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Because differences often exist between species in their tolerances to environmental conditions, locations characterized by extreme parameter values (i.e., high temperature, low DO, high turbidity) may provide refuges from predation or competition by altering the outcome of inter-species interactions. This thesis examined the effects and relative importance of water temperature, dissolved oxygen (DO) and turbidity on habitat use by fish species and resulting changes in community composition. The effects of abiotic factors on predator-prey interactions were tested using field surveys, laboratory experiments, field experiments and computer modeling. Field surveys were conducted in Blind Channel, Delta Marsh, Manitoba, and on Lake Winnipeg, Manitoba, to determine if small bodied forage species preferentially used high temperature, low DO or high turbidity habitats and whether predator species avoided these locations. Prey species were more abundant in these extreme locations at both small (Blind Channel) and large (Lake Winnipeg) spatial scales, but predator avoidance was only documented in Blind Channel. The tolerances of fish species to moderate hypoxia (< 3 mg/L DO) was tested in the laboratory to verify that differences did exist among species and that the observed species distributions were not solely the effect of temperature. To quantify the potential for moderately hypoxic locations to provide a refuge from predation for small fish, a field manipulation was conducted in Blind Channel; hypoxic habitats were created without altering water temperature, decoupling the natural covariation between these two factors that occurs in aquatic systems. The abundance of small forage fish was higher in the hypoxic locations compared to controls and while predators still visited the hypoxic habitats, their mean visit duration was reduced from around 300 min to less than 1 min. An individual based computer model was used to test and illustrate current understanding of the relative importance of temperature, DO and turbidity on predator habitat selection decisions and fish community composition. The model showed that DO had a stronger effect on community composition than temperature, and that reduced foraging success from high turbidity was able to overpower the other two factors. Hypoxia affects habitat selection decisions by fish species and can provide refuges from predation and competition, helping maintain higher species diversity. Water temperature appears to have a weaker effect on fish distributions than DO while turbidity primarily affects visual predators, though the strength of turbidity effects depends on the magnitude and duration of individual events.

Modular tissue engineering involves assembling tissue constructs with integral vasculature from units containing adipose-derived mesenchymal stromal cells (adMSCs) and endothelial cells. Here, the effects of implant volume and adMSC density on the vascularization of modular tissues were explored. Both parameters affected the contributions of host- and graft-derived vessels, without affecting total vessel density. Increasing implant volume from 0.01 to 0.10 mL increased HIF1&alpha; expression and graft-derived vessel density, suggesting a role of hypoxia in graft-derived vessel formation. However, increasing adMSC density within small-volume implants did not increase HIF1&alpha; expression. Vascularization of small-volume implants of high (4.3&bull;10^6 cells/mL) and low (1.0&bull;10^6 cells/mL) adMSC densities was dominated by host vessel ingrowth at day 7. By increasing adMSC density, a high proportion of host-derived vessels was maintained to day 14, presumably via paracrine effects. Further dissection of the role of hypoxia in modular tissue engineering remains a promising avenue to pursue.

Modular tissue engineering involves assembling tissue constructs with integral vasculature from units containing adipose-derived mesenchymal stromal cells (adMSCs) and endothelial cells. Here, the effects of implant volume and adMSC density on the vascularization of modular tissues were explored. Both parameters affected the contributions of host- and graft-derived vessels, without affecting total vessel density. Increasing implant volume from 0.01 to 0.10 mL increased HIF1&alpha; expression and graft-derived vessel density, suggesting a role of hypoxia in graft-derived vessel formation. However, increasing adMSC density within small-volume implants did not increase HIF1&alpha; expression. Vascularization of small-volume implants of high (4.3&bull;10^6 cells/mL) and low (1.0&bull;10^6 cells/mL) adMSC densities was dominated by host vessel ingrowth at day 7. By increasing adMSC density, a high proportion of host-derived vessels was maintained to day 14, presumably via paracrine effects. Further dissection of the role of hypoxia in modular tissue engineering remains a promising avenue to pursue.

