statistical analysis --- p.28, Chapter 3.2 --- Establishment of in vitro model of primary mouse NSPs and the effect of TPO on their proliferation --- p.29, Chapter 3.2.1 --- Mouse embryo dissection for the extraction of NSP --- p.29, Chapter 3.2.2 --- Culturing of NSP --- p.30, Chapter 3.2.3 --- Immunofluorescence staining for stem cell markers --- p.31, Chapter 3.2.4 --- Neurosphere assay with different combinations of mitogens --- p.31, Chapter 3.2.5 --- Neurosphere assay with different concentrations of TPO --- p.32, Chapter 3.2.6 --- Neurosphere assay under hypoxia --- p.32, Chapter 3.2.7 --- Statistical analysis --- p.33, Chapter Chapter 4 --- Effects of thrombopoietin on neonatal rat models of hypoxia-ischemia brain damage --- p.39, Chapter 4.1 --- Summary of experimental settings --- p.39, Chapter 4.2 --- Results --- p.39, Chapter 4.2.1 --- Mortality --- p.39, Chapter 4.2.2 --- Effects of TPO on p7 mild damage model 1 week post-surgery --- p.40, Chapter 4.2.2.1 --- Body and brain weights --- p.40, Chapter 4.2.2.2 --- Gross injury score --- p.41, Chapter 4.2.2.3 --- Cortex and hippocampus area --- p.41, Chapter 4.2.2.4 --- Blood cell counts --- p.42, Chapter 4.2.3 --- Effects of TPO on p7 severe damage model 1 week post-surgery --- p.43, Chapter 4.2.3.1 --- Body and brain weights --- p.43, Chapter 4.2.3.2 --- Gross injury score --- p.43, Chapter 4.2.3.3 --- Cortex area --- p.44, Chapter 4.2.3.4 --- Blood cell counts --- p.44, Chapter 4.2.4 --- Effects of TPO on p7 severe damage model 3 week post-surgery --- p.45, Chapter 4.2.4.1 --- Body and brain weights --- p.45, Chapter 4.2.4.2 --- Gross injury score --- p.46, Chapter 4.2.4.3 --- Blood cell counts --- p.46, Chapter 4.2.4.4 --- Functional outcomes --- p.46, Chapter 4.2.5 --- Effects of TPO on pl4 severe damage model 1 week post-surgery --- p.47, Chapter 4.2.5.1 --- Body and brain weights --- p.47, Chapter 4.2.5.2 --- Gross injury score --- p.48, Chapter 4.2.5.3 --- Cortex area --- p.48, Chapter 4.2.5.4 --- Blood cell counts --- p.49, Chapter 4.3 --- Discussion --- p.49, Chapter Chapter 5 --- Effects of thrombopoietin on the proliferation of primary mouse neural stem/ progenitor cells in culture --- p.83, Chapter 5.1 --- Summary of experimental settings --- p.83, Chapter 5.2 --- Results --- p.83, Chapter 5.2.1 --- Effect of EGF or bFGF withdrawal on NSP proliferation --- p.84, Chapter 5.2.2 --- Dose effect of TPO treatment on NSP proliferation --- p.85, Chapter 5.2.3 --- Effect of hypoxia --- p.85, Chapter 5.2.4 --- Effect of TPO treatment in combination with hypoxia --- p.86, Chapter 5.2.5 --- Detection of neural progenitor cell marker --- p.87, Chapter 5.3 --- Discussion --- p.88, Chapter Chapter 6 --- General discussion --- p.101, Bibliography --- p.106, http://library.cuhk.edu.hk/record=b5893561, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Hypoxia is a common patho-physiological phenomenon in many types of diseases, including tumors, myocardial infarction and cerebral ischemia. It is believed that hypoxia not only affects the cellular regulation pathways, but also interferes genome, transcriptome and proteome inside tumor, eventually enhances tumor development by increasing malignancy and metastatic potential, induction of resistance towards radiotherapy and chemotherapy, activation of angiogenic mechanism, etc. One of the major biological events for hypoxia is induction of apoptosis, which is believed to provide a selective pressure for tumor progression. However, the mechanism of hypoxia induced apoptosis is not well established. In the present study, the molecular mechanism of hypoxia induced apoptosis was investigated and was found to be different in human squamous carcinoma A431 cells and human hepatocellular carcinoma HepG2 cells. In HepG2 cells, the conventional intrinsic apoptotic pathway that involved the activation of caspase-9 and -3 was found to be triggered by hypoxia through a newly identified p53 - Bnip-3 shunt. On the other hand, caspase-4 and -10 were found to be activated under hypoxia and may be related to hypoxia induced DNA fragmentation in A431 cells. Reoxygenation prior to hypoxia is the event after blood reperfusion in tumor vasculature. It is demonstrated in this study that reoxygenation is a distinctive stress from hypoxia, and it is very likely to be induced by reactive oxygen species. Apart from apoptosis, the mechanism for the development of drug resistance after hypoxia is also not yet clearly identified. In this study, resistance towards several common chemotherapeutic drugs after cells were subjected to hypoxia/reoxygenation cycles were demonstrated. Among them, the possible role of the genes related to methotrexate and cisplatin resistance were also investigated., Ho Yiu Fung., "August 2006.", Adviser: Tim-Tak Kwok., Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1393., Thesis (Ph.D.)--Chinese University of Hong Kong, 2006., Includes bibliographical references (p. 159-176)., Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web., Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web., s in English and Chinese., School code: 1307., http://library.cuhk.edu.hk/record=b6074282, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Hypoxia is a common patho-physiological phenomenon in many types of diseases, including tumors, myocardial infarction and cerebral ischemia. It is believed that hypoxia not only affects the cellular regulation pathways, but also interferes genome, transcriptome and proteome inside tumor, eventually enhances tumor development by increasing malignancy and metastatic potential, induction of resistance towards radiotherapy and chemotherapy, activation of angiogenic mechanism, etc. One of the major biological events for hypoxia is induction of apoptosis, which is believed to provide a selective pressure for tumor progression. However, the mechanism of hypoxia induced apoptosis is not well established. In the present study, the molecular mechanism of hypoxia induced apoptosis was investigated and was found to be different in human squamous carcinoma A431 cells and human hepatocellular carcinoma HepG2 cells. In HepG2 cells, the conventional intrinsic apoptotic pathway that involved the activation of caspase-9 and -3 was found to be triggered by hypoxia through a newly identified p53 - Bnip-3 shunt. On the other hand, caspase-4 and -10 were found to be activated under hypoxia and may be related to hypoxia induced DNA fragmentation in A431 cells. Reoxygenation prior to hypoxia is the event after blood reperfusion in tumor vasculature. It is demonstrated in this study that reoxygenation is a distinctive stress from hypoxia, and it is very likely to be induced by reactive oxygen species. Apart from apoptosis, the mechanism for the development of drug resistance after hypoxia is also not yet clearly identified. In this study, resistance towards several common chemotherapeutic drugs after cells were subjected to hypoxia/reoxygenation cycles were demonstrated. Among them, the possible role of the genes related to methotrexate and cisplatin resistance were also investigated., Ho Yiu Fung., "August 2006.", Adviser: Tim-Tak Kwok., Source: Dissertation Abstracts International, Volume: 68-03, Section: B, page: 1393., Thesis (Ph.D.)--Chinese University of Hong Kong, 2006., Includes bibliographical references (p. 159-176)., Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web., Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web., s in English and Chinese., School code: 1307., http://library.cuhk.edu.hk/record=b6074282, Use of this resource is governed by the terms and conditions of the Creative Commons “Attribution-NonCommercial-NoDerivatives 4.0 International” License (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Summary: The uncontrolled release of glutamate is thought to be a key event in the death of the anoxic/ischemic mammalian brain. However the origin of glutamate, vesicular and/or cytoplasmic, is unknown. Likewise, the anoxic turtle releases a surge of glutamate upon anoxic depolarization. Therefore, this study investigated the origin of glutamate release in the isolated cerebellum of the freshwater turtle (Trachemys scripta). The results showed that: during anoxia, low extracellular glutamate levels are maintained, an ability lost during in vitro ischemia, by a reduction in glutamate release. Upon anoxic depolarization glutamate release originates from the cytoplasm. The lack of vesicular glutamate release is likely the result of an inhibition of vesicular exocytosis. However during in vitro ischemia, the inhibitory signal which blocks vesicular glutamate release during anoxia is lost. This allows a biphasic pattern of glutamate release during ischemia originating initially from vesicular stores which then causes cytoplasmic glutamate release., Collection: FAU Electronic Theses and Dissertations Collection, Thesis (M.S.)--Florida Atlantic University, 2001., Charles E. Schmidt College of Science