Antarctic fish from the Perciform suborder Notothenioidei inhabit arguably the most thermally stable ocean environment on earth. In order to populate the subzero environment Antarctic fish have evolved numerous adaptations. However, specialisation to -1.9°C has incurred a trade off, thermal flexibility is lost likely due to modifications to the cold and as a result Notothenioidei are extremely stenothermic. Climate change mediated warming is predicted to increase the ocean temperature surrounding the Antarctic continent by 2°C within the next century. This increase is projected to affect individuals, populations and the community structures of those inhabiting the area and therefore the physiological study of the acclimation ability and thermal limitations of Antarctic fish is an area scientific interest. The present study is a series of discrete experiments relating to one species, Trematomus bernacchii, a circumpolar benthic Notothenioidei found in nearly all inshore waters surrounding the Antarctic coastline. These studies included investigation of the response of this species to both chronic and acute temperature exposure prior to and following a feeding event, a reduction in environmental oxygen and an exhaustive exercise event, as well as examination of T. bernacchii ability to recovery from these challenges. T. bernacchii demonstrated variable success when acclimated to +3°C. Failure appeared to be determined by the recovery period following capture and aquarium housing, 7 days housing following capture resulted in 100% mortality, conversly 3 months resulted in 100% survival. Following successful acclimation T. bernacchii showed physiological adjustment as acclimated resting metabolic rate mirrored that of T. bernacchii tested at environmental temperature, 20.63 ± 1.3 compared to 22.38 ± 1.02 mg. O₂. kg⁻¹. h⁻¹. The previously undefined specific dynamic action response (SDA), in T. bernacchii was characteristic of polar species. At environmental temperatures SDA scope was small 14.52 ± 3.52 mg O₂. kg⁻¹. h⁻¹, and lengthy ,72 hours; SDA duration was reduced to 9 hours in acclimated fish. Resting metabolic rate was elevated following acute exposure to +3°C, 34.27 ± 2.35 mg O₂. kg⁻¹. h⁻¹, masking the SDA response and associated parameters. T. bernacchii were relatively sensitive to hypoxia, Pcrit over four acute temperature exposures, ranged between 69 and 102mmHg, higher than the average range for teleosts (40 – 60 mmHg). Above -1°C Pcrit increased, rising with acute temperature exposure. Ventilation rate was temperature dependent and completely absent at +4 and +6°C. A bradycardia (beginning at 60 and 70mmHg) was observed at all temperature exposures, this response was consistent as all heart rates reduced by 25%. Recovery from both hypoxia and acute temperature exposure was rapid. Following an exhaustive exercise event aerobic Scope of T. bernacchii was constrained over an acute temperature increase, reducing from 38.58 ± 5.64 to 24.41 ± 4.92 mg.O₂. kg⁻¹.h⁻¹ over a 7°C temperature increase, respiratory scope too was reduced such that at +4 and +6°C scope was absent. Heart rate of T. bernacchii was highly constrained at -1°C, increasing by 2.54 ± 0.9 bpm following exercise. Acute temperature increase resulted in an increase in cardiac scope, maximum 6.29 ± 1.2 bpm at +2°C, due likely to a thermally mediated loss of cholinergic tonus following exhaustive exercise. Recovery of all parameters was temperature dependent and rapid upon return to -1°C. The present study is the first to quantify and assess the effect of acute and chronic temperature exposure on the SDA response of T. bernacchii. Furthermore, it supplements the current literature on acclimation ability, acute temperature exposure, aerobic scope and hypoxia tolerance for this species. This work will be of use in future investigations of the effects of rapid climate change on Antarctic notothenioid fish and the interconnected ecosystem.

Noninvasive measurements of myocardial carboxymyoglobin levels (%MbCO) and oxygen tensions (PtO2) are difficult to obtain experimentally. We have developed a compartmental model which allows prediction of myocardial %MbCO levels and PtO2 for varied carbon monoxide (CO) exposures. The cardiac compartment in the model consists of vascular subcompartments which contain two tissue subcompartments varying in capillary density. Mass-balance equations for oxygen (O2) and CO are applied for all compartments. Myocardial oxygen consumption and blood flow are quantified from predictive formulas based on heart rate. Model predictions are validated with experimental data at normoxia, hypoxia, exercise and hyperoxia. CO exposures of varying concentration and time (short-high, long-low), CO rebreathing during 100% O2, and exposure during exercise is simulated. Results of the simulations demonstrate that during CO exposures and subsequent therapies, the temporal changes of %MbCO in the heart differ from those of carboxyhemoglobin levels (%HbCO). Analysis of correlation between %HbCO, %MbCO and PtO2 was done to understand myocardial injury due to CO hypoxia. This thesis demonstrates that the model is able to anticipate the uptake and distribution of CO in the human myocardium and thus can be used to estimate the extravascular burden (MbCO, PtO2 ) of CO on the human heart.

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Hypoxia can result in brain injury. Hypoxic brain injury can also result in excess stress hormones and activated immune responses. In this study, we examined multiple spontaneous motor behaviors, concentrations of stress hormones, and gene expression of immune responses in rats after perinatal hypoxia. Hypoxic animals exhibited impaired spontaneous motor behaviors in several tests. Perinatal hypoxia also caused increased levels of stress hormones and altered expression of genes associated with adaptive and innate immunity at different time points after hypoxia exposure. Findings demonstrate stress hormones and immune responses are available to play an important role in perinatal brain injury and can impact delayed behavioral development.

Prolonged prenatal hypoxia has shown to cause fetal growth restriction inchickens due to restricted oxygen to the somatic tissue. The body goes through a critical periodof development. Insults during this critical period may have lifelong effects on the individual.Currently heart failure is treated either with symptomatic therapy using diuretics or by targetingthe renin-angiotensin-aldosterone system. Developing new successful treatments is importantwith the aging population and the increased rate of heart failure. Previous studies have shownsystolic contractile dysfunction in 5 week old broiler chicken hearts when the eggs have beenincubated in hypoxia until hatching. S100A1 in cardiomyocytes regulates the calcium-controllednetwork which plays a big role in cardiac contractility and in this study, using qPCR on S100A1(GOI), GADPH and β-actin to try and determine if the changes made to the heart while the fetusis developing is due to a lack of S100A1 expression resulting in a decreased handling of Ca2+uptake which causes contractile dysfunction A Roche Lightcycler 480 was used together with theRoche template running triplets of each sample at 15-15-15 seconds for 45 cycles No statisticalsignificance was observed between the control group and the experimental group. However inthis study only S100A1 gene is being considered but a better understanding of the whole S100family might give a better understanding of mechanisms causing the progressive deterioration ofcardiac function