Summary: This study investigated the homeostasis of extracellular potassium ion concentration ([K+]e) and correlated energy levels in the anoxic frog brain (Rana pipiens). The results showed K+ ion homeostasis was maintained for 3hrs in anoxia. It confirmed a constant decline in brain ATP in anoxia. It was concluded that ion homeostasis in the frog does not rely on the maintenance of normoxic levels of ATP. When Na+/K+ATPase was inhibited, it was found that initial K+ efflux was decreased in the anoxic frog. This could be due to decreased ion permeability in anoxia, an adaptive strategy seen in other anoxic tolerant organisms. However, the study showed once a threshold [K+]e was reached, the final K + efflux pattern was unchanged. This [K+]e appears to represent a membrane potential threshold. Critical energy levels were determined representing the energy minimum to maintain ion homeostasis in the anoxic frog brain., Charles E. Schmidt College of Science, Degree granted: Thesis (M.S.)--Florida Atlantic University, 2000., Collection: FAU Electronic Theses and Dissertations Collection

OBJECTIVES: To study the changes after hypoxia-ischemia (HI), and to observe both, the vulnerability of the different regions of the brain to HI and the heat shock protein-72 kDa (HSP72) induction and its efects on the neuronal cell. MATERIAL AND METHODS: 7-days-old rats were exposed to left carotid artery ligation followed by 2 h of HI and then they were sacrificed at different time points. Brains extracted at 1-72 h were immunohistochemically study using the HSP-72 and the microtubule associated protein-2 (MAP2) stainings. Brains extracted at 1-4 weeks underwent histopathological study. RESULTS: Loss of MAP2 immunostaining was detected since the 1st hour post-insult, being highest at 24 h. MAP2 reappeared at 72 h in almost all the brain regions of the ligated hemisphere, except the hippocampal CA3 region. At 1-2 weeks post HI, we observed atrophic and cystic lesions. 15-20% of rats did not show any anatomical lesion up to 4 weeks post HI. The HSP72 synthesis was early in the dentate gyrus of the hippocampus, but a delayed induction was observed in the CA3 region; this region showed an increased vulnerability to HI. CONCLUSIONS: Absence of anatomical lesion was observed in 15-20% of rats exposed to HI. Atrophic or cystic lesions are observed since 1-2 weeks after the insult, despite an apparent immunohistochemical recovery at 72 h., OBJETIVOS: Observar las diferencias de vulnerabilidad de las diferentes regiones cerebrales frente a la hipoxia isquemia (HI), y la inducción de la síntesis de marcadores de injuria neuronal y su efecto posterior en la neurona. MATERIALES Y MÉTODOS: Se ligó la arteria carótida izquierda a ratas de 7 días de edad, seguido de 2 h de hipoxia, sacrificándolas a diferentes intervalos de tiempo. Se realizó un estudio inmunohistoquímico con la proteína del golpe del calor de 72 kDa (HSP72) y la proteína asociada al microtúbulo tipo 2 (MAP2) durante las primeras 72 h. RESULTADOS: La pérdida de inmunotinción del MAP2 se observó desde la 1 h, siendo máxima a las 24 h, pero a las 72 h se observó una reaparición en la mayoría de regiones del hemisferio izquierdo, excepto la región CA3 del hipocampo. Entre 1 y 2 semanas después se observó lesiones de tipo atrófico y cístico. 15-20% de ratas no sufrió daño anatómico hasta las 4 semanas. Hubo síntesis temprana de HSP72 en el giro dentado del hipocampo, mientras que en la región CA3 su inducción fue tardía, observándose aquí mayor vulnerabilidad a la HI. CONCLUSIONES: En 15 a 20% de ratas sometidas a HI no se observa daño anatómico hasta las 4 semanas. La lesión atrófica o cística se consolida entre 1 y 2 semanas después del insulto, a pesar de una aparente recuperación inmunohistoquímica a las 72 h.

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Marihuana, or its principal active ingredient, delta-9-tetrahydrocannabinol (delta9-THC), impairs performance on complex behavioral tasks in animals and man. Although there exists some evidence that altitude-induced hypoxia potentiates the physiological effects of marihuana, the interaction between altitude and marihuana on behavioral tasks has not been established., Two baboons were trained to perform on a delayed matching-to-sample task at ground level and altitudes of 8,000 and 12,000 feet. The animals were orally administered doses of delta9-THC, ranging from 0.25 to 2.0 mg/kg, 2 hours prior to experimental sessions at each altitude. No effects on accuracy of matching performance were observed for any of the drug doses or altitudes used. Amount of work output, as measured by number of trials completed and speed of responding, was not affected by delta9-THC at ground level but was markedly reduced by the higher drug doses at the 8,000- and 12,000-feet altitudes., This interaction suggests that the behavioral impairment produced by marihuana can be potentiated by hypoxia.

General aviation pilots are increasingly ascending to altitudes exceeding ten thousand feet. As one becomes exposed to heights above twelve thousand feet, blood oxygen saturation diminishes in accordance with a predicable schedule. Recommended measures for the provision of adequate supplemental oxygen are described.

To assess the effects of propranolol on tolerance to rapid decompression, a series of experiments was conducted measuring time of useful function (TUF) in rats exposed to a rapid decompression profile in an altitude chamber. In other experiments TUF was measured for rats exposed to an oxygen/nitrogen gas mixture which produced a hypoxic condition equivalent to that in the decompression experiments. The findings were, 1.Rats become less tolerant to hypoxia of an onset rate comparable to that of rapid decompression when given propranolol, and this intolerance is further exacerbated by an increase in physical exertion., 2.Younger animals are more susceptible to this type of hypoxia, but propranolol has no greater effect on hypoxia tolerance in younger animals., 3.None of the reduced tolerance can be attributed to a shift in the oxyhemoglobin dissociation curve., In rats the curve is shifted slightly to the left, whereas in man there is a reported shift to the right. Because propranolol impairs tolerance to hypoxia in experimental animals, it is important to assess its effects on human tolerance.

The report describes evaluation of two prototype phase dilution rebreathing masks as compared to an open port rebreathing mask design. Human subjects wearing the prototype masks and engaged in three minute periods of rest and exercise were exposed to altitudes of 14,000, 18,000, 25,000, 30,000 and 34,000 feet in an altitude chamber., Each subject was instrumented to obtain a variety of physiological parameters including end expiratory gas composition, blood oxygen saturation (ear oximetry), ECG, and respiratory rate (impedance pneumograph). Oxygen flow and system pressure as provided by an automatic constant-flow regulator were also determined. The automatic constant-flow regulator when used in conjunction with either of the prototype phase dilution rebreather test masks and proper orifices maintained the subjects' indicated blood oxygen saturations equal to or in excess of their ground level (1,273 feet) baselines., With the same oxygen flow rates the prototype porous and dilution valve masks provided higher tracheal oxygen partial pressures than the open port masks at all altitudes tested during rest and exercise. The prototype phase dilution rebreather masks appear to be more efficient since at the same flow rates a greater amount of oxygen was derived from the supply and less oxygen lost to the ambient environment as compared to the open port type mask.

The Supersonic Transport represents a quantum step in civil aeronautics. It will cruise at altitudes having low ambient gaseous pressures far exceeding human capacities for compensatory respiration. In consideration of this evolutionary step, tentative airworthiness standards with respect to SST pressurization capabilities in the event of depressurization emergencies are discussed and a series of evolved SST cabin altitude-time profiles, together with the basis of their development, are then presented.

The concept of time of useful consciousness fails to take into account the progressive decay that occurs in performance under hypoxic conditions. This study, using a means of quantitatively assessing such a decrement, presents data obtained in a series of chamber runs at 27,500 and 35,000 feet. The performance-decrement functions appear to follow the arterial-oxygen-saturation curves.

This report present some of the technical background necessary for understanding the aeromedical importance of sickle-cell disease and the sickle-trait carrier, whose erythrocytes contain mixtures of hemoglobin S and normal hemoglobin A. This carrier state (type AS) is not limited to Negroes; it has been found, with lower frequency, in people exhibiting no evidence of African inheritance., Reports of type AS people who died suddenly, exhibiting sickle cells at necropsy, and other reports of sickling crises in these individuals at mild altitudes, have led some authors to conclude that airmen and air passengers who are type AS are at considerable risk. Other reports, particularly those based on the flying experiences of large numbers of pilots with sickle trait, as well as on the results of experimental exposures of type AS people to simulated altitude, indicate that isolated instances of sudden death and altitude intolerance are infrequent in this genotype.

The ultimate limitations in flight performance and in future civil air carrier equipment are the limitations imposed by what may be termed “human tolerances.” This is particularly applicable to the matter of the supersonic transport. The discussion of man’s maximum adaptive capacities for the majority of stresses potentially encountered in atmospheric and transatmospheric flights points to the weakest links in the man-machine complex of air and space transportation. An attempt is made to point out the means by which the human tolerances can be maximally adapted to the advanced technology.

Ten healthy female pilots, 20-49 years old and weighing more than 110 pounds were tested for tolerances to hypoxia orthostatic stress, and physical work at 1 and 3 d after donating about 450 mL of blood on one occasion, and 6 mL (sham control) on a second separate occasion. Testing included consecutive 30-min seated exposures to each of four oxygen-nitrogen mixtures (equal to air breathing at 6,000, 8,000, 10,000 and 12,400 ft of altitude), 5 min of quiet standing, and seated pedal ergometry graded to produce a heart rate of 140 beats per min., The findings of this study indicated that, if the complete absence of adverse symptoms at ground level, a pilot may return to flying between 1 and 3 d after blood donation with the recommended initial precautions that: cabin altitude be limited to 6,000 during flight; and +Gz stress exceeding the equivalent of short-duration level turns at 30 deg of bank angle be avoided. Until complete restoration of the pilot's in-flight physiological tolerances has occurred, the presence of a copilot and on-board availability of supplemental oxygen are also recommended.

Ten healthy men, 20-35 years old, were tested for tolerance to hypoxia, orthostatic stress, and physical fatigue after a period of rest, and, on another occasion, after a period of physical exertion. Exertion consisted of four 10-min periods of pedal ergometry; each period consisted of a 30-watt (W) load imposed for 2 min, 60 W for 4 min, and 100 W for 4 min. Testing included a 100-min exposure to an oxygen/nitrogen gas mixture equivalent to 3658 m of altitude, 2 min of lower body negative pressure (LBNP) at -40 torr differential pressure, and 6 min of 50 W pedal ergometry. Psychomotor testing was conducted during hypoxic exposure., Although some statistically significant (p or = 0.05) physiological decrements were associated with prior physical exertion, psychomotor performance and mentation were not significantly affected. In this study, prior physical exertion produced no adverse effects on physiological tolerances, mentation, or psychomotor performance.

In a study of 54 human subjects using three alcohol consumption levels and three simulated cabin conditions it was found that alcohol caused an increase in heart rate and an increase in skin temperature. Internal body temperature was lower with alcohol but did increase as blood alcohol levels decreased. The performance tests used apparently were not critical enough to detect differences due to single influences. Blood alcohol determinations for subjects receiving the high level of alcohol yielded significantly higher levels of blood alcohol for subjects at 20,000 ft. than at the other altitudes. However, the readings at 20,000 ft. were not significantly different than readings obtained at the other altitudes for subjects receiving the lower dose of alcohol.

This report continues a review (see FAA-AM-76-15) of the evidence for mixed dominance of the Hbs beta gene in people with the sickle cell trait. These individuals, whose erythrocytes contain a mixture of hemoglobins (HbA/HbS), are healthy and have a normal life expectancy. They are tolerant to moderate altitudes; their erythrocytes become sickled only at oxygen tensions that would be hazardous to any person., However, there is a possibility that other debilitating factors (e.g., alcoholism, pulmonary disorders) can, in a small fraction of those with the trait, produce an abnormal susceptibility to hypoxia. Those so debilitated would not be medically qualified to serve as air crewmembers. This report presents an experimental plan for estimating the proportion of such individuals in a population of young people with the sickle trait and outlines methods to be used in the study.

Twenty rats were given propranolol, 1.8 mg/kg body weight, by mouth for 12 days. On day 13, these and 20 control rats were tested for time of useful function (TUF) after rapid decompression in a hypobaric chamber. The criterion for TUF was the animal's ability to remain upright in a motor-driven exercise wheel. The decompression profile was achieved by rapidly reducing the pressure to a level equivalent to an altitude of 34,000 ft (10,363 m), holding for 1 min, then recompressing and holding at 29,000 ft (8,839 m) for the remainder of the test. On day 13 the propranolol-treated rats had a significant shift to the right in the oxygen-hemoglobin dissociation curve (ODC), their average P50 was about 3.5 torr greater than that of control animals. Although shifts to the right in the ODC normally occur during adaptation to altitudes, this was of no advantage to the drug-treated group, which had an average TUF of only about 170 s (approximately 50 s less than that of control rats). This finding is consistent with the results of Eaton et al., who found that rats with left-from-normal shifts in the ODC survived longer than did control rats at altitudes approximatley equal to those used in the present study. In other expermients we showed that one metabolite of propranolol, 4-hydroxypropranolol, can produce rightward shifts in the ODC. This result may help explain why chronic administration of the drug causes such shifts, though its concentration in the blood is far less that that required to produce the effect in vitro. Decrements in the TUF seen in these and other (FAA Office of Aviation Medicine Report No. AM-79-10) experiments were probably the result of several mechanisms, including shifts in the ODC, central depression, and cardiovascular effects.

Regionalization of specialized perinatal care is a fully viable and progressing concept. The two major components of regionalized care are the level III care facility and the air transport service. In descending importance, the medical transport team, the pilot and aircraft, and related technology and equipment are the three most important components of the transport service., Although significant reductions in perinatal morbidity and mortality have already resulted from development of regional care, additional progress is possible and desirable. Areas of possible improvement are: earlier precrisis diagnosis of maternal and/or fetal risk at level I care; supplementary training of medical transport personnel in perinatal aspects of Aviation Medicine, Physiology, and Safety; technology or preflight stabilization of the pregnant mother or the neonate; adjunct medical training of transport pilots; exclusive use of multiengine, fixed-wing, all-weather aircraft; and technology of in-flight life support and monitoring equipment and methods.

A new design, hanging, quick-don crew pressure breathing oxygen mask applicable to jet-transport operations was tested and evaluated in three phases, consisting of (1) exposing five masked subjects to a stepwise altitude-chamber flight profile with a maximum altitude of 43,000 feet; (2) rapidly decompressing five masked subjects from 8,000 to 40,000 feet in 45 to 50 seconds; and (3) similarly decompressing these subjects and donning the mask during the decompression., Donning was accomplished in 2.5 to 6.3 seconds after the donning signal, at altitudes varying between 28,000 to 31,000 feet. When used with a pressure-breathing regulator incorporating the military pressure-breathing schedule, the mask maintained subjects in a satisfactory physiological condition at 43,000 feet. When worn prior to and during a rapid decompression, the mask provided adequate protection. When donned during the rapid-decompression profile, there was a significant transient decrease in blood saturation without loss of consciousness followed by a rapid recovery of blood saturation.

The paper describes altitude chamber experiments conducted with human subjects using a new continuous-flow disposable passenger mask applicable for emergency use to maximum altitudes of 41,000 feet. This mask design differs in configuration from the previous omni-directional maska designed to meet the requirements of Nationaal Aerospace Standard 1179 and FAA Technical Standard Order C-64 in that the inner face flap or seal has been eliminated and the cylindrical shape reduced to a modified cone. The primary goal of this study was to determine if design modification of the mask induced an increase or decrease in physiological efficiency.

Twelve healthy young men were evaluated in each of four experimental conditions involving the possible combinations of two exercise conditions given prior to performance testing (1 h of heavy exercise vs. no exercise) and two altitude conditions (ground level vs. 12,500 ft) which were administered during performance testing. Performance was measured during a 2 1/4-h test session with the Multiple Task Performance Battery (MTBP) which involved time-shared performance in monitoring of warning lights and meters, mental arithmetic, problem solving, and tracking., Heart rate was statistically higher after exercise than after no exercise and statistically higher at 12,500 ft than at ground level. Norepinephrine excretion was higher during exercise experiments than during no-exercise experiments. There was no altitude effect for this measurement. The overall composite score of MTPB performance was significantly lower at 12,500 ft than at ground level. The adverse effect of higher altitude was greatest in the tracking task. The 1-h period of vigorous physical exercise had no statistically significant main effect on overall MTPB scores., Residual effects of exercise resulting in increased arousal may account for the tendency for performance to be slightly higher in the case of problem solving. The interaction of altitude with exercise was also significant in the case of tracking performance. The most important aspect of the interaction was that tracking performance was significantly better at 12,500 ft following exercise. This finding is possibly due to the increase in cardiovascular circulation induced by prior exercise and exercise "breaks" should be examined in future research